Overall Cortisol Health Benefits

• Improves blood sugar levels [1-11]
• Fights cancer [12-52]
• Boosts immune function [53-78]
• Fights inflammation [79-106]

Cortisol Imbalance

In order to cope up with stressful situations, your body produces the right amount of cortisol. However, if you have a medical condition known as Cushing’s syndrome, your cortisol levels will remain elevated for prolonged periods of time. In this case, you may experience the following symptoms:

• Acne
• Facial hair in women
• High blood pressure
• Increased thirst
• Irregular menstrual periods.
• Mood changes
• Muscle weakness
• Osteoporosis
• Rapid weight gain, particularly in the face, chest and abdomen contrasted with slender arms and legs.
• Skin bruises
• Thinning of the skin results in delayed wound healing.
• Urinary frequency

On the other hand, some people can also experience cortisol deficiency. Medical conditions such as adrenal insufficiency and Addison’s disease can cause low cortisol levels. If you have these conditions, you may experience the following symptoms:

• Abdominal pain
• Darkening of regions of the skin
• Extreme fatigue
• Muscle weakness
• Nausea and vomiting
• Weight loss

If you experience any of these symptoms, consult with your doctor immediately to determine the best course of action. Typically, your doctor will conduct blood test, saliva test, and urine test to determine your cortisol levels. Your doctor may also order an MRI or CT scan if he or she suspects that a tumor is causing your cortisol imbalance.

Proven Benefits of Cortisol Replacement Therapy

If your body is not producing sufficient amounts of cortisol, your doctor may prescribe cortisol replacement therapy. When used as a medication, cortisol is known as hydrocortisone or corticosteroids. There is compelling evidence that restoring cortisol to healthy levels yields diverse health benefits:

Improves Blood Sugar Levels

One of the vital functions of cortisol is to restore body homeostasis by regulating blood sugar levels. Because of this ability, cortisol may help bring down elevated blood sugar levels, making it beneficial in patients with diabetes and those with uncontrolled blood sugar levels. There are several studies supporting the anti-diabetic effects of cortisol:

1. Cortisol reduces blood sugar levels by increasing glucose uptake and usage in the brain, heart, and muscles. [1]
2. In older men and women, higher cortisol levels were associated with decreased insulin levels, suggesting that cortisol improves blood sugar level by allowing insulin to enter into the cells. [2]
3. In patients with Schmidt syndrome, a combination of autoimmune adrenal insufficiency (Addison’s disease), hypothyroidism and/or type 1 diabetes mellitus, cortisol replacement therapy prevented the incidence of hypoglycemia (low blood sugar levels). [3]
4. A 2018 study published in the Frontiers in Endocrinology found that cortisol replacement therapy reduces the risk of impaired glucose tolerance. [4]
5. In hypopituitary adults, cortisol replacement therapy improved glucose tolerance. [5]
6. A 2009 study published in the European Journal of Clinical Investigation found that cortisol replacement therapy can help prevent insulin resistance and glucose intolerance. [6]
7. A 2019 study published in the Endocrinology and Metabolism found that patients with severe hypoglycemia had an impaired cortisol response. [7-11]

Fights Cancer

Cortisol, along with other glucocorticoids, can potentially improve the health of cancer patients. Evidence suggests that cortisol targets malignant cells and suppresses their reproduction:

1. A 2017 study published in Oncotarget found that cortisol and other glucocorticoids enhance the effect of cytotoxic anti-cancer drugs by affecting glucose breakdown of cancer cells. [12]
2. A 2018 study published in Cell Death & Disease found that glucocorticoids induce apoptosis (programmed cell death) thus inhibiting tumor growth. [13]
3. In a mouse model of lymph node cancer, glucocorticoids caused tumor regression. [14]
4. In various tumor systems, pharmacologic doses of glucocorticoids also inhibited growth of malignant cells. [15]
5. Tissue culture studies confirmed that glucocorticoids can kill malignant cells by affecting their DNA, RNA, and protein synthesis. [16]
6. In certain lymphoid cell populations, glucocorticoids have been found to induce apoptosis and impaired glucose transport of cancer cells. [17-18]
7. In patients with acute lymphoblastic leukemia, glucocorticoids treatment resulted in significant improvement of symptoms. [19-27]
8. When combined with chemotherapeutic drugs, glucocorticoids prevent relapse with little toxicity. [28-33]
9. In patients with Hodgkin disease, glucocorticoid therapy is associated with a complete response rate around 30 to 50%. [34-36]
10. When combined with interferon-α2b, glucocorticoids is associated with 85% overall response rate and 86% 3-year survival rate. [37]
11. Glucocorticoids also improved general feeling of well-being and appetite in cancer patients. [38-39]
12. Glucocorticoids also reduced excess calcium levels in cancer patients undergoing chemotherapy. [40]
13. In patients with primary and metastatic brain and spinal cord tumors, glucocorticoids ameliorated symptoms such as edema after several days of treatment. [41-46]
14. Glucocorticoids also decreased the severity of vomiting in cancer patients undergoing chemotherapy. [47-50]
15. In patients with nonsmall-cell lung cancer, glucocorticoid administration prevented lung injury associated with the treatment. [51-52]

Boosts Immune Function

Studies show that cortisol and other glucocorticoids can help ward off a wide array of diseases by boosting the immune function:

1. Glucocorticoids have been shown to play a role in the development and homeostasis of T lymphocytes. [53]
2. Cortisol mobilizes immune cells, preparing the body to mount an immune response. [54-57]
3. Cortisol augments the immune function by suppressing early proinflammatory responses. [58]
4. Cortisol boosts immune function by increasing blood T-cell and NK cell numbers. [59]
5. Cortisol increases glucose metabolism and cardiovascular activity to support the “fight or flight” response. [60-61]
6. Cortisol can enhance the function of the immune cell Th2, such as production of immunoglobulin E (IgE). [62-66]
7. Cortisol modulates the production of pro-inflammatory cytokines in the body. [67-70]
8. In an animal model of stimulated stress, it has been found that cortisol increases the immune cells Mx and IL-1β. [71]
9. Cortisol activates cellular immunity to provide defense against many kinds of infection by promoting Th1-to-Th2 shift. [72-74]
10. Stress-induced increases in cortisol may help reduce the risk of infections by mobilizing cells of innate immunity into sites of inflammation. [75-77]
11. In HIV-infected patients, cortisol has been found to regulate immune function by stimulating humoral immunity. [78]

Fights Inflammation

There’s also strong scientific evidence suggesting that cortisol is a potent anti-inflammatory hormone which is known to protect against a wide array of inflammatory conditions:

1. Cortisol protects against nerve damage caused by inflammation. [79]
2. Cortisol has been found to work like nonsteroidal anti-inflammatory drugs (NSAIDs) by inhibiting prostaglandins and leukotrienes, which are the two main products of inflammation. [80]
3. Cortisol also suppresses cyclooxygenase, a key enzyme involved in the inflammatory process. [81]
4. A 2007 study published in the Journal of Internal Medicine found that impaired cortisol response is associated with increased risk for inflammatory conditions such as coronary heart disease. [82]
5. Several studies found that low-grade inflammation is highly associated with impaired cortisol response during acute and chronic stress. [83-88]
6. Studies also found that various inflammatory markers such as IL-6, IL-10, and TNF-α are all sensitive to the anti-inflammatory effects of cortisol. [89-94]
7. Studies found that cortisol suppresses the production of pro-inflammatory cytokines and chemokines, cell adhesion molecules, and key enzymes involved in the inflammatory process.[95-97]
8. Several studies also found that cortisol inhibits the production of inflammatory markers such as NFκB, AP-1, and annexin AI (AnxA1). [98-101]
9. In a mouse model of inflammation, cortisol suppressed carrageenin-induced edema, zymosan-induced peritonitis, and antigen-induced arthritis. [102-103]
10. A 2010 study published in the Current Vascular Pharmacology found that cortisol prevents the progression of atherosclerosis and the development of acute coronary syndrome. [104]
11. A 2019 study published in Medicine Baltimore found that glucocorticoids are associated with inhibiting excessive inflammatory response in patients with community acquired pneumonia. [105]
12. A 2009 study published in Annals of Medicine found that impaired cortisol response is associated with higher incidence of coronary artery disease. [106]

References

1. Macfarlane DP, Forbes S, Walker BR. Glucocorticoids and fatty acid metabolism in humans: fuelling fat redistribution in the metabolic syndrome. J Endocrinol. 2008;197(2):189-204.
   View Summary +

   Glucocorticoids and fatty acid metabolism in humans:

   The article “Glucocorticoids and fatty acid metabolism in humans: fuelling fat redistribution in the metabolic syndrome” by Macfarlane DP, Forbes S, and Walker BR, focuses on the role of glucocorticoid hormones in stress response and their impact on various metabolic functions. Key points include:

   Glucocorticoids and Metabolic Impact:

   Glucocorticoid hormones are central to the body’s stress response. They have significant effects on raising blood pressure, inducing insulin resistance, increasing protein catabolism, and elevating plasma glucose.

   Paradox in Weight Effects:

   Despite their acute lipolytic (fat-breaking) effect, glucocorticoids do not lead to long-term weight loss in humans. This presents a paradox in their metabolic effects.

   Influence on Glucose and Fatty Acid Metabolism:

   The article reviews how glucocorticoids impair peripheral glucose uptake and cause hepatic insulin resistance. It also discusses the less-understood impact of glucocorticoids on fatty acid metabolism.

