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| Figure 1: Overview of Addison's Disease | Figure 1: Overview of Addison's Disease | ||
| Image from: http://www.organsofthebody.com | Image from: http://www.organsofthebody.com | ||
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| - | Figure 2: Age at diagnosis for deceased Addison patients | + | Figure 2: Age at diagnosis for deceased Addison patients. |
| - | Image from: http://www.eje-online.org/ | + | Image from: http://www.eje-online.org/content/160/2/233/F2.expansion.html |
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| ====== Signs and Symptoms ====== | ====== Signs and Symptoms ====== | ||
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| + | Table 1: Michels & Michels, 2014 | ||
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| <style justify>The symptoms of Addison’s disease begin gradually. As the disease progresses and more of the adrenal glandular tissue is destroyed, symptoms tend to worsen from mild to severe. This can take up to a few years, and because these symptoms are generalized and similar to many other health conditions, Addison’s disease may not even be diagnosed until the patient suffers from an Addisonian crisis (Sarkar et al., 2012). | <style justify>The symptoms of Addison’s disease begin gradually. As the disease progresses and more of the adrenal glandular tissue is destroyed, symptoms tend to worsen from mild to severe. This can take up to a few years, and because these symptoms are generalized and similar to many other health conditions, Addison’s disease may not even be diagnosed until the patient suffers from an Addisonian crisis (Sarkar et al., 2012). | ||
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| Early symptoms of Addison’s include worsening fatigue, generalized lethargy and muscle weakness, loss of appetite, leading to weight loss, hypotension, and low mood and irritability. Oftentimes, patients also present with hyponatremia and hyperkalemia (Sarkar et al., 2012). This is classified as pathological when serum sodium concentrations drop below 135 mmol/L (Simon, 2016) and serum potassium concentrations are higher than 5.5 mEq/L (Lederer, 2016). Although uncommon, hypoglycaemia can occur, which leads to common symptoms experienced with low blood sugar levels, like dizziness and, in extreme cases, loss of consciousness (Sarkar et al., 2012). The patient also complains of gastrointestinal upset, nausea, vomiting, diarrhea, dehydration, and a peculiar craving for salt. Dehydration and salt cravings are linked to the drop in aldosterone levels (Sarkar et al., 2012). Table _ gives a brief overview of the major symptoms experienced by patients, along with the prevalence of each one. | Early symptoms of Addison’s include worsening fatigue, generalized lethargy and muscle weakness, loss of appetite, leading to weight loss, hypotension, and low mood and irritability. Oftentimes, patients also present with hyponatremia and hyperkalemia (Sarkar et al., 2012). This is classified as pathological when serum sodium concentrations drop below 135 mmol/L (Simon, 2016) and serum potassium concentrations are higher than 5.5 mEq/L (Lederer, 2016). Although uncommon, hypoglycaemia can occur, which leads to common symptoms experienced with low blood sugar levels, like dizziness and, in extreme cases, loss of consciousness (Sarkar et al., 2012). The patient also complains of gastrointestinal upset, nausea, vomiting, diarrhea, dehydration, and a peculiar craving for salt. Dehydration and salt cravings are linked to the drop in aldosterone levels (Sarkar et al., 2012). Table _ gives a brief overview of the major symptoms experienced by patients, along with the prevalence of each one. | ||
| - | As the disease progresses, early symptoms worsen, along with the appearance of new symptoms. The most characteristic late symptom of Addison’s is generalized hyperpigmentation of the skin and mucosal surfaces (Sarkar et al., 2012). These include any sun-exposed skin and over pressure points, like elbows and knees. Observable hyperpigmentation of mucosal surfaces presents as intraoral and buccal pigmentation, as shown in Figure _ (Sarkar et al., 2012). These are due to the abnormal interaction of ACTH with the melanocortin-1 receptor on keratinocytes. In autoimmune Addison’s, hyperpigmentation is seen in association with vitiligo due to the destruction of melanocytes (Sarkar et al., 2012). | ||
