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Addisons Disease: Symptoms and Effects
Introduction
Addisons disease is a condition which develops in the human body most frequently as a result of autoimmune adrenalitis and damages adrenal tissue, which ultimately hinders the production of cortisol (Rumsby and Woodward 168). The adrenal cortex, which is unable to produce enough glucocorticoids and mineralocorticoids, may potentially cause an adrenal crisis (Barthel et al. 165). Medical professionals have to able to detect this disease in patients as soon as possible since it can be extremely life-threatening and lead to death.
Physiology and Anatomy
The adrenal glands are a part of the endocrine system that can be found above each kidney and have a triangular shape (Johns Hopkins Medicine). These glands are divided into two parts the inner one, the medulla, and the outer one, the adrenal cortex. The main function of the latter is to produce steroid hormones, while the purpose of the former is to secret hormones which are responsible for controlling stress response (Johns Hopkins Medicine). The adrenal cortex comprises three important areas that produce different hormones and are vital for the proper functioning of peoples bodies and organs (Johns Hopkins Medicine). Zona glomerulosa produces a mineralocorticoid hormone called aldosterone, which regulates blood pressure and blood pH by adjusting the electrolytes level (Johns Hopkins Medicine). Zona fasciculata secrets cortisol, which is a glucocorticoid hormone that reduces inflammation in the body and monitors the use of proteins, carbohydrates, and fats (Johns Hopkins Medicine). Finally, Zona Reticularis produces weak male hormones, androgenic steroids, and dehydroepiandrosterone (DHEA), which are later converted into estrogens or androgens (Johns Hopkins Medicine). Thus, a lack of hormone production in adrenal glands increases the risk of Addisons Disease, which can lead to death if not treated.
Symptoms and Effects
Knowing the symptoms of the disease is crucial when diagnosing it since this condition is relatively rare. Patients with Addisons Disease often experience overall weakness, fatigue, and considerable weight loss, as well as problems with the gastrointestinal tract (Barthel et al. 165). These symptoms develop over several years and can be unnoticeable for patients who may link them to other conditions. Frequently, patients become diagnosed with Addisons Disease after experiencing substantial stress, which highlights deficiencies in cortisol and aldosterone in their body. Low levels of these hormones can ultimately cause orthostasis, hypotension, and even adrenal crisis, which is an acute condition with potentially lethal complications (Dineen et al. 3). Another symptom of Addisons Disease is hyperpigmentation, which is caused by an adrenocorticotrophic hormone (ACTH), which stimulates the melanocortin 1 receptor and leads to a darkened skin tone. Hyperpigmentation is not limited to one particular area and can spread across the entire body, including on buccal mucosa and lips vermilion border (Michels and Michels 564). Although it must be noted that these symptoms are not always caused by Addisons Disease and can be results of other conditions, thus, professionals have to conduct necessary tests before diagnosing.
Causes and Risk Factors
Several decades ago, tuberculosis, which initiated bilateral adrenal destruction, was the main cause of Addisons Disease in the world, yet, nowadays, it affects most people in developing countries (Fofi et al. 23). In the majority of patients in developed nations, the onset of primary adrenal insufficiency is caused by other autoimmune diseases, for example, autoimmune adrenalitis (Fofi et al. 23). Autoimmune adrenalitis, which destroys the adrenal cortex, can be both an isolated disorder and occurring together with other types of autoimmune diseases in autoimmune polyendocrinopathy syndrome (APS), a rare autosomal recessive syndrome. Infectious diseases, especially chronic ones such as bilateral adrenal tumors, including lung cancer, melanoma, sarcoidosis, histoplasmosis may provoke Addisons Disease. The adrenal cortex in patients bodies can also be destroyed as a result of hemorrhage caused by meningococcemia. Moreover, chronic conditions such as AIDS often suppress the secretion of cortisol and aldosterone in the human body, which may trigger Addisons Disease or worsen other symptoms (Lang 42). Researchers still find new conditions influencing Addisons Disease, which makes it difficult to trace the primary adrenal deficiency to one particular cause.