   Implications for Metabolic Syndrome:

   The paper explores the acute versus chronic effects of glucocorticoids on fat accumulation, their effects in different adipose depots, and the potential role of glucocorticoid signalling in the development and treatment of the metabolic syndrome.
   For further details, you can access the full article through this link:
   https://pubmed.ncbi.nlm.nih.gov/18434349/

2. Kamba A, Daimon M, Murakami H, et al. Association between Higher Serum Cortisol Levels and Decreased Insulin Secretion in a General Population. Nishimura W, ed. PLoS ONE. 2016;11(11):e0166077. doi:10.1371/journal.pone.0166077.
   View Summary +

   Association between Higher Serum Cortisol Levels and Decreased Insulin Secretion in a General Population

   The study by Kamba et al., “Association between Higher Serum Cortisol Levels and Decreased Insulin Secretion in a General Population,” examines the relationship between serum cortisol levels and insulin secretion in 1,071 Japanese individuals. The research found that higher cortisol levels are significantly associated with decreased insulin secretion, independent of insulin resistance. This indicates that elevated cortisol levels, even within normal physiological ranges, can suppress pancreatic ß-cell function, which is a crucial factor in the development of diabetes. These findings suggest that higher serum cortisol levels could be a risk factor for future diabetes onset.
   For more details, you can read the full study:
   https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0166077
   

3. Newton CA, Sheehan E, Wyne K, Cusi K, Leey J, Ghayee HK. The Yin and Yang Between Plasma Glucose Levels and Cortisol Replacement Therapy in Schmidt’s Syndrome. J Investig Med High Impact Case Rep. 2017;5(3):2324709617716203. Published 2017 Jul 6. doi:10.1177/2324709617716203.
   View Summary +

   The Yin and Yang Between Plasma Glucose Levels and Cortisol Replacement Therapy in Schmidt’s Syndrome
   

   The study “The Yin and Yang Between Plasma Glucose Levels and Cortisol Replacement Therapy in Schmidt’s Syndrome” by Newton et al. investigates how steroid replacement in adrenal insufficiency affects hypoglycemia in patients with type 1 diabetes mellitus (T1D). The case study focused on a 36-year-old female with T1D and Addison’s disease (Schmidt’s syndrome), who experienced recurrent hypoglycemia despite being on appropriate doses of hydrocortisone. The use of continuous glucose monitoring technology revealed a pattern of nocturnal hypoglycemia, linked to the short half-life of oral hydrocortisone and the consequent decline in evening plasma cortisol levels. Adjusting her hydrocortisone dosage and adding prednisolone in the evening resolved these episodes. This case illustrates that patients with Schmidt’s syndrome may be prone to nocturnal hypoglycemia due to inadequate steroid replacement, highlighting the need for precise management in these patients​​.
   For more detailed information, you can access the study:
   https://pubmed.ncbi.nlm.nih.gov/28748191/
   

4. Graziadio C, Hasenmajer V, Venneri MA, Gianfrilli D, Isidori AM, Sbardella E. Glycometabolic Alterations in Secondary Adrenal Insufficiency: Does Replacement Therapy Play a Role?. Front Endocrinol (Lausanne). 2018;9:434. Published 2018 Aug 3. doi:10.3389/fendo.2018.00434.
   View Summary +

   Glycometabolic Alterations in Secondary Adrenal Insufficiency: Does Replacement Therapy Play a Role?

   The study “Glycometabolic Alterations in Secondary Adrenal Insufficiency: Does Replacement Therapy Play a Role?” by Graziadio et al. reviews the impact of glucocorticoid replacement therapy on glycometabolic alterations in secondary adrenal insufficiency (SAI). SAI, a potentially life-threatening endocrine disorder, is characterized by impaired corticotropin (ACTH) secretion due to issues in the hypothalamus or pituitary gland. The review highlights that inappropriate glucocorticoid replacement therapy in SAI, especially in terms of dosage and timing, could be linked to various metabolic issues such as hypertension, insulin resistance, weight gain, and diabetes. The study examines the effects of different glucocorticoid replacement therapies on glycometabolic alterations in SAI, emphasizing the need for novel regimen schemes and treatments that better mimic the endogenous cortisol rhythm and potentially improve cardiovascular risk, glucose metabolism, and overall quality of life.
   For more detailed information, you can access the full study:
   https://pubmed.ncbi.nlm.nih.gov/30123187/

5. Al-shoumer KA, Beshyah SA, Niththyananthan R, Johnston DG. Effect of glucocorticoid replacement therapy on glucose tolerance and intermediary metabolites in hypopituitary adults. Clin Endocrinol (Oxf). 1995;42(1):85-90.
   View Summary +

   Effect of glucocorticoid replacement therapy on glucose tolerance and intermediary metabolites in hypopituitary adults

   The study “Effect of glucocorticoid replacement therapy on glucose tolerance and intermediary metabolites in hypopituitary adults” by Al-shoumer et al. explores how glucocorticoid replacement affects glucose metabolism in hypopituitary adults. The study involved eight hypopituitary adults undergoing a 3-hour oral glucose tolerance test on two separate days, with varying timings of glucocorticoid intake. The findings indicate that pre-prandial glucocorticoid replacement therapy led to mild increases in blood glucose and insulin levels, even when plasma cortisol concentrations were within acceptable limits. The study concludes that glucocorticoid replacement therapy in hypopituitary adults can affect glucose tolerance, suggesting that more research is needed to determine optimal glucocorticoid replacement regimens​​.
   For more detailed information, you can access the full study
   https://pubmed.ncbi.nlm.nih.gov/7889636/
   

6. Van raalte DH, Ouwens DM, Diamant M. Novel insights into glucocorticoid-mediated diabetogenic effects: towards expansion of therapeutic options?. Eur J Clin Invest. 2009;39(2):81-93.
   View Summary +

   The study “Novel insights into glucocorticoid-mediated diabetogenic effects: towards expansion of therapeutic options?” by Van Raalte et al. discusses the diabetogenic effects of glucocorticoids (GCs) used in pharmacological treatments. While GCs are effective anti-inflammatory agents, their chronic use is associated with significant metabolic side effects like central adiposity, insulin resistance, glucose intolerance, and diabetes. These effects are similar to various components of the metabolic syndrome (MetS). The study highlights emerging treatments aiming to separate GCs’ anti-inflammatory and metabolic actions, including selective glucocorticoid receptor ligands and 11beta-hydroxysteroid dehydrogenase type 1 inhibitors. This review provides updated insights into the mechanisms of GC-induced metabolic disturbances, especially their role in insulin resistance and beta-cell dysfunction​​.
   For more detailed information, you can access the study
   https://pubmed.ncbi.nlm.nih.gov/19200161/
   

7. Rhyu YA, Jang JY, Park S, et al. Impaired Cortisol and Growth Hormone Counterregulatory Responses among Severe Hypoglycemic Patients with Type 2 Diabetes Mellitus. Endocrinol Metab (Seoul). 2019;34(2):187–194. doi:10.3803/EnM.2019.34.2.187.
   View Summary +

   Impaired Cortisol and Growth Hormone Counterregulatory Responses among Severe Hypoglycemic Patients with Type 2 Diabetes Mellitus
   

   The study “Impaired Cortisol and Growth Hormone Counterregulatory Responses among Severe Hypoglycemic Patients with Type 2 Diabetes Mellitus” by Rhyu et al. examines the cortisol and growth hormone responses in type 2 diabetes mellitus (DM) patients experiencing severe hypoglycemia. The study involved measuring plasma cortisol and growth hormone levels in 112 type 2 DM patients who had severe hypoglycemia and visited the emergency department from 2006 to 2015. The findings revealed that 20.5% of the patients had an impaired cortisol response, and 73.2% had an impaired growth hormone response. Factors like advanced age, shorter DM duration, and higher BMI were significantly associated with an impaired growth hormone response. The study concludes that a considerable number of type 2 DM patients have impaired cortisol and/or growth hormone responses to severe hypoglycemia, and these impairments are linked to specific demographic and clinical characteristics​​.
   For more detailed information, you can access the full study
   https://pubmed.ncbi.nlm.nih.gov/31257746/

8. Cryer PE. Mechanisms of hypoglycemia-associated autonomic failure in diabetes. N Engl J Med. 2013;369:362–372.
   View Summary +

   Mechanisms of hypoglycemia-associated autonomic failure in diabetes
   

   This article delves into the intricate mechanisms behind hypoglycemia-associated autonomic failure (HAAF) observed in diabetes. Cryer explores how recurrent episodes of hypoglycemia in individuals with diabetes can lead to a blunted autonomic response to subsequent hypoglycemic events. The author delves into the physiological pathways that contribute to the reduced ability of the body to detect and counteract low blood sugar levels. Understanding these mechanisms is critical in managing diabetes and preventing potential adverse effects of hypoglycemia.
   For further details, please refer to the original article:
   https://www.nejm.org/doi/full/10.1056/NEJMra1215228
   

9. Rizza RA, Cryer PE, Gerich JE. Role of glucagon, catecholamines, and growth hormone in human glucose counterregulation. Effects of somatostatin and combined alpha- and beta-adrenergic blockade on plasma glucose recovery and glucose flux rates after insulin-induced hypoglycemia. J Clin Invest. 1979;64:62–71.
   View Summary +

   Role of glucagon, catecholamines, and growth hormone in human glucose counterregulation. Effects of somatostatin and combined alpha- and beta-adrenergic blockade on plasma glucose recovery and glucose flux rates after insulin-induced hypoglycemia
   

   The study “Role of glucagon, catecholamines, and growth hormone in human glucose counterregulation” by Rizza et al. explores the mechanisms of glucose counterregulation in response to insulin-induced hypoglycemia. Conducted on 13 normal subjects, the study examined the effects of pharmacologically induced deficiencies of glucagon, growth hormone, and catecholamines. It found that recovery from hypoglycemia primarily involved a compensatory increase in glucose production, with the potential participation of glucagon, epinephrine, cortisol, and growth hormone. The study concluded that intact glucagon secretion is necessary for normal glucose counterregulation, while adrenergic mechanisms become critical when glucagon secretion is impaired​​.
   For more detailed information, you can access the full study:
   https://pubmed.ncbi.nlm.nih.gov/36413/
   

10. Feldman JM, Plonk JW, Bivens CH. The role of cortisol and growth hormone in the counter-regulation of insulin-induced hypoglycemia. Horm Metab Res. 1975;7:378–381.
    View Summary +

    The role of cortisol and growth hormone in the counter-regulation of insulin-induced hypoglycemia
    

    The study “The role of cortisol and Growth Hormone in the counter-regulation of Insulin-induced Hypoglycemia” by Feldman et al. examined the impact of cortisol and growth hormone on insulin-induced hypoglycemia. The study involved four volunteers who underwent insulin tolerance tests with and without administration of cyproheptadine, which reduces cortisol and growth hormone secretion. The results showed that despite significant reductions in cortisol and growth hormone secretion due to cyproheptadine, there was a similar pattern of decline and recovery in plasma glucose levels in both tests. This suggests that while normal basal levels of cortisol and growth hormone are necessary for counter-regulation after insulin-induced hypoglycemia, their augmented secretion might not be essential for this response, as increases in epinephrine and glucagon secretion could also contribute to restoring normal plasma glucose concentrations​​.
    For more detailed information, you can access the full study:
    https://pubmed.ncbi.nlm.nih.gov/1183916/
    

11. Boyle PJ, Cryer PE. Growth hormone, cortisol, or both are involved in defense against, but are not critical to recovery from, hypoglycemia. Am J Physiol. 1991;260:E395–E402.
    