| - | Because these symptoms are slow to progress and very generalized, an event of illness or accident can spontaneously worsen the condition and lead to an Addisonian crisis. The crisis is characterized by sudden, penetrating pains in the lower back, abdomen, or legs, combined with severe vomiting and diarrhea (Sarkar et al., 2012). This leads to severe dehydration, drastic drop in blood pressure, and loss of consciousness. Other associated symptoms include pale, cold, and clammy skin, sweating, and rapid, shallow breathing (Sarkar et al., 2012). It is important that a patient suffering from an Addisonian crisis seeks emergency medical assistance. If left untreated, it can lead to shock, seizures, coma, or even death (Sarkar et al., 2012). Table _ describes the clinical features of Addison’s disease as symptoms, signs, and associated biochemical changes. | ||
| + | As the disease progresses, early symptoms worsen, along with the appearance of new symptoms. The most characteristic late symptom of Addison’s is generalized hyperpigmentation of the skin and mucosal surfaces (Sarkar et al., 2012). These include any sun-exposed skin and over pressure points, like elbows and knees. Observable hyperpigmentation of mucosal surfaces presents as intraoral and buccal pigmentation, as shown in Figure 3 (Sarkar et al., 2012). These are due to the abnormal interaction of ACTH with the melanocortin-1 receptor on keratinocytes. In autoimmune Addison’s, hyperpigmentation is seen in association with vitiligo due to the destruction of melanocytes (Sarkar et al., 2012). | ||
| + | Because these symptoms are slow to progress and very generalized, an event of illness or accident can spontaneously worsen the condition and lead to an Addisonian crisis. The crisis is characterized by sudden, penetrating pains in the lower back, abdomen, or legs, combined with severe vomiting and diarrhea (Sarkar et al., 2012). This leads to severe dehydration, drastic drop in blood pressure, and loss of consciousness. Other associated symptoms include pale, cold, and clammy skin, sweating, and rapid, shallow breathing (Sarkar et al., 2012). It is important that a patient suffering from an Addisonian crisis seeks emergency medical assistance. If left untreated, it can lead to shock, seizures, coma, or even death (Sarkar et al., 2012). | ||
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| + | Figure 3: Sarkar et al., 2012 | ||
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| ====== Diagnosis ====== | ====== Diagnosis ====== | ||
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| + | Figure 4: Michels & Michels, 2014 | ||
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| <style justify>Due to the subtlety and non-specificity of Addison’s disease, early diagnosis can be difficult. Presentation of the symptoms relates to the degree of cortisol, mineralocorticoid, and adrenal androgen deficiency (higher degree of deficiency equates to more severe symptoms) (Michels & Michels, 2014). There are three main types of tests that are used in combination to diagnose Addison’s: | <style justify>Due to the subtlety and non-specificity of Addison’s disease, early diagnosis can be difficult. Presentation of the symptoms relates to the degree of cortisol, mineralocorticoid, and adrenal androgen deficiency (higher degree of deficiency equates to more severe symptoms) (Michels & Michels, 2014). There are three main types of tests that are used in combination to diagnose Addison’s: | ||
| **1. Metabolic Tests** | **1. Metabolic Tests** | ||