Statistics
As it was mentioned earlier, Addisons disease is a relatively rare disorder that has a prevalence of 411 per 100 000 and an incidence of 0.8 per 100 000 population/year (OConnell and Siafarikas 834). The condition is thirty times less prevalent than type 1 diabetes and two-hundred times less frequent than autoimmune thyroid diseases. During childhood, boys are more likely to develop this condition since they account for 75% of all patients, while among adults, women constitute the majority of cases, which is 70%. Females are also more susceptible to Addisons disease if it occurs in combination with polyglandular autoimmune syndromes. When the condition is isolated, it more frequently affects males under twenty years old (Fofi et al. 24). The syndrome is widespread among specific ethnic groups such as Sardinian (1:14,000), Finnish (1:25,000) and Norwegian populations (1:90,000) (Mitchell and Pearce 308). Nevertheless, it is worth mentioning that Addisons disease can be found across different segments of society, and people of any age, gender, and race. The statistics of western countries demonstrate a much better picture than those of developing countries, where the problem is exacerbated by the healthcare issues.
Treatment
Treatment for Addison disease implies a hormone therapy using glucocorticoids and mineralocorticoids, only if the level of aldosterone is also quite low, the standard treatment regimen involves taking hydrocortisone or prednisone (Michels and Michels 564). For example, the latest study has shown that glucocorticoid therapy helps decrease GDF15 hormone responsible for reducing food intake in patients with Addisons disease (Melvin et al. 1432). According to the recommended guidelines of the Endocrine Society, cortisone acetate or hydrocortisone can be given to patients three times a day in equal doses (Rumsby and Woodward 175). Although, there is an alternative to these drugs, particularly in the form of prednisolone, which can be offered to patients who require a simpler therapy in order to improve comfort (Barthel et al. 167). Moreover, as demonstrated in one study, dual-release hydrocortisone preparation showed better results than conventional hydrocortisone therapy. The research indicated that this type of treatment contributed to more effective lipids metabolism and significantly reduced central adiposity, which impaired the glucose level (Giordano et al. 367). Thus, hydrocortisone therapy must be the primary means of treating Addisons disease in the majority of cases.
Conclusion
Addisons disease or primary adrenal deficiency is a serious condition that affects people of all ages, genders, and races and constitutes adrenal glands insufficient production of hormones such as cortisol and aldosterone. This condition occurs when the outer layer of the adrenal glands, the adrenal cortex, suffers damage and stops to secret the aforementioned hormones, which are vital for the human body. The main symptoms of this disorder are weakness, fatigue, weight loss, and hyperpigmentation, which causes the skin tone to become darkened. Nowadays, the development of Addisons disease is largely attributed to other autoimmune conditions such as autoimmune adrenalitis and infectious diseases, for example, adrenal tumors. The disorder is quite uncommon, and it is most prevalent among adult females and males during their first twenty years of life. The primary treatment for Addisons Disease is hormone therapy based on glucocorticoids, namely, hydrocortisone, which has been proved to be the most effective solution.
Works Cited
Barthel, Andreas, et al. An Update on Addisons Disease. Experimental and Clinical Endocrinology & Diabetes, vol. 127, 2019, pp. 165175.
Dineen, Rosemary, et al. Adrenal Crisis: Prevention and Management in Adult Patients. Therapeutic Advances in Endocrinology and Metabolism, vol. 10, 2019, pp. 112.
Fofi, Claudia, et al. Renal Involvement in Adrenal Insufficiency (Addison Disease): Can we Always Recognize it? Internal and Emergency Medicine, vol. 15, 2019, pp. 2331.
Giordano, Roberta et al. Improvement of Anthropometric and Metabolic Parameters, and Quality of Life Following Treatment with Dual-Release Hydrocortisone in Patients with Addisons Disease. Endocrine, vol 51, no. 2, 2015, pp. 360368.
Johns Hopkins Medicine. Adrenal Glands. Johns Hopkins Medicine, 2020.
Lang, Florian, editor. Encyclopedia of Molecular Mechanisms of Disease. Springer, 2009.
Melvin, Audrey, et al. GDF15 Is Elevated in Conditions of Glucocorticoid Deficiency and Is Modulated by Glucocorticoid Replacement. The Journal of Clinical Endocrinology & Metabolism, vol. 105, no. 5, 2020, pp. 14271434.
Michels, Aaron, and Nicole Michels. Addison Disease: Early Detection and Treatment Principles. American Family Physician, vol. 89, no. 7, 2014, pp. 563568.
Mitchell, Anna L., and Simon H.S. Pearce. Autoimmune Addison Disease: Pathophysiology and Genetic Complexity. Nature Reviews Endocrinology, vol. 8, no. 5, pp. 306316.
OConnell, Susan, and Aris Siafarikas. Addison Disease: Diagnosis and Initial Management. Australian Family Physician, vol. 39, no. 11, 2010, pp. 834837.
Rumsby, Gill., and Gary M. Woodward, editors. Disorders of Steroidogenesis. Springer, 2019.
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