    View Summary +

    Growth hormone, cortisol, or both are involved in defense against, but are not critical to recovery from, hypoglycemia
    

    The study “Growth hormone, cortisol, or both are involved in defense against, but are not critical to recovery from, hypoglycemia” by Boyle and Cryer examined the roles of growth hormone and cortisol in the defense against prolonged hypoglycemia. The study involved control subjects and patients with deficiencies in these hormones due to hypopituitarism. The results indicated that while growth hormone and cortisol play a role in defending against prolonged hypoglycemia, they are not essential for the recovery from it. The study suggests that the roles of these hormones are more than just permissive in this context​​.
    For more detailed information, you can access the full study:
    https://pubmed.ncbi.nlm.nih.gov/2003593/

12. Aoki S, Morita M, Hirao T, et al. Shift in energy metabolism caused by glucocorticoids enhances the effect of cytotoxic anti-cancer drugs against acute lymphoblastic leukemia cells. Oncotarget. 2017;8(55):94271–94285. Published 2017 Oct 9. doi:10.18632/oncotarget.21689.
    View Summary +

    Shift in energy metabolism caused by glucocorticoids enhances the effect of cytotoxic anti-cancer drugs against acute lymphoblastic leukemia cells
    

    The study “Shift in energy metabolism caused by glucocorticoids enhances the effect of cytotoxic anti-cancer drugs against acute lymphoblastic leukemia cells” by Aoki et al. investigates the interaction between glucocorticoids (GCs) and cytotoxic anti-cancer drugs in the treatment of acute lymphoblastic leukemia (ALL). The research found that dexamethasone (Dex), a type of GC, suppresses glycolysis in ALL cells, leading to an increase in mitochondrial oxidative phosphorylation. Additionally, autophagy, which is a cellular degradation process, was found to regulate mitochondrial viability. Mitochondria enhanced by Dex became more susceptible to anti-cancer drugs that inhibit respiratory complexes, like etoposide and daunorubicin, resulting in increased production of reactive oxygen species and enhanced cytotoxicity. This study suggests that the shift in energy metabolism induced by GCs—from glycolysis to mitochondrial oxidative phosphorylation mediated by autophagy—can be a crucial factor in enhancing the efficacy of anti-cancer drugs in treating ALL​​.
    For more detailed information, you can access the full study
    https://pubmed.ncbi.nlm.nih.gov/29212227/

13. Ayroldi E, Cannarile L, Delfino DV, Riccardi C. A dual role for glucocorticoid-induced leucine zipper in glucocorticoid function: tumor growth promotion or suppression?. Cell Death Dis. 2018;9(5):463. Published 2018 May 1. doi:10.1038/s41419-018-0558-1.
    View Summary +

    A dual role for glucocorticoid-induced leucine zipper in glucocorticoid function: tumor growth promotion or suppression?
    

    The study “A dual role for glucocorticoid-induced leucine zipper in glucocorticoid function: tumor growth promotion or suppression?” examines the varying effects of glucocorticoids (GCs) in cancer treatment. The effectiveness of GCs is influenced by several factors including the type of tumor, the specific GC therapy used, the expression level of the glucocorticoid receptor (GR), and the presence of external stimuli from immune cells and the tumor microenvironment​​.
    For more detailed information, you can access the full study:
    https://pubmed.ncbi.nlm.nih.gov/29721169/
    

14. Heilman FR , Kendall EC . The influence of 11-dehydro-17-hydroxycorticosterone (compound E) on the growth of malignant tumor in the mouse. Endocrinology. 1944;34:416–26.
    View Summary +

    The influence of 11-dehydro-17-hydroxycorticosterone (compound E) on the growth of malignant tumor in the mouse. Endocrinology

    The study “The influence of 11-dehydro-17-hydroxycorticosterone (compound E) on the growth of malignant tumor in the mouse” by Heilman and Kendall, published in 1944 in Endocrinology, explores the effects of a specific compound, 11-dehydro-17-hydroxycorticosterone (known as compound E), on the growth of malignant tumors in mice. This research is significant as it dates back to the early days of exploring the effects of corticosteroids on cancer growth. This area has greatly expanded in the following decades.
    For more detailed information:
    https://academic.oup.com/endo/article-abstract/34/6/416/2773861

15. Vollmer EP . A viewpoint on animal tumors as test systems for steroids. In: Hormonal steroids, biochemistry, pharmacology, and therapeutics. Proc First Int Cong Horm Steroids. 1965;2:351.
    View Summary +

    A viewpoint on animal tumors as test systems for steroids. In: Hormonal steroids, biochemistry, pharmacology, and therapeutics. Proc First Int Cong Horm Steroids
    

    The document “A viewpoint on animal tumors as test systems for steroids” by Vollmer EP, presented in the proceedings of the First International Congress on Hormonal Steroids in 1965, discusses the use of animal tumors as test systems for studying the effects of steroids. This viewpoint contributes to the broader understanding of how steroids interact with cancerous tissues and their potential implications in medical treatments.

16. Baxter GD , Collins RJ , Harmon BV. et al. Cell death by apoptosis in acute leukemia. J Pathol. 1989;158:123–9.
    View Summary +

    Harmon BV. et al. Cell death by apoptosis in acute leukemia. J Pathol

    The study “Cell death by apoptosis in acute leukaemia” by Baxter GD, Collins RJ, Harmon BV, et al., published in 1989, focuses on the process of apoptosis in acute leukemia cells. The research demonstrated that freshly isolated childhood T-cell acute lymphoblastic leukemia cells undergo rapid chromatin fragmentation into nucleosomal sized fragments, a hallmark of apoptosis, when incubated in growth medium post-isolation from blood. This pattern of DNA fragmentation was also observed in other types of acute leukemia, including T-cell acute lymphoblastic leukemia, common acute lymphoblastic leukemia, and acute myeloid leukemia. In contrast, normal leukocytes did not show such fragmentation under similar conditions. The study underscores the significance of apoptosis in the pathophysiology of acute leukemia​​.
    For more detailed information, you can access the study:
    https://pubmed.ncbi.nlm.nih.gov/2754542/
    

17. Rosen JM , Fina JJ , Millholland RJ , Rosen F . Inhibition of glucose uptake in lymphosarcoma 1798 by cortisol and its relationship to the biosynthesis of deoxyribonucleic acid. J Biol Chem. 1970;245:2074–80.
    View Summary +

    Inhibition of glucose uptake in lymphosarcoma 1798 by cortisol and its relationship to the biosynthesis of deoxyribonucleic acid
    

    The study conducted by Rosen, Fina, Millholland, and Rosen in 1970 investigated the impact of cortisol on the glucose uptake in lymphosarcoma 1798 cells and its correlation with the synthesis of DNA. The research found that cortisol, a hormone released in response to stress, hindered the absorption of glucose in these specific cancer cells. Additionally, the study explored the connection between this inhibition of glucose uptake and the production of deoxyribonucleic acid (DNA), a fundamental component of cell growth and division.
    For more detailed information, you can access the study:
    https://www.jbc.org/article/S0021-9258(18)63208-9/abstract
    

18. Cohen JJ. Lymphocyte death induced by glucocorticoids. In: Schleimer RP, Claman HN, Oronsky AL, editors. Anti-inflammatory steroid action: basic and clinical aspects. San Diego: Academic; 1989. p. 110.
    View Summary +

    Anti-inflammatory steroid action: basic and clinical aspects
    

    The work “Lymphocyte death induced by glucocorticoids” by Cohen JJ, as referenced in “Anti-inflammatory steroid action: basic and clinical aspects” edited by Schleimer RP, Claman HN, and Oronsky AL, discusses the impact of glucocorticoids on lymphocyte cell death. While specific details of the content are not available through my current resources, the title suggests an exploration of how glucocorticoid steroids influence lymphocyte apoptosis, a key process in the immune response. This topic is crucial in understanding the balance between the body’s need to combat inflammation and potential immune suppression effects of glucocorticoids.
    For more information, you can refer to the mention of this work in the NCBI Bookshelf:
    https://www.ncbi.nlm.nih.gov/books/NBK12432/
    

19. Vietti TJ , Sullivan MP , Berry DH . et al. The response of acute childhood leukemia to an initial and a second course of prednisone. J Pediatr. 1965;66:18–26.
    View Summary +

    The response of acute childhood leukemia to an initial and a second course of prednisone
    

    The study “The response of acute childhood leukemia to an initial and a second course of prednisone” by Vietti TJ, Sullivan MP, Berry DH, et al., published in 1965 in the Journal of Pediatrics, focused on the effects of prednisone treatment in cases of acute childhood leukemia. While specific details of the study’s findings are not directly accessible through my current resources, it appears the study investigated the therapeutic response of acute childhood leukemia to one or more courses of prednisone treatment. This research is significant for its early exploration of the effectiveness of prednisone, a corticosteroid, in treating childhood leukemia, a critical area in pediatric oncology.
    For more information about the study, you can refer to these sources:
    https://www.sciencedirect.com/science/article/pii/S0022347665803341
    

20. Koizumi S , Fujimoto T . Improvement in treatment of childhood acute lymphoblastic leukemia: a 10-year study by the Children’s Cancer and Leukemia Study Group. Int J Hematol. 1994;59:99–112.
    View Summary +

    Improvement in treatment of childhood acute lymphoblastic leukemia: a 10-year study by the Children’s Cancer and Leukemia Study Group
    

    The study “Improvement in treatment of childhood acute lymphoblastic leukemia: a 10-year study by the Children’s Cancer and Leukemia Study Group” conducted by Koizumi S, Fujimoto T, and colleagues, published in 1994 in the International Journal of Hematology, examined advancements in the treatment of childhood acute lymphoblastic leukemia (ALL) over a decade. Unfortunately, I couldn’t access the specific content of the study to provide a detailed summary. However, this research likely contributed significantly to the understanding of ALL treatment in children, marking important progress in pediatric oncology.
    For more detailed information, you can access the study through this link:
    https://pubmed.ncbi.nlm.nih.gov/8018909/
    

21. Yang CP , Lin ST , Liang DC . et al. Treatment of childhood acute lymphoblastic leukemia with protocol TCL-842 in Taiwan: the Taiwan Children’s Cancer Study Group. J Formos Med Assoc. 1993;92:431–9.
    View Summary +

    Treatment of childhood acute lymphoblastic leukemia with protocol TCL-842 in Taiwan

    The study referenced, conducted by Yang CP, Lin ST, Liang DC, et al. in 1993, focused on the treatment of childhood acute lymphoblastic leukemia (ALL) using protocol TCL-842 in Taiwan. The research was carried out by the Taiwan Children’s Cancer Study Group and aimed to evaluate the effectiveness and outcomes of treating pediatric patients diagnosed with acute lymphoblastic leukemia using the TCL-842 protocol in Taiwan.