| - | A metabolic panel is a complete blood analysis that serves as a broad-spectrum medical screening tool. This type of test provides a rough evaluation of kidney and liver function, and the balance of serum electrolytes and fluid, using a blood sample drawn from the patient in question (2005). Along with this, the physician also requests serum cortisol levels to be tested early in the morning (8 a.m.). Low cortisol levels are the most evident clinical feature of Addison’s (Michels & Michels, 2014). If the results demonstrate low serum cortisol concentrations (<83 nmol/L), hyponatremia (<135 mmol/L) (Simon, 2016), and hyperkalemia (>5.5 mEq/L) (Lederer, 2016), the physician then requests a cosyntropic stimulation test (Michels & Michels, 2014). This type of test measures cortisol response to ACTH levels. An abnormal rise in ACTH levels (>11 pmol/L) is indicative of underlying cortisol deficiency (Michels & Michels, 2014). Therefore, this type of test is the first-line test for confirming diagnosis of Addison’s disease. Initially, plasma levels of cortisol, ACTH, aldosterone, and renin should be measured, followed by administration of 250 mcg of synthetic ACTH (Michels & Michels, 2014). After 30-60 minutes of intravenous ACTH administration, serum cortisol levels are measured again (Michels & Michels, 2014). Less than 497-552 nmol/L peak cortisol levels in the blood is diagnostic for adrenal insufficiency (Michels & Michels, 2014). A summary of the metabolic panel is shown in Figure _. | + | A metabolic panel is a complete blood analysis that serves as a broad-spectrum medical screening tool. This type of test provides a rough evaluation of kidney and liver function, and the balance of serum electrolytes and fluid, using a blood sample drawn from the patient in question (2005). Along with this, the physician also requests serum cortisol levels to be tested early in the morning (8 a.m.). Low cortisol levels are the most evident clinical feature of Addison’s (Michels & Michels, 2014). If the results demonstrate low serum cortisol concentrations (<83 nmol/L), hyponatremia (<135 mmol/L) (Simon, 2016), and hyperkalemia (>5.5 mEq/L) (Lederer, 2016), the physician then requests a cosyntropic stimulation test (Michels & Michels, 2014). This type of test measures cortisol response to ACTH levels. An abnormal rise in ACTH levels (>11 pmol/L) is indicative of underlying cortisol deficiency (Michels & Michels, 2014). Therefore, this type of test is the first-line test for confirming diagnosis of Addison’s disease. Initially, plasma levels of cortisol, ACTH, aldosterone, and renin should be measured, followed by administration of 250 mcg of synthetic ACTH (Michels & Michels, 2014). After 30-60 minutes of intravenous ACTH administration, serum cortisol levels are measured again (Michels & Michels, 2014). Less than 497-552 nmol/L peak cortisol levels in the blood is diagnostic for adrenal insufficiency (Michels & Michels, 2014). A summary of the metabolic panel is shown in Figure 4. |
| **2. Immunologic Tests** | **2. Immunologic Tests** | ||
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| {{:adgland.jpg|}} | {{:adgland.jpg|}} | ||
| - | Figure 3 | + | Figure 5: The three zones of the adrenal cortex. |
| Image from https://www.britannica.com/science/adrenal-gland. | Image from https://www.britannica.com/science/adrenal-gland. | ||
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| {{:hpaa.png|}} | {{:hpaa.png|}} | ||
| - | Figure 4 | + | Figure 6: The hypothalamus, pituitary gland & adrenal glands make up the HPA axis. |
| Image from http://www.integrativepro.com/Resources/Integrative-Blog/2016/The-HPA-Axis. | Image from http://www.integrativepro.com/Resources/Integrative-Blog/2016/The-HPA-Axis. | ||
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| - | Figure 5 | + | Figure 7: Comparing Primary Adrenal Insufficiency to Secondary/Tertiary Adrenal Insufficiency. |
| Image from: http://www.prn.org/index.php/complications/article/hiv_osteoporosis_adrenal_insufficiency_85. | Image from: http://www.prn.org/index.php/complications/article/hiv_osteoporosis_adrenal_insufficiency_85. | ||
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| {{:ADpatho.png|}} | {{:ADpatho.png|}} | ||
| - | Figure 6: Molecular Immunopathogenesis of Primary Adrenal Insufficiency | + | Figure 8: Molecular Immunopathogenesis of Primary Adrenal Insufficiency. |
| Image from: (Charmandari, Nicolaides & Chrousos, 2014) | Image from: (Charmandari, Nicolaides & Chrousos, 2014) | ||
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| {{:screen_shot_2017-03-09_at_4.50.30_pm.png|}} | {{:screen_shot_2017-03-09_at_4.50.30_pm.png|}} | ||
| - | Figure 7: Oral tablets which replenish bodily hormones. | + | Figure 9: Oral tablets which replenish bodily hormones. |
