Role of Autoimmunity in Three Endocrine Disorders

Role of Autoimmunity in Three Endocrine Disorders

A number of endocrine illnesses are immune mediated and can now be reliably predicted. Autoimmune disorders can occur in a person and people related to them. Families with history of autoimmunity, and has had antibody screening done, becomes aware of those that carry such risk. Knowing the prevalence of such disorders and the diseases associated with them can help in early diagnosis and prevent them from becoming more serious. Autoimmunity affects several glands in the body. Studies reveal that alleles are very important in the determination of tissue-specific targeting (Aaron W. Michels & George S. Eisenbarth, 2010).

The Process of Autoimmunity

Autoimmunity is necessary for the body to maintain its health by countering effects of external virulent and organic attacks. It involves regulatory networks that provide the body with immunity against infection. It has not yet been determined why instances arise where autoimmunity processes sometimes become causal in destroying some healthy tissues. The autoimmune conditions identified so far range from systemic to tissue specific disorders. Such conditions can start at any stage of life — childhood to adulthood. The function of the immune system is protecting an individual from infections. With the onset of an autoimmune disease, the immune system launches an ill-informed attack on healthy cells. Most of the conditions are genetic. Demographics like women — particularly Hispanic-America, African-America and Native-American women — have a higher risk of developing some autoimmune disorders. The disorders develop from a relatively overactive response of the immune system to body and tissues. Instead of attacking pathogens, the body attacks itself having confused cells of given body part for pathogens. The attack can be at only particular organs as is the case with autoimmune thyroiditis, or at a particular tissue in several places as is the case with Good Pasture’s disease, which can affect both the kidney’s and the lung’s basement membrane (Sean Zeelie, 2012).

1. Autoimmunity in Endocrine System

The most common autoimmune condition is Hashimoto’s thyroiditis (HT). About 10% of the general population is affected by HT. It results in a gradual decline of thyroid function, development of goiter, and the infiltration of T-cell on histology. The condition is more prevalent among women than it is in men. Women are 7 times more likely to develop the condition than men. There is no significant association between HT and HLA even though its occurrence is most likely in genetically susceptible populations. CTLA-4 and thyroglobulin mutations are associated with the condition. T-cells play a very important function in disease pathogenesis as it reacts with thyroid antigens and secretes inflammatory cytokines. Autoantibodies build up in HT to form TSHR, thyroglobin and peroxidase. The belief is that the auto-antibodies result from damage caused thyroid follicular cells brought about by T. cells. Thyroid peroxidase is the main autoantigen. There is a close association between disease activity and autoantibodies to TPO (Aaron W. Michels & George S. Eisenbarth, 2010).

Evidence exists showing the presence of genetic components in most cases of autoimmune endocrine diseases. Studies of familial inheritance of thyroiditis and type 1 diabetes have yielded some of the best pieces of evidence. The concordance rate among siblings is about 3% to 4% while the rate among monogenic twins is about 50%. As compared to the risk of the general population, which is about 0.3%, the two former groups suffer a significantly higher risk. This risk, as data collected points out, is due to genetics as well as other factors like environmental factors (Mark S. Anderson, 2008).

Grave’s Disease and Addison’s Disease

Evidence shows that when one develops type 1 diabetes, their risk of contracting other autoimmune diseases increases. This is due to the genetic susceptibility arising from developing such a condition. The autoimmune process going on in pancreatic cells might also have an effect on other organs and so leading to the individual developing organ-nonspecific autoimmune conditions. Grave’s disease and Hashimoto’s thyroiditis are diabetes 1 most frequently occurring co-morbidities (15-30%). Others include celiac disease (4-9%), addison’s disease (0.5%), vitiligo (2-10%) and autoimmune gastritis (5-10%). Type 1 diabetes patients who develop other autoimmune diseases record a reduction in quality of life and increased mortality and morbidity (Aleksandra Krzwska & Iwona Ben-Skowronek, 2016).

As is the case with various autoimmune conditions, Graves’ disease mostly results from a combination of environmental and