22. Bassan R , Battista R , Montaldi A . et al. Reinforced HEAV’D therapy for adult acute lymphoblastic leukemia: improved results and revised prognostic criteria. Hematol Oncol. 1993;11:169–77.
    View Summary +

    Reinforced HEAV’D therapy for adult acute lymphoblastic leukemia: improved results and revised prognostic criteria
    

    The study “Improvement in treatment of childhood acute lymphoblastic leukemia: a 10-year study by the Children’s Cancer and Leukemia Study Group” by Koizumi S and Fujimoto T, published in 1994 in the International Journal of Hematology, focuses on advancements in the treatment of childhood acute lymphoblastic leukemia over ten years. This research likely provides insights into the evolution of treatment strategies, effectiveness, and patient outcomes for this specific type of childhood cancer.
    For more detailed information, you can access the study through this link:
    https://pubmed.ncbi.nlm.nih.gov/8018909/
    

23. Todeschini G , Meneghini V , Pizzolo G . et al. Relationship between daunorubicin dosage delivered during induction therapy and outcome in adult acute lymphoblastic leukemia. Leukemia. 1994;8:376–81.
    View Summary +

    Relationship between daunorubicin dosage delivered during induction therapy and outcome in adult acute lymphoblastic leukemia
    

    The study by Todeschini G, Meneghini V, Pizzolo G, et al. investigated the impact of daunorubicin dosage during induction therapy on the outcomes of adult patients with acute lymphoblastic leukemia (ALL). The study employed a chemotherapeutic regimen, ALLVR589, which included high doses of daunorubicin (270 mg/m²) during induction and high-dose Ara-C in post-remission. The protocol also involved conventional chemo-radio prophylaxis of the central nervous system and periodic reinductions over three years. The study evaluated 60 patients, with a 93% complete remission rate and a 55% event-free survival rate after a median follow-up of 44 months. The findings indicated that increasing daunorubicin dosage in induction might help improve adult ALL outcomes by reducing relapse occurrence​​.
    For more detailed information, you can refer to the study directly via
    https://pubmed.ncbi.nlm.nih.gov/9519775/
    

24. Nagura E , Kimura K , Yamada K . et al. Nationwide randomized comparative study of doxorubicin, vincristine and prednisolone combination therapy with and without l-asparaginase for adult acute lymphoblastic leukemia. Cancer Chemother Pharmacol. 1994;33:359–65.
    View Summary +

    Nationwide randomized comparative study of doxorubicin, vincristine and prednisolone combination therapy with and without l-asparaginase for adult acute lymphoblastic leukemia

    The study by Nagura E, Kimura K, Yamada K, et al. was a nationwide randomized clinical trial in Japan, comparing the efficacy of combination chemotherapy for adult acute lymphoblastic leukemia (ALL) using doxorubicin, vincristine, and prednisolone, with and without L-asparaginase (AdVP vs L-AdVP). The study involved 198 patients across 58 institutions. The complete remission (CR) rates were similar between the two groups: 63.1% for AdVP and 64.6% for L-AdVP. The median survival times and 7-year survival rates were slightly higher for L-AdVP but not statistically significant. Additionally, while pancreatitis occurred more frequently with L-AdVP, other side effects like hyperbilirubinemia, diabetes mellitus, diarrhea, and hypofibrinogenemia showed no significant difference. The study concluded that adding a single course of L-asparaginase to the induction phase did not significantly enhance the antileukemic treatment effect in adult ALL
    https://pubmed.ncbi.nlm.nih.gov/8306408/
    

25. Bassan R , Battista R , Viero P . et al. Intensive therapy for adult acute lymphoblastic leukemia: preliminary results of the idarubicin/vincristine/l-asparaginase/prednisolone regimen. Semin Oncol. 1993;20(Suppl 8):39–46.
    View Summary +

    Intensive therapy for adult acute lymphoblastic leukemia
    

    The study by Bassan R, Battista R, Viero P, et al., conducted between June 1991 and September 1992, evaluated an intensive therapy regimen for adult acute lymphoblastic leukemia (ALL). This regimen, known as IVAP (idarubicin, vincristine, L-asparaginase, and prednisolone), was tested in different dosages (IVAP-1, IVAP-2, IVAP-3) on 80 patients. The complete remission rate with IVAP-1 was 44% among newly diagnosed patients aged 15 to 60 years, primarily due to high toxicity. However, IVAP-2 showed better outcomes with 89% achieving complete remission and reduced hematologic and nonhematologic toxicity. The study also explored the use of recombinant human granulocyte colony-stimulating factor, which didn’t reduce the duration of granulocytopenia but showed a lower incidence of infections. These preliminary results suggested that IVAP-2 (idarubicin 20 mg/m²) was a highly effective and well-tolerated regimen for remission induction in adult ALL patients.
    For more detailed information, please refer to the study:
    https://pubmed.ncbi.nlm.nih.gov/7507263/
    

26. Thyss A , Suciu S , Bertrand Y . et al. Systemic effect of intrathecal methotrexate during the initial phase of treatment of childhood acute lymphoblastic leukemia. J Clin Oncol. 1997;15(5):1824–30.
    View Summary +

    Systemic effect of intrathecal methotrexate during the initial phase of treatment of childhood acute lymphoblastic leukemia
    

    The study by Thyss A, Suciu S, Bertrand Y, et al., focused on the systemic effect of intrathecal methotrexate (IT MTX) during the initial phase of treatment in childhood acute lymphoblastic leukemia (ALL). This retrospective study analyzed 1,044 children with ALL, restricting the analysis to 732 cases with an initial blast count greater than 1,000/microL. The results showed that the timing of IT MTX administration had a significant impact on response to therapy: 90.4% response rate in group 1 (IT MTX administered earlier), 76.9% in group 2, and 70% in group 3. The study concluded that IT MTX has a therapeutic systemic effect in childhood ALL, and its earlier use leads to a higher percentage of responders. The results indicated that response to prephase therapy should not be considered solely as an in vivo test for corticosteroid sensitivity.
    For more detailed information, you can refer to the study directly via this link:
    https://pubmed.ncbi.nlm.nih.gov/9164191/
    

27. Annino L , Vegna M , Camera A . et al. Treatment of adult acute lymphoblastic leukemia: long-term follow up of the GIMEME ALL0288 randomized study. Blood. 2002;99(3):863–71.
    View Summary +

    Treatment of adult acute lymphoblastic leukemia
    

    The GIMEMA ALL 0288 study, led by Annino L, Vegna M, Camera A, et al., assessed the treatment of adult acute lymphoblastic leukemia (ALL). Conducted from January 1988 to April 1994 with 778 eligible patients, the study focused on the effects of a 7-day prednisone pretreatment, the addition of cyclophosphamide to a conventional 4-drug induction regimen, and the impact of early post-complete remission (CR) intensification using an 8-drug consolidation. Key findings included a 65% response rate to prednisone pretreatment, an 82% CR achievement rate, and the importance of prednisone response as a predictor of CR achievement, overall survival, continuous CR, and disease-free survival. The addition of cyclophosphamide significantly influenced CR achievement, but neither induction intensification nor early consolidation appeared to impact the duration of CR and disease-free survival. The median survival times were 2.2 years (overall survival), 2.4 years (continuous CR), and 2 years (disease-free survival)​​.
    For more detailed information, you can access the study on:
    https://pubmed.ncbi.nlm.nih.gov/11806988/
    

28. Sabbath KD , Weitberg AB , Calabresi P . Potentially curable neoplasms. Dis Mon. 1986;32:593–652.
    View Summary +

    Potentially curable neoplasms

    The article authored by Sabbath KD, Weitberg AB, and Calabresi P in the 1986 issue of the “Disease-a-Month” journal, titled “Potentially curable neoplasms,” offers an extensive and comprehensive overview of various cancer types considered potentially curable during that era. Spanning from pages 593 to 652, the article likely delves into the classification of these curable neoplasms, discussing the available treatments, including surgery, chemotherapy, and radiation therapy. It provides insights into the prognosis, survival rates, and outcomes associated with these cancers, shedding light on the advancements, clinical trials, and emerging treatments existing at that time. Furthermore, the content may touch upon clinical considerations, diagnostic approaches, and multidisciplinary care strategies aimed at improving the management and treatment outcomes for these specific types of potentially curable cancers.

29. Winick NJ , Smith SD , Shuster J . et al. Treatment of CNS relapse in children with acute lymphoblastic leukemia: a Pediatric Oncology Group study. J Clin Oncol. 1993;11:271–8.
    View Summary +

    Treatment of CNS relapse in children with acute lymphoblastic leukemia: a Pediatric Oncology Group study.
    

    The study by Winick NJ, Smith SD, Shuster J, et al., examined the efficacy and toxicity of chemotherapy and cranial radiation for treating children with acute lymphoblastic leukemia (ALL) following their first isolated central nervous system (CNS) relapse. In this Pediatric Oncology Group study, 120 children underwent a treatment protocol that included a four-drug reinduction and triple intrathecal therapy, followed by cranial radiation and systemic consolidation and maintenance therapy. All patients achieved a second complete remission, but there were 61 protocol failures, including various types of relapse. The overall event-free survival at 4 years was 46%. The study concluded that marrow relapse remains the primary site of failure, indicating the need for intensified systemic therapy in future protocols​​.
    For further details, you can refer to the study on:
    https://pubmed.ncbi.nlm.nih.gov/8426204/
    

30. Buhrer C , Hartmann R , Fengler R . et al. Importance of effective central nervous system therapy in isolated bone marrow relapse of childhood acute lymphoblastic leukemia. BFM (Berlin-Frankfurt-Munster) Relapse Study Group. Blood. 1994;83:3468–72.
    View Summary +

    Importance of effective central nervous system therapy in isolated bone marrow relapse of childhood acute lymphoblastic leukemia
    

    The study by Buhrer C, Hartmann R, Fengler R, et al., focused on the importance of effective central nervous system (CNS) therapy in children with late isolated first bone marrow relapse of acute lymphoblastic leukemia (ALL). In the multicenter trial, ALL-REZ BFM 85, intermediate-dose systemic and intrathecal methotrexate was used. Due to a high rate of second CNS relapses, subsequent trials (ALL-REZ BFM 87) included cranial radiotherapy (cRT) and prolonged triple intrathecal therapy. The study found that cRT and prolonged intrathecal therapy effectively prevented CNS relapses, reduced overall relapse rates, and increased overall survival rates in children with late isolated bone marrow relapse of ALL​​.
    For more detailed information, you can access the study via this link:
    https://pubmed.ncbi.nlm.nih.gov/8204875/
    

31. Martino R , Brunet S , Sureda A . et al. Treatment of refractory and relapsed adult acute leukemia using a uniform chemotherapy protocol. Leuk Lymphoma. 1993;11:393–8.
    View Summary +

    Treatment of refractory and relapsed adult acute leukemia using a uniform chemotherapy protocol
    

    The study by Martino R, Brunet S, Sureda A, et al., involved 29 adult patients with relapsed (21) or refractory (8) de novo acute leukemia (12 ALL and 17 ANLL). These patients were treated with a remission-induction salvage chemotherapy protocol that included vindesine, mitoxantrone, cyclophosphamide, intermediate-dose cytosine arabinoside, prednisolone, and methotrexate. The results showed that 59% of ANLL patients and 67% of ALL patients achieved complete remission (CR). Notably, 86% of cases refractory to first-line therapy entered CR. Severe pancytopenia was a common side effect, and 17% of patients died due to complications while aplastic. The study concluded that this protocol is effective as remission-induction salvage therapy for adult acute leukemias​​.
    https://pubmed.ncbi.nlm.nih.gov/8124212/
    

32. Ryalls MR , Pinkerton CR , Meller ST . et al. High-dose methylprednisolone sodium succinate as a single agent in relapsed childhood acute lymphoblastic leukaemia. Med Pediatr Oncol. 1992;20:119–23.
    View Summary +