| Image from: http://www.mcguffmedical.com, http://www.drsfostersmith.com | Image from: http://www.mcguffmedical.com, http://www.drsfostersmith.com | ||
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| **Injection Alternatives** | **Injection Alternatives** | ||
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| Since some individuals experience nausea leading to vomiting as a symptom, intravenous or intramuscular cortisol injections can replace the oral tablets (Mayo Clinic, 2015). | Since some individuals experience nausea leading to vomiting as a symptom, intravenous or intramuscular cortisol injections can replace the oral tablets (Mayo Clinic, 2015). | ||
| It is strongly recommended that individuals with the disease carry a cortisol injection kit with them in case of Addisonian/Adrenal Crisis (Canadian Addison Society, 2017). In the appropriate hospital setting, receiving an intravenous dose of hydrocortisone and dextrose sugar in saline solution would be an ideal treatment for the adrenal crisis (Mayo Clinic, 2015). Otherwise, the individual or family member can follow the appropriate instructions to inject the hydrocortisone intramuscularly into a large muscle, typically the thigh (quadricep muscle) (Canadian Addison Society, 2017). | It is strongly recommended that individuals with the disease carry a cortisol injection kit with them in case of Addisonian/Adrenal Crisis (Canadian Addison Society, 2017). In the appropriate hospital setting, receiving an intravenous dose of hydrocortisone and dextrose sugar in saline solution would be an ideal treatment for the adrenal crisis (Mayo Clinic, 2015). Otherwise, the individual or family member can follow the appropriate instructions to inject the hydrocortisone intramuscularly into a large muscle, typically the thigh (quadricep muscle) (Canadian Addison Society, 2017). | ||
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| {{:screen_shot_2017-03-09_at_4.49.57_pm.png|}} | {{:screen_shot_2017-03-09_at_4.49.57_pm.png|}} | ||
| - | Figure 8: Injection kit should be carried on the person in case of Addisonian crisis. | + | Figure 10: Injection kit should be carried on the person in case of Addisonian crisis. |
| Image from: http://www.addisons.org | Image from: http://www.addisons.org | ||
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| {{:screen_shot_2017-03-09_at_5.06.20_pm.png|}} | {{:screen_shot_2017-03-09_at_5.06.20_pm.png|}} | ||
| - | Figure 9: Intramuscular injection into a large muscle is usually recommended; typically the thigh. | + | Figure 11: Intramuscular injection into a large muscle is usually recommended; typically the thigh. |
| Image from: www.addisonsociety.ca | Image from: www.addisonsociety.ca | ||
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| - | Oral tablets, intravenous injections and intramuscular injections are current hormone replacement therapies for Addison’s Disease, however, there have been many clinical trials considering continuous subcutaneous hydrocortisone infusions (CSHI) as a better treatment option. A 2014 study investigated the efficacy of CSHI versus conventional oral hydrocortisone (OHC) replacement and the subcutaneous infusions showed improvements in normalization of ACTH and cortisol levels and improvements in quality of life (Oksnes et al., 2014). As shown in figure, the infusions got the morning blood cortisol levels back to normal ranges as opposed to the oral tablets (Oksnes et al., 2014). Cortisol levels should be high in the morning and the infusions reestablished this to the normal range (Oksnes et al., 2014). | + | Oral tablets, intravenous injections and intramuscular injections are current hormone replacement therapies for Addison’s Disease, however, there have been many clinical trials considering continuous subcutaneous hydrocortisone infusions (CSHI) as a better treatment option. A 2014 study investigated the efficacy of CSHI versus conventional oral hydrocortisone (OHC) replacement and the subcutaneous infusions showed improvements in normalization of ACTH and cortisol levels and improvements in quality of life (Oksnes et al., 2014). As shown in figure 12, the infusions got the morning blood cortisol levels back to normal ranges as opposed to the oral tablets (Oksnes et al., 2014). Cortisol levels should be high in the morning and the infusions reestablished this to the normal range (Oksnes et al., 2014). |