    High-dose methylprednisolone sodium succinate as a single agent in relapsed childhood acute lymphoblastic leukaemia

    The study by Ryalls MR, Pinkerton CR, Meller ST, et al., assessed the effectiveness of high-dose methylprednisolone sodium succinate as a single agent in treating relapsed childhood acute lymphoblastic leukemia. The study involved 20 children who received methylprednisolone (1 g/m²) daily for 5 to 8 days. Results showed a reduction in bone marrow blasts and complete clearance of cerebrospinal fluid blasts in some patients with central nervous system relapses. Additionally, there was tumor shrinkage in patients with testicular relapses and pain relief in a patient with navicular bone relapse. The treatment demonstrated minimal toxicity and was found to be effective, especially in treating established CNS disease​​.
    For more detailed information, you can refer to the study on:
    https://pubmed.ncbi.nlm.nih.gov/1734216/
    

33. Yetgin S , Gurgey A , Tuncer AM . et al. A comparison of the effect of high-dose methylprednisolone with conventional-dose prednisolone in acute lymphoblastic leukemia patients with randomization. Leuk Res. 1998;22(6):485–93.
    View Summary +

    A comparison of the effect of high-dose methylprednisolone with conventional-dose prednisolone in acute lymphoblastic leukemia patients with randomization

    The study by Yetgin S, Gurgey A, Tuncer AM, et al., compared the efficacy of high-dose methylprednisolone (HDMP) with conventional-dose prednisolone in the treatment of children with acute lymphoblastic leukemia (ALL). In this trial, 166 children with ALL were randomized into two groups, with one group receiving conventional-dose prednisolone and the other receiving high-dose methylprednisolone during remission-induction chemotherapy. The results showed that 97% of children achieved complete remission, with a significantly higher 3-year event-free survival rate in the group receiving HDMP. This suggests that HDMP is more effective, especially for high-risk patients, in improving long-term event-free survival​​.
    For more detailed information, you can access the study on:
    https://pubmed.ncbi.nlm.nih.gov/9678714/
    

34. Pfreundschuh MG , Rueffer U , Lathan B . et al. Dexa-BEAM in patients with Hodgkin’s disease refractory to multidrug chemotherapy regimens: a trial of the German Hodgkin’s Disease Study Group. J Clin Oncol. 1994;12:580–6.
    View Summary +

    Dexa-BEAM in patients with Hodgkin’s disease refractory to multidrug chemotherapy regimens
    

    The study by Pfreundschuh MG, Rueffer U, Lathan B, et al., was a prospective phase II trial to evaluate the efficacy of Dexa-BEAM (dexamethasone, carmustine, etoposide, cytarabine, and melphalan) as salvage chemotherapy for patients with Hodgkin’s disease refractory to multidrug regimens. Fifty-five patients, who progressed or relapsed after extensive chemotherapy, were treated with Dexa-BEAM. The response rate was 60%, with 31% achieving complete remission and 29% partial remission. The study found Dexa-BEAM to be an effective salvage treatment, comparable in efficacy and toxicity to high-dose chemotherapy/autologous bone marrow transplantation (HDCT/ABMT). The results underscore the need for further trials to define the role of HDCT with and without ABMT in these patients​​.
    For more detailed information, you can access the study via this link:
    https://pubmed.ncbi.nlm.nih.gov/8120557/
    

35. Fairey AF , Mead GM , Jones HW . et al. CAPE/PALE salvage chemotherapy for Hodgkin’s disease patients relapsing within 1 year of ChlVPP chemotherapy. Ann Oncol. 1993;4:857–60.
    View Summary +

    CAPE/PALE salvage chemotherapy for Hodgkin’s disease patients relapsing within 1 year of ChlVPP chemotherapy

    The study by Fairey AF, Mead GM, Jones HW, et al., focused on the CAPE/PALE salvage chemotherapy regimen for patients with Hodgkin’s disease who relapsed within one year of receiving ChlVPP chemotherapy. This study involved 25 patients who had failed to achieve complete remission or showed disease progression within a year after ChlVPP treatment. The CAPE/PALE regimen, consisting of cyclophosphamide, adriamycin, prednisolone, etoposide, and lomustine, was administered for six courses at three-week intervals. The results showed that 52% of the patients achieved complete remission, and after a minimum follow-up of 38 months, five patients remained free from disease progression. The regimen was well-tolerated, indicating that CAPE/PALE produces results comparable to other salvage regimens for Hodgkin’s disease, though new strategies are needed for this patient group​​.
    For more detailed information, you can access the study at:
    https://utsouthwestern.elsevierpure.com/en/publications/capepale-salvage-chemotherapy-for-hodgkins-disease-patients-relap

36. Smith MR , Khanuja PS , al-Katib A . et al. Continuous infusion ABDIC therapy for relapsed or refractory Hodgkin’s disease. Cancer. 1994;73:1264–9.
    View Summary +

    Continuous infusion ABDIC therapy for relapsed or refractory Hodgkin’s disease
    

    The study by Smith MR, Khanuja PS, al-Katib A, et al., evaluated the efficacy of continuous infusion ABDIC (doxorubicin, bleomycin, dacarbazine, lomustine, and prednisone) therapy in patients with relapsed or refractory Hodgkin’s disease. Conducted between May 1988 and January 1992, it involved 19 patients treated with the ABDIC regimen. The total response rate was 63%, with 10 patients having a partial response and 2 achieving complete response. Seven patients later underwent bone marrow transplantation, two of whom remained disease-free for over 35 months. The treatment was generally well-tolerated, with nausea and bone marrow suppression as major toxicities. This study concluded that ABDIC is an active and tolerable therapy, especially effective as cytoreductive therapy followed by bone marrow transplantation, potentially offering long-term disease-free survival for heavily pretreated patients​​.
    For more detailed information, you can access the study at:
    https://pubmed.ncbi.nlm.nih.gov/7508818/

37. Solal-Celigny P , Lepage E , Brousse N . et al. Recombinant interferon alfa-2b combined with a regimen containing doxorubicin in patients with advanced follicular lymphoma. Groupe d’Etude des Lymphomes de l’Adulte. N Engl J Med. 1993;329:1608–14.
    View Summary +

    Recombinant interferon alfa-2b combined with a regimen containing doxorubicin in patients with advanced follicular lymphoma
    

    The study by Solal-Celigny P, Lepage E, Brousse N, et al., evaluated the addition of recombinant interferon alfa-2b to a chemotherapy regimen containing doxorubicin in patients with advanced follicular non-Hodgkin’s lymphoma. The trial involved 242 patients who were treated with a regimen of cyclophosphamide, doxorubicin, teniposide, and prednisone (CHVP). Among these, 123 patients also received interferon alfa-2b. The results showed that the group receiving both CHVP and interferon alfa had a higher response rate, longer event-free survival, and higher 3-year survival rate compared to those receiving CHVP only. The addition of interferon alfa increased efficacy without serious toxicity, though some patients couldn’t tolerate side effects like fatigue and hepatitis​​.
    For more detailed information, you can access the study at:
    https://pubmed.ncbi.nlm.nih.gov/8232429/
    

38. Tchekmedyian NS . Clinical approaches to nutritional support in cancer. Curr Opin Oncol. 1993;5:633–8.
    View Summary +

    Clinical approaches to nutritional support in cancer. Curr Opin Oncol
    

    The study by Tchekmedyian NS discusses clinical approaches to nutritional support in cancer. It highlights that anorexia and weight loss are common complications in cancer and AIDS patients. Assessment of dietary records and nutritional needs is crucial for initial intervention. Various pharmacological strategies, including corticosteroids, anabolic steroids, cyproheptadine, hydrazine sulfate, dronabinol, and megestrol acetate, have been tested to counter anorexia and weight loss. Notably, megestrol acetate has shown improvements in appetite and weight in both cancer and AIDS patients. Enteral and parenteral nutrition may benefit certain patients but are generally not recommended for those with end-stage disease​​.
    For more detailed information, you can access the study at:
    https://pubmed.ncbi.nlm.nih.gov/8364079/
    

39. Lai YL , Fang FM , Yeh CY . Management of anorexic patients in radiotherapy: a prospective randomized comparison of megestrol and prednisolone. J Pain Symptom Manage. 1994;9:265–8.
    View Summary +

    Management of anorexic patients in radiotherapy: a prospective randomized comparison of megestrol and prednisolone

    The study by Lai YL, Fang FM, Yeh CY, et al., evaluated the effects of megestrol acetate and prednisolone in treating anorexia induced during whole pelvis external irradiation in cancer patients. The prospective study involved 52 patients randomized to receive either megestrol acetate, prednisolone, or a placebo for 21 consecutive days. The results indicated improvements in body weight, appetite, performance status, and sense of well-being in both the megestrol acetate and prednisolone groups, with a statistically significant appetite improvement in the megestrol acetate group compared to the placebo group. No complications were reported during the trial​​.
    For more detailed information, you can access the study at:
    https://pubmed.ncbi.nlm.nih.gov/8089543/
    

40. Attie MF . Treatment of hypercalcemia. Endocrinol Metab Clin North Am. 1987;18:807–28.
    View Summary +

    Treatment of hypercalcemia

    The article by Attie MF, titled “Treatment of Hypercalcemia”, published in “Endocrinol Metab Clin North Am” in 1987, focuses on the management of severe hypercalcemia, a potentially life-threatening condition often caused by cancers that enhance bone resorption. The treatment primarily involves addressing the underlying disease, restoring extracellular volume, correcting electrolyte deficiencies, and reducing bone resorption. Key interventions include the use of bisphosphonates and plicamycin (mithramycin), which are effective in reducing bone resorption. Calcitonin, though less effective than bisphosphonates or plicamycin, acts more rapidly and can be used in combination to enhance the decrease in serum calcium levels. Additionally, glucocorticoids can be effective in hypercalcemia associated with high vitamin D levels, as seen in conditions like sarcoidosis or some lymphomas. The article emphasizes the importance of early intervention with these agents due to their delayed hypocalcemic action and discusses potential future strategies for predicting and managing hypercalcemia in cancer patients.
    For more detailed information, you can access the study at:
    https://pubmed.ncbi.nlm.nih.gov/2673775/
    

41. Edwards MSB , Prados M . Current management of brain stem gliomas. Pediatr Neurosci. 1987;13:309–15.
    View Summary +

    Current management of brain stem gliomas

    The study by Edwards MSB and Prados M discusses the current management of brain stem gliomas, which account for 10-20% of central nervous system tumors in children. The management of these tumors is complex and controversial, with generally poor long-term survival prospects. However, brain stem gliomas are a heterogeneous group, and some have better prognoses than others. Advances in diagnostic imaging, especially magnetic resonance imaging, have enhanced the ability to differentiate among these tumor types. Additionally, advancements in radiation therapy might offer improved survival rates for children with brain stem gliomas

42. Weissman DE . Glucocorticoid treatment for brain metastases and epidural spinal cord compression: a review. J Clin Oncol. 1988;6:543–51.
    View Summary +

    Glucocorticoid treatment for brain metastases and epidural spinal cord compression

    The article authored by Weissman DE in the Journal of Clinical Oncology in 1988, titled “Glucocorticoid treatment for brain metastases and epidural spinal cord compression: a review,” likely provides an insightful examination of the use of glucocorticoids in the treatment of brain metastases and epidural spinal cord compression. This review probably explores the efficacy, mechanisms of action, and clinical outcomes associated with the administration of glucocorticoids in managing these specific conditions. It may discuss the impact of glucocorticoid therapy on reducing inflammation, relieving symptoms, and potentially improving the quality of life for patients with brain metastases or epidural spinal cord compression.
    https://europepmc.org/article/med/3280744

43. Sorensen S , Helweg-Larsen S , Mouridsen H , Hansen HH . Effect of high-dose dexamethasone in carcinomatous metastatic spinal cord compression treated with radiotherapy: a randomised trial. Eur J Cancer. 1994;30A:22–7.
    View Summary +

    Effect of high-dose dexamethasone in carcinomatous metastatic spinal cord compression treated with radiotherapy
    

    This study conducted a randomized trial to assess the impact of high-dose dexamethasone as an adjunct to radiotherapy in treating carcinomatous metastatic spinal cord compression. The research aimed to evaluate the efficacy of dexamethasone in managing this condition. The trial likely investigated the effects of dexamethasone dosage alongside radiotherapy on alleviating symptoms and improving outcomes for patients with spinal cord compression due to cancer metastases.
    For more detailed information:
    https://www.sciencedirect.com/science/article/pii/S0959804905800115
    

44. Hildebrand J , Gangji D . Supportive care of neurologic complications. Curr Opin Oncol. 1992;4:632–41.
    View Summary +

    Supportive care of neurologic complications
    

    The publication by Hildebrand and Gangji in “Current Opinion in Oncology” in 1992 addresses the supportive care methods for neurologic complications in oncology. It likely discusses various supportive care strategies focused on managing neurologic complications that arise during cancer treatment or due to the disease itself. This publication might cover aspects such as symptom management, palliative care, and interventions to alleviate neurologic symptoms encountered in individuals with cancer, providing insights into optimizing patient comfort and quality of life during treatment.
    You can refer to the article via this DOI link:
    https://doi.org/10.1097/00001622-199208000-00006
    

45. Vech CJ , Hovestadt A , Verbiest HB . et al. Dose-effect relationship of dexamethasone on Karnofsky performance in metastatic brain tumors: a randomized study of doses of 4, 8, and 16 mg per day. Neurology. 1994;44:675–80.
    View Summary +

    Dose-effect relationship of dexamethasone on Karnofsky performance in metastatic brain tumors
    

    The study by Vech CJ, Hovestadt A, Verbiest HB, et al., titled “Dose-effect relationship of dexamethasone on Karnofsky performance in metastatic brain tumors: a randomized study of doses of 4, 8, and 16 mg per day,” published in “Neurology” in 1994, examines the impact of different doses of dexamethasone on the Karnofsky Performance Status in patients with metastatic brain tumors. This randomized trial investigates how 4 mg, 8 mg, and 16 mg per day doses of dexamethasone affect patient functionality and quality of life, providing insights into optimizing treatment for these patients.
    https://n.neurology.org/content/44/4/675.short
    

46. Wolff JEA , Hauch H , Kuhl J . et al. Dexamethasone increases hepatotoxicity of MTX in children with brain tumors. Anticancer Res. 1998;18(4B):2895–9.
    View Summary +

    Dexamethasone increases hepatotoxicity of MTX in children with brain tumors

    The study “Dexamethasone increases hepatotoxicity of MTX in children with brain tumors” by Wolff JEA, Hauch H, Kuhl J, et al., published in “Anticancer Research” in 1998, investigates the adverse effects of combining dexamethasone with methotrexate (MTX) in treating children with brain tumors. The research specifically focuses on the increased risk of liver toxicity (hepatotoxicity) associated with this combination of drugs, which is a critical concern in pediatric oncology.
    For more details and to view the study:
    https://pubmed.ncbi.nlm.nih.gov/9713483/
    

47. Aapro MS . Corticosteroids as antiemetics. Recent Results Cancer Res. 1988;108:102–11.
    View Summary +

    Corticosteroids as antiemetics
    

    The article by Aapro MS titled “Corticosteroids as antiemetics,” published in “Recent Results in Cancer Research” in 1988, discusses the use of corticosteroids as a treatment for preventing or controlling nausea and vomiting, particularly in the context of cancer treatment. This study delves into the effectiveness, mechanisms, and clinical applications of corticosteroids as antiemetic agents, contributing to the broader understanding of managing side effects in cancer therapy.
    For more detailed information visit:
    https://link.springer.com/chapter/10.1007/978-3-642-82932-1_13
    

48. Aapro MS . Controlling emesis related to cancer therapy. Eur J Cancer. 1991;27:356–61.
    View Summary +

    Controlling emesis related to cancer therapy

    The article by Aapro MS, titled “Controlling emesis related to cancer therapy,” published in the “European Journal of Cancer” in 1991, focuses on strategies and treatments for managing nausea and vomiting in cancer patients undergoing therapy. This work highlights the importance of effective emesis control to improve patient comfort and adherence to cancer treatment regimens. It underscores the challenges and approaches in managing these common and often debilitating side effects associated with cancer therapies.
    For more detailed information visit:

49. Tsavaris N , Mylonakis N , Bacoyiannis C . et al. Comparison of ondansetron versus ondansetron plus methylprednisolone as antiemetic prophylaxis during cisplatin-containing chemotherapy. J Pain Symptom Manage. 1994;9:254–8.
    View Summary +

    Comparison of ondansetron versus ondansetron plus methylprednisolone as antiemetic prophylaxis during cisplatin-containing chemotherapy

    The study by Tsavaris N, Mylonakis N, Bacoyiannis C, et al., titled “Comparison of ondansetron versus ondansetron plus methylprednisolone as antiemetic prophylaxis during cisplatin-containing chemotherapy,” published in the “Journal of Pain and Symptom Management” in 1994, investigates the effectiveness of ondansetron alone versus a combination of ondansetron and methylprednisolone in preventing nausea and vomiting in patients undergoing chemotherapy with cisplatin. This research is significant in optimizing antiemetic treatment strategies for cancer patients, enhancing their comfort and tolerance to chemotherapy.
    For more detailed information visit:
    https://www.sciencedirect.com/science/article/pii/0885392494901023
    

50. Sorbe B , Hogberg T , Himmelmann A . et al. Efficacy and tolerability of tropisetron in comparison with a combination of tropisetron and dexamethasone in the control of nausea and vomiting induced by cisplatin-containing chemotherapy. Eur J Cancer. 1994;30A:629–34.
    View Summary +

    Efficacy and tolerability of tropisetron in comparison with a combination of tropisetron and dexamethasone in the control of nausea and vomiting induced by cisplatin-containing chemotherapy

    The study by Sorbe B, Hogberg T, Himmelmann A, et al., titled “Efficacy and tolerability of tropisetron in comparison with a combination of tropisetron and dexamethasone in the control of nausea and vomiting induced by cisplatin-containing chemotherapy,” published in the “European Journal of Cancer” in 1994, compares the effectiveness and side effects of the antiemetic tropisetron alone versus its combination with dexamethasone. This research is key to understanding how these drugs can be used to manage the nausea and vomiting often associated with cisplatin chemotherapy, aiming to improve patient comfort and treatment adherence.
    For more detailed information visit:
    https://www.sciencedirect.com/science/article/pii/0959804994905347
    

51. Spain RC . The case for mitomycin in non-small cell lung cancer. Oncology. 1993;50(Suppl 1):35–50.
    View Summary +

    The case for mitomycin in non-small cell lung cancer. Oncology
    

    The article “The case for mitomycin in non-small cell lung cancer” by Spain RC, published in “Oncology” in 1993, discusses the role of mitomycin in the treatment of non-small cell lung cancer. The article explores the effectiveness, application, and outcomes associated with the use of mitomycin in this context, contributing to the understanding of chemotherapy options in lung cancer treatment.
    For more detailed information, you can refer to the article through this URL:
    https://pubmed.ncbi.nlm.nih.gov/8387177/​​
    

52. Liu GT , Glaser JS , Schatz NJ . High-dose methylprednisolone and acetazolamide for visual loss in pseudotumor cerebri. Am J Ophthalmol. 1994;118:88–96.
    View Summary +

    High-dose methylprednisolone and acetazolamide for visual loss in pseudotumor cerebri
    

    The study “High-dose methylprednisolone and acetazolamide for visual loss in pseudotumor cerebri” by Liu GT, Glaser JS, Schatz NJ, published in “American Journal of Ophthalmology” in 1994, explores the effectiveness of a treatment regimen involving high doses of methylprednisolone and acetazolamide for acute, severe visual loss associated with pseudotumor cerebri. The study highlights that this treatment approach is safe and effective, particularly in cases of florid papilledema, a condition often linked with pseudotumor cerebri. It also notes that the absence of immediate improvement may necessitate optic nerve sheath decompression.
    For further details, you can access the study through this link:
    https://pubmed.ncbi.nlm.nih.gov/8387177/
    

53. Pazirandeh A, Xue Y, Prestegaard T, Jondal M, Okret S (May 2002). “Effects of altered glucocorticoid sensitivity in the T cell lineage on thymocyte and T cell homeostasis”. FASEB Journal. 16 (7): 727–9.
    View Summary +

    Effects of altered glucocorticoid sensitivity in the T cell lineage on thymocyte and T cell homeostasis
    

    The study “Effects of altered glucocorticoid sensitivity in the T cell lineage on thymocyte and T cell homeostasis” by Pazirandeh A, Xue Y, Prestegaard T, Jondal M, Okret S, published in the FASEB Journal in May 2002, examines how changes in glucocorticoid sensitivity affect thymocyte and T cell homeostasis. The research is significant in understanding the hormonal influences on thymocyte and peripheral T-cell numbers, contributing to the broader knowledge of immune system regulation and the impact of glucocorticoids on it.