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| {{:screen_shot_2017-03-09_at_5.12.05_pm.png|}} | {{:screen_shot_2017-03-09_at_5.12.05_pm.png|}} | ||
| - | Figure 10: Morning cortisol levels in the CSHI condition are up to normal circadian levels; OHC condition levels are still low. | + | Figure 12: Morning cortisol levels in the CSHI condition are up to normal circadian levels; OHC condition levels are still low. |
| Image from: (Oksnes et al., 2014) | Image from: (Oksnes et al., 2014) | ||
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| {{:screen_shot_2017-03-09_at_2.13.42_pm.png|}} | {{:screen_shot_2017-03-09_at_2.13.42_pm.png|}} | ||
| - | Figure 11: All-cause mortality in Addison's patients, between 1987-2001, in Sweden. | + | Figure 13: All-cause mortality in Addison's patients, between 1987-2001, in Sweden. |
| Image from: Bergthorsdottir et al., 2006 | Image from: Bergthorsdottir et al., 2006 | ||
| </style> | </style> | ||
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| {{:screen_shot_2017-03-09_at_2.43.38_pm.png|}} | {{:screen_shot_2017-03-09_at_2.43.38_pm.png|}} | ||
| - | Figure 12: Medical bracelets help convey information. | + | Figure 14: Medical bracelets help convey information. |
| Image from: http://www.myidentitydoctor.com | Image from: http://www.myidentitydoctor.com | ||
| </style> | </style> | ||
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| ====== References ====== | ====== References ====== | ||
| - | Adrenal Insufficiency & Addison's Disease | NIDDK. (n.d.). Retrieved March 01, 2017, from https://www.niddk.nih.gov/health-information/endocrine-diseases/adrenal-insufficiency-addisons-disease#prepare | + | Adam, A., & Dixon, A. (2008). Preface. Grainger & Allison's Diagnostic Radiology, Xv. doi:10.1016/b978-0-443-10163-2.50002-6 |
| - | Neto, R. A., & Carvalho, J. F. (2014). Diagnosis and classification of Addison's disease (autoimmune adrenalitis). Autoimmunity Reviews, 13(4-5), 408-411. doi:10.1016/j.autrev.2014.01.025 | + | Addison’s Disease. (2015). Mayo Clinic. Retrieved February 28, 2017 from, http://www.mayoclinic.org/diseases-conditions/addisons-disease/diagnosis-treatment/treatment/txc-20156064 |
| - | "Addison Disease". MedicineNet. Archived from the original on 24 June 2007. Retrieved 2007-07-25. | + | "Addison Disease". MedicineNet. Archived from the original on 24 June 2007. Retrieved 2007-07-25. |
| - | + | ||
| - | Odeke, S., & Nagelberg, S. (2001). Addison disease. eMedicine Journal, 2, 5. | + | |
| - | + | ||
| - | Volpé, R. (1990). Autoimmune diseases of the endocrine system. Boca Raton: CRC Press. | + | |
| - | + | ||
| - | Lovas, K., & Husebye, E. S. (2002). High prevalence and increasing incidence of Addison's disease in western Norway. Clinical Endocrinology,56(6), 787-791. doi:10.1046/j.1365-2265.2002.t01-1-01552.x | + | |
| “Addison's disease - Treatment". NHS Choices. Retrieved 2017-02-25. | “Addison's disease - Treatment". NHS Choices. Retrieved 2017-02-25. | ||
| + | |||
| + | Adrenal Insufficiency & Addison's Disease | NIDDK. (n.d.). Retrieved March 01, 2017, from https://www.niddk.nih.gov/health-information/endocrine-diseases/adrenal-insufficiency-addisons-disease#prepare | ||
| Alschuler, L. (2016). The HPA Axis. Retrieved from http://www.integrativepro.com/Resources/Integrative-Blog/2016/The-HPA-Axis | Alschuler, L. (2016). The HPA Axis. Retrieved from http://www.integrativepro.com/Resources/Integrative-Blog/2016/The-HPA-Axis | ||
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| HLA-DRB1 gene. (2014). Genetics Home Reference. Retrieved 2 March 2017, from https://ghr.nlm.nih.gov/gene/HLA-DRB1 | HLA-DRB1 gene. (2014). Genetics Home Reference. Retrieved 2 March 2017, from https://ghr.nlm.nih.gov/gene/HLA-DRB1 | ||
| - | Michels A, Michels N (1 Apr 2014). "Addison disease: early detection and treatment principles". Am Fam Physician. 89 (7): 563–8. PMID 24695602. | + | Husebye, E. S., Allolio, B., Arlt, W., Badenhoop, K., Bensing, S., Betterle, C., … Pearce, S. H. |
| + | (2013). Consensus statement on the diagnosis, treatment and follow-up of patients with primary adrenal insufficiency. The Journal of Internal Medicine, 275 (2): 104-115. | ||
| + | |||
| + | Injection Kit. (2017). Canadian Addison Society. Retrieved February 28, 2017 from http://www.addisonsociety.ca/injection-kit.html | ||
| + | |||
| + | Lederer, E. (2016). Hyperkalemia. Medscape. | ||
| + | |||
| + | Lovas, K., & Husebye, E. S. (2002). High prevalence and increasing incidence of Addison's disease in western Norway. Clinical Endocrinology,56(6), 787-791. doi:10.1046/j.1365-2265.2002.t01-1-01552.x | ||
| + | |||
| + | Michels, A., & Michels, N. (2014). Addison disease: early detection and treatment principles. Indian Journal of Clinical Practice, 25(6). | ||
| Miller, W. L., & Bose, H. S. (2011). Early steps in steroidogenesis: intracellular cholesterol trafficking thematic review series: genetics of human lipid diseases. Journal of lipid research, 52(12), 2111-2135. | Miller, W. L., & Bose, H. S. (2011). Early steps in steroidogenesis: intracellular cholesterol trafficking thematic review series: genetics of human lipid diseases. Journal of lipid research, 52(12), 2111-2135. | ||
| Mitchell, A. L., & Pearce, S. H. (2012). Autoimmune Addison disease: pathophysiology and genetic complexity. Nature reviews Endocrinology, 8(5), 306-316. | Mitchell, A. L., & Pearce, S. H. (2012). Autoimmune Addison disease: pathophysiology and genetic complexity. Nature reviews Endocrinology, 8(5), 306-316. | ||
| + | |||
| + | N. A. Comprehensive Metabolic Panel. (2005). Lab Tests Online. | ||
| + | |||
| + | Neto, R. A., & Carvalho, J. F. (2014). Diagnosis and classification of Addison's disease (autoimmune adrenalitis). Autoimmunity Reviews, 13(4-5), 408-411. doi:10.1016/j.autrev.2014.01.025 | ||
| + | |||
| + | Odeke, S., & Nagelberg, S. (2001). Addison disease. eMedicine Journal, 2, 5. | ||
| + | |||
| + | Oksnes, M., Björnsdottir S., Isaksson, M., Methlie, P., Carlsen, S., Nilsen, R. M., … Løvås, K. | ||
| + | (2014). Continuous Subcutaneous Hydrocortisone Infusion versus Oral Hydrocortisone Replacement for Treatment of Addison's Disease: A Randomized Clinical Trial. The Journal of Clinical Endocrinology & Metabolism, 99 (5): 1665-1674. | ||
| “Overview: Addison’s disease”. Mayo Clinic. Retrieved from http://www.mayoclinic.org/diseases-conditions/addisons-disease/manage/ptc-20156068. | “Overview: Addison’s disease”. Mayo Clinic. Retrieved from http://www.mayoclinic.org/diseases-conditions/addisons-disease/manage/ptc-20156068. | ||
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| Pavlaki, A. N., & Magiakou, M. A. (2011). Glucocorticoid Therapy and Adrenal Suppression. | Pavlaki, A. N., & Magiakou, M. A. (2011). Glucocorticoid Therapy and Adrenal Suppression. | ||
| - | Addison’s Disease. (2015). Mayo Clinic. Retrieved February 28, 2017 from, http://www.mayoclinic.org/diseases-conditions/addisons-disease/diagnosis-treatment/treatment/txc-20156064 | + | Sarkar, S. B., Sarkar, S., Ghosh, S., & Bandyopadhyay, S. (2012). Addison’s disease. Contemporary Clinical Dentistry, 3(4), 484–486. http://doi.org/10.4103/0976-237X.107450 |
| - | Husebye, E. S., Allolio, B., Arlt, W., Badenhoop, K., Bensing, S., Betterle, C., … Pearce, S. H. | + | Simon, E. (2016). Hyponatremia. Medscape. |
| - | (2013). Consensus statement on the diagnosis, treatment and follow-up of patients with primary adrenal insufficiency. The Journal of Internal Medicine, 275 (2): 104-115. | + | |
| + | Ten, S., New, M., & Maclaren, N. (2001). Addison’s disease 2001. The Journal of Clinical Endocrinology & Metabolism, 86(7), 2909-2922. | ||
| - | Injection Kit. (2017). Canadian Addison Society. Retrieved February 28, 2017 from http://www.addisonsociety.ca/injection-kit.html | + | Volpé, R. (1990). Autoimmune diseases of the endocrine system. Boca Raton: CRC Press. |
| - | Michels, A. & Michels, N. (2014). Addison Disease: Early Detection and Treatment Principles. Am Fam Physician. 89 (7): 563-568. | ||
| - | Oksnes, M., Björnsdottir S., Isaksson, M., Methlie, P., Carlsen, S., Nilsen, R. M., … Løvås, K. | ||
| - | (2014). Continuous Subcutaneous Hydrocortisone Infusion versus Oral Hydrocortisone Replacement for Treatment of Addison's Disease: A Randomized Clinical Trial. The Journal of Clinical Endocrinology & Metabolism, 99 (5): 1665-1674. | ||
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