    For more detailed information, you can refer to the article through this URL:
    https://pubmed.ncbi.nlm.nih.gov/11923224/​​
    

54. Morey JN, Boggero IA, Scott AB, Segerstrom SC. Current Directions in Stress and Human Immune Function. Curr Opin Psychol. 2015;5:13–17. doi:10.1016/j.copsyc.2015.03.007.
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    Current Directions in Stress and Human Immune Function
    

    The article “Current Directions in Stress and Human Immune Function” by Morey JN, Boggero IA, Scott AB, Segerstrom SC, published in “Current Opinion in Psychology” in 2015, explores the relationship between stress and the human immune system. This paper reviews recent research on how psychological stress can affect immune function, contributing to the understanding of the complex interactions between mental states and physical health. The focus on current trends and findings in this field highlights the evolving knowledge of how stress influences immune responses, with implications for both psychological and physical well-being.
    https://doi.org/10.1016/j.copsyc.2015.03.007
    

55. Dhabhar FS, Malarkey WB, Neri E, McEwen BS. Stress-induced redistribution of immune cells—From barracks to boulevards to battlefields: a tale of three hormones–Curt Richter Award Winner. Psychoneuroendocrinology. 2012;37:1345–1368.
    View Summary +

    Stress-induced redistribution of immune cells—From barracks to boulevards to battlefields

    The article “Stress-induced redistribution of immune cells—From barracks to boulevards to battlefields: a tale of three hormones–Curt Richter Award Winner” by Dhabhar FS, Malarkey WB, Neri E, McEwen BS, published in “Psychoneuroendocrinology” in 2012, examines the impact of stress on the distribution of immune cells in the body. It focuses on how stress hormones influence the movement of immune cells, likening it to a military deployment from barracks (resting state) to boulevards (circulation) and battlefields (sites of immune activity). This research provides insightful understanding of the interaction between stress and immune response.

    For more detailed information, you can refer to the article through this link:
    https://www.sciencedirect.com/science/article/abs/pii/S030645301200083X?via%3Dihub

56. Rohleder N. Acute and chronic stress induced changes in sensitivity of peripheral inflammatory pathways to the signals of multiple stress systems–2011 Curt Richter Award Winner. Psychoneuroendocrinology. 2012;37:307–316.
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    Acute and chronic stress induced changes in sensitivity of peripheral inflammatory pathways to the signals of multiple stress systems–2011 Curt Richter Award Winner

    The article by Rohleder N, titled “Acute and chronic stress induced changes in sensitivity of peripheral inflammatory pathways to the signals of multiple stress systems–2011 Curt Richter Award Winner,” published in “Psychoneuroendocrinology” in 2012, investigates how both acute and chronic stress affect the sensitivity of peripheral inflammatory pathways. The research focuses on how stress influences the body’s inflammatory response, examining the complex interactions between stress-related systems and inflammatory processes. This work is significant in understanding the broader implications of stress on physical health, particularly concerning inflammation.
    For more detailed information, you can refer to the article using the following link:
    https://www.sciencedirect.com/science/article/abs/pii/S0306453011003259

57. Jefferies WM. Cortisol and immunity. Med Hypotheses. 1991;34(3):198-208.
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    Cortisol and immunity. Med Hypotheses
    

    The article “Cortisol and immunity” by Jefferies WM, published in “Medical Hypotheses” in 1991, discusses the relationship between cortisol, a key stress hormone, and the immune system. It delves into the ways cortisol influences immune responses, potentially affecting various aspects of health and disease. This research is crucial for understanding the hormonal regulation of immunity and its implications for stress management and treatment of immune-related conditions.
    To access the full article, you can use this link:
    https://www.sciencedirect.com/science/article/abs/pii/030698779190040E
    

58. Yeager MP, Guyre CA, Sites BD, Collins JE, Pioli PA, Guyre PM. The Stress Hormone Cortisol Enhances Interferon-υ-Mediated Proinflammatory Responses of Human Immune Cells. Anesth Analg. 2018;127(2):556-563.
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    The Stress Hormone Cortisol Enhances Interferon-υ-Mediated Proinflammatory Responses of Human Immune Cells

    The study “The Stress Hormone Cortisol Enhances Interferon-υ-Mediated Proinflammatory Responses of Human Immune Cells” by Yeager MP, Guyre CA, Sites BD, Collins JE, Pioli PA, Guyre PM, published in “Anesthesia & Analgesia” in 2018, explores the impact of cortisol, a stress hormone, on the proinflammatory responses of human immune cells. This research highlights how cortisol can amplify the effects of interferon-υ, a key mediator in inflammatory processes, providing insights into the complex relationship between stress, hormonal responses, and immune system activation.
    For more detailed information, the article can be accessed here:
    https://journals.lww.com/anesthesia-analgesia/Fulltext/2018/08000/The_Stress_Hormone_Cortisol_Enhances.34.aspx
    

59. Dhabhar FS. Enhancing versus Suppressive Effects of Stress on Immune Function: Implications for Immunoprotection versus Immunopathology. Allergy Asthma Clin Immunol. 2008;4(1):2–11. doi:10.1186/1710-1492-4-1-2.
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    Enhancing versus Suppressive Effects of Stress on Immune Function: Implications for Immunoprotection versus Immunopathology
    

    The article “Enhancing versus Suppressive Effects of Stress on Immune Function: Implications for Immunoprotection versus Immunopathology” by Dhabhar FS, published in “Allergy, Asthma & Clinical Immunology” in 2008, examines the dual role of stress in influencing immune function. It discusses how stress can both enhance and suppress immune responses, with implications for both protecting against and exacerbating various diseases. This research is significant in understanding the complex role of stress in immune regulation, providing insights into its potential impacts on health and disease.
    https://doi.org/10.1186/1710-1492-4-1-2
    

60. Schedlowski M, Jacobs R, Stratman G. Changes of natural killer cells during acute psychological stress. J Clin Immunol. 1993;13:119–26. doi: 10.1007/BF00919268.
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    Changes of natural killer cells during acute psychological stress. J Clin Immunol
    

    The study “Changes of natural killer cells during acute psychological stress” by Schedlowski M, Jacobs R, Stratman G, published in the “Journal of Clinical Immunology” in 1993, investigates the impact of acute psychological stress on natural killer (NK) cell activity. This research is crucial for understanding how stress can affect an essential component of the immune system, specifically focusing on NK cells known for their role in combating infections and tumors.
    https://doi.org/10.1007/BF00919268
    

61. Heffner KL. Neuroendocrine effects of stress on immunity in the elderly: implications for inflammatory disease. Immunol Allergy Clin North Am. 2011;31(1):95–108. doi:10.1016/j.iac.2010.09.005.
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    Neuroendocrine effects of stress on immunity in the elderly: implications for inflammatory disease
    

    The article “Neuroendocrine effects of stress on immunity in the elderly: implications for inflammatory disease” by Heffner KL, published in “Immunology and Allergy Clinics of North America” in 2011, explores the connection between stress, neuroendocrine responses, and immune function in older adults. It particularly focuses on how these interactions may influence the development and course of inflammatory diseases in the elderly. This research is significant for understanding the unique impact of stress on the aging immune system and its implications for managing inflammatory conditions in this population.
    https://doi.org/10.1016/j.iac.2010.09.005
    

62. Agarwal SK, Marshall GD., Jr. Dexamethasone promotes type 2 cytokine production primarily through inhibition of type 1 cytokines. Journal of Interferon and Cytokine Research. 2001;21:147–55.
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    Dexamethasone promotes type 2 cytokine production primarily through inhibition of type 1 cytokines
    

    The study “Dexamethasone promotes type 2 cytokine production primarily through inhibition of type 1 cytokines” by Agarwal SK and Marshall GD., Jr., published in the “Journal of Interferon and Cytokine Research” in 2001, investigates the effects of dexamethasone, a synthetic corticosteroid, on cytokine production. The research finds that dexamethasone primarily encourages the production of type 2 cytokines by inhibiting type 1 cytokines. This is significant in understanding the immunomodulatory effects of dexamethasone, particularly its influence on immune responses and potential implications for treating various inflammatory and autoimmune conditions.
    https://www.liebertpub.com/doi/abs/10.1089/107999001750133159
    

63. Elenkov IJ, Chrousos GP. Stress hormones, proinflammatory and antiinflammatory cytokines, and autoimmunity. Annals of the New York Academy of Sciences. 2002;966:290–303.
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    Stress hormones, proinflammatory and antiinflammatory cytokines, and autoimmunity. Annals of the New York Academy of Sciences.

    The article “Stress hormones, proinflammatory and antiinflammatory cytokines, and autoimmunity” by Elenkov IJ and Chrousos GP, published in the “Annals of the New York Academy of Sciences” in 2002, examines the interplay between stress hormones and cytokines in the context of autoimmunity. It highlights how stress hormones can influence the balance between proinflammatory and antiinflammatory cytokines, thereby affecting autoimmune diseases. This research is important for understanding the complex interactions between the endocrine and immune systems and their role in the development and progression of autoimmune disorders.
    For more detailed information:
    https://www.sciencedirect.com/science/article/pii/S0077892302933328?via%3Dihub
    

64. Buske-Kirschbaum A, Fischbach S, Rauh W, et al. Increased responsiveness of the hypothalamus-pituitary-adrenal (HPA) axis to stress in newborns with atopic disposition. Psychoneuroendocrinology. 2004;29:705–11.
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    Increased responsiveness of the hypothalamus-pituitary-adrenal (HPA) axis to stress in newborns with atopic disposition
    

    The study “Increased responsiveness of the hypothalamus-pituitary-adrenal (HPA) axis to stress in newborns with atopic disposition” by Buske-Kirschbaum A, Fischbach S, Rauh W, et al., published in “Psychoneuroendocrinology” in 2004, investigates the response of the hypothalamus-pituitary-adrenal axis to stress in newborns predisposed to atopy (allergic hypersensitivity). This research is pivotal in understanding the early life stress responses in infants at risk of developing allergic conditions, offering insights into the relationship between stress, the endocrine system, and the development of atopic diseases.
    For more detailed information, the article can be accessed here:
    https://www.sciencedirect.com/science/article/abs/pii/S0306453003001673?via%3Dihub
    

65. Wright RJ, Finn P, Contreras JP, et al. Chronic caregiver stress and IgE expression, allergen-induced proliferation, and cytokine profiles in a birth cohort predisposed to atopy. Journal of Allergy and Clinical Immunology. 2004;113:1051–7.
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    Chronic caregiver stress and IgE expression, allergen-induced proliferation, and cytokine profiles in a birth cohort predisposed to atopy
    

    The study “Chronic caregiver stress and IgE expression, allergen-induced proliferation, and cytokine profiles in a birth cohort predisposed to atopy” by Wright RJ, Finn P, Contreras JP, et al., published in the “Journal of Allergy and Clinical Immunology” in 2004, explores the relationship between chronic stress in caregivers and immune responses in their children predisposed to atopy. It specifically examines the impact on IgE expression, allergen-induced cell proliferation, and cytokine profiles, offering insights into how environmental stressors can influence allergic responses in susceptible individuals.
    For more detailed information:
    https://www.sciencedirect.com/science/article/abs/pii/S0091674904003724?via%3Dihub
    

66. Kiecolt-Glaser JK, Heffner KL, Glaser R, et al. How stress and anxiety can alter immediate and late phase skin test responses in allergic rhinitis. Psychoneuroendocrinology. 2009;34:670–80.
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    How stress and anxiety can alter immediate and late phase skin test responses in allergic rhinitis
    

    The study “How stress and anxiety can alter immediate and late phase skin test responses in allergic rhinitis” by Kiecolt-Glaser JK, Heffner KL, Glaser R, et al., published in “Psychoneuroendocrinology” in 2009, investigates the impact of stress and anxiety on skin test responses in individuals with allergic rhinitis. It explores how psychological factors can influence both immediate and late-phase allergic reactions. This research sheds light on the complex relationship between stress, anxiety, and immune responses in individuals with allergic conditions.
    For more detailed information:
    https://www.sciencedirect.com/science/article/abs/pii/S0091674904003724?via%3Dihub
    

67. Elenkov IJ, Kvetnansky R, Hashiramoto A, et al. Low- versus high-baseline epinephrine output shapes opposite innate cytokine profiles: presence of Lewis- and Fischer-like neurohormonal immune phenotypes in humans? Journal of Immunology. 2008;181:1737–45.
    View Summary +

    Low- versus high-baseline epinephrine output shapes opposite innate cytokine profiles: presence of Lewis- and Fischer-like neurohormonal immune phenotypes in humans?

    The study “Low- versus high-baseline epinephrine output shapes opposite innate cytokine profiles: presence of Lewis- and Fischer-like neurohormonal immune phenotypes in humans?” by Elenkov IJ, Kvetnansky R, Hashiramoto A, et al., published in the “Journal of Immunology” in 2008, explores the relationship between baseline epinephrine levels and innate cytokine profiles. It suggests the presence of distinct neurohormonal immune phenotypes in humans based on their epinephrine output, with implications for understanding individual variations in immune responses.
    https://www.jimmunol.org/content/181/3/1737
    

68. Elenkov IJ, Chrousos GP. Stress hormones, proinflammatory and antiinflammatory cytokines, and autoimmunity. Annals of the New York Academy of Sciences. 2002;966:290–303.
    View Summary +

    Stress hormones, proinflammatory and antiinflammatory cytokines, and autoimmunity
    

    The article “Stress hormones, proinflammatory and antiinflammatory cytokines, and autoimmunity” by Elenkov IJ and Chrousos GP, published in the “Annals of the New York Academy of Sciences” in 2002, explores the complex interactions between stress hormones, proinflammatory, and antiinflammatory cytokines in the context of autoimmunity. It discusses how stress can modulate the immune response, potentially contributing to the development and exacerbation of autoimmune diseases. This research provides valuable insights into the role of stress in the pathophysiology of autoimmune conditions.
    For more detailed information, please refer to the article through:
    https://www.sciencedirect.com/science/article/pii/S0077892302933328?via%3Dihub
    

69. Salicru AN, Sams CF, Marshall GD. Cooperative effects of corticosteroids and catecholamines upon immune deviation of the type-1/type-2 cytokine balance in favor of type-2 expression in human peripheral blood mononuclear cells. Brain, Behavior, and Immunity. 2007;21:913–20.
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    Cooperative effects of corticosteroids and catecholamines upon immune deviation of the type-1/type-2 cytokine balance in favor of type-2 expression in human peripheral blood mononuclear cells

    The study “Cooperative effects of corticosteroids and catecholamines upon immune deviation of the type-1/type-2 cytokine balance in favor of type-2 expression in human peripheral blood mononuclear cells” by Salicru AN, Sams CF, Marshall GD, published in “Brain, Behavior, and Immunity” in 2007, investigates the combined impact of corticosteroids and catecholamines on immune responses. It focuses on how these compounds work together to shift the cytokine balance towards type-2 expression in human peripheral blood mononuclear cells. This research highlights the complex interplay between hormonal and immune factors in regulating immune responses.
    For more information:
    https://www.sciencedirect.com/science/article/abs/pii/S0889159107000526?via%3Dihub
    

70. Kronfol Z, House JD. Depression, cortisol, and immune function. Lancet. 1984;1(8384):1026-7.
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    Depression, cortisol, and immune function.

    The article “Depression, cortisol, and immune function” by Kronfol Z and House JD, published in “Lancet” in 1984, discusses the relationship between depression, cortisol (a stress hormone), and immune function. It briefly addresses how depression may influence cortisol levels and, in turn, affect immune responses. The study contributes to the understanding of the complex interplay between mental health, hormonal regulation, and immune function.

    For more information visit:
    https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(84)91542-4/fulltext
    

71. Niklasson L, Sundh H, Olsen RE, et al. Effects of cortisol on the intestinal mucosal immune response during cohabitant challenge with IPNV in Atlantic salmon (Salmo salar). PLoS ONE. 2014;9(5):e94288.
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    Effects of cortisol on the intestinal mucosal immune response during cohabitant challenge with IPNV in Atlantic salmon (Salmo salar)
    

    The study “Effects of cortisol on the intestinal mucosal immune response during cohabitant challenge with IPNV in Atlantic salmon (Salmo salar)” by Niklasson L, Sundh H, Olsen RE, et al., published in “PLoS ONE” in 2014, investigates the influence of cortisol, a stress hormone, on the intestinal mucosal immune response in Atlantic salmon during a challenge with IPNV (Infectious Pancreatic Necrosis Virus). It explores how cortisol levels may impact the fish’s immune defense mechanisms in the context of viral infection.
    For more information:
    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0094288
    

72. Chiappelli, F., Manfrini, E., Franceschi, C., Cossarizza, A., & Black, K. L. (1994). Steroid regulation of cytokines: Relevance for Th1 to Th2 shift? In E. R. de Kloet, E. C. Azmitia, & P. W. Landfield (Eds.), Annals of the New York Academy of Sciences: Vol. 746. Brain corticosteroid receptors: Studies on the mechanism, function, and neurotoxicity of corticosteroid action (pp. 204–215). New York: New York Academy of Sciences.
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    Steroid regulation of cytokines: Relevance for Th1 to Th2 shift?

    The chapter “Steroid regulation of cytokines: Relevance for Th1 to Th2 shift?” by Chiappelli, F., Manfrini, E., Franceschi, C., Cossarizza, A., & Black, K. L., published in the book “Annals of the New York Academy of Sciences” in 1994, discusses the influence of steroids on cytokine regulation and its potential relevance to the shift between Th1 and Th2 immune responses. It contributes to the understanding of how steroids may modulate the balance between these immune pathways.
    For more information:
    https://nyaspubs.onlinelibrary.wiley.com/doi/abs/10.1111/j.1749-6632.1994.tb39201.x
    

73. Marshall GD, Jr, Agarwall SK, Lloyd C, Cohen L, Henniger EM, Morris GJ. Cytokine dysregulation associated with exam stress in healthy medical students. Brain, Behavior, and Immunity. 1998;12:297–307.
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    Cytokine dysregulation associated with exam stress in healthy medical students

    The study “Cytokine dysregulation associated with exam stress in healthy medical students” by Marshall GD Jr, Agarwal SK, Lloyd C, Cohen L, Henniger EM, Morris GJ, published in “Brain, Behavior, and Immunity” in 1998, investigates the impact of exam-related stress on cytokine regulation in healthy medical students. The research reveals dysregulation of cytokine levels during the stress of exams, providing insights into the potential immune responses triggered by psychological stress in this population.
    https://www.sciencedirect.com/science/article/pii/S0889159198905372
    

74. Rook GA. Glucocorticoids and immune function. Baillieres Best Pract Res Clin Endocrinol Metab. 1999;13(4):567-81.
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    Glucocorticoids and immune function
    

    The article “Glucocorticoids and immune function” by Rook GA, published in “Bailliere’s Best Practice & Research in Clinical Endocrinology & Metabolism” in 1999, explores the complex interactions between glucocorticoids and the immune system. It discusses how these hormones can both suppress and modulate immune responses, shedding light on their role in immune function and their therapeutic applications in various medical conditions.
    https://www.sciencedirect.com/science/article/pii/S1521690X99900441
    

75. Benschop RJ, Rodriguez-Feuerhahn M, Schedlowski M. Catecholamine-induced leukocytosis: early observations, current research, and future directions. Brain Behav Immun. 1996;10(2):77–91.
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    Catecholamine-induced leukocytosis: early observations, current research, and future directions
    

    The article “Catecholamine-induced leukocytosis: early observations, current research, and future directions” by Benschop RJ, Rodriguez-Feuerhahn M, Schedlowski M, published in “Brain, Behavior, and Immunity” in 1996, explores the phenomenon of catecholamine-induced leukocytosis. It discusses early observations, current research findings, and future directions in understanding how catecholamines, such as adrenaline and noradrenaline, can influence the mobilization of white blood cells. This research provides insights into the mechanisms by which stress-related hormones can impact the immune system.
    For more information:
    https://www.sciencedirect.com/science/article/pii/S088915910580003X?via%3Dihub
    

76. Dhabhar FS, Malarkey WB, Neri E, McEwen BS. Stress-induced redistribution of immune cells – from barracks to boulevards to battlefields: a tale of three hormones – Curt Richter Award winner. Psychoneuroendocrinology. 2012;37(9):1345–1368.
    View Summary +

    Stress-induced redistribution of immune cells – from barracks to boulevards to battlefields: a tale of three hormones
    

    The article “Stress-induced redistribution of immune cells – from barracks to boulevards to battlefields: a tale of three hormones” by Dhabhar FS, Malarkey WB, Neri E, McEwen BS, published in “Psychoneuroendocrinology” in 2012, discusses the impact of stress on the redistribution of immune cells in the body. It focuses on the role of three hormones in this process and provides insights into how stress can influence immune responses and overall health.
    For more information:
    https://www.sciencedirect.com/science/article/pii/S0306453012000579?via%3Dihub
    

77. Dhabhar FS, McEwen BS. Enhancing versus suppressive effects of stress hormones on skin immune function. Proc Natl Acad Sci USA. 1999;96(3):1059–1064.
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    Enhancing versus suppressive effects of stress hormones on skin immune function
    

    The study “Enhancing versus suppressive effects of stress hormones on skin immune function” by Dhabhar FS and McEwen BS, published in the “Proceedings of the National Academy of Sciences of the USA” in 1999, explores the dual role of stress hormones in modulating skin immune function. It highlights how stress hormones can have both enhancing and suppressive effects on the skin’s immune responses, shedding light on the complexity of stress-immune system interactions.
    https://www.pnas.org/doi/abs/10.1073/pnas.96.3.1059
    

78. Norbiato G, Bevilacqua M, Vago T, Taddei A, Clerici . Glucocorticoids and the immune function in the human immunodeficiency virus infection: a study in hyperco
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    Glucocorticoids and the immune function in the human immunodeficiency virus infection

    The study by Norbiato et al. examines the impact of glucocorticoids on immune function in individuals with HIV infection. It focuses on hypercortisolemia, a condition characterized by high cortisol levels, and its effects on the immune system. The research investigates how glucocorticoids may influence immune responses in the context of HIV infection, providing insights into the complex interactions between hormones and the immune system in this population.

    For more details checkout:
    https://academic.oup.com/jcem/article-abstract/82/10/3260/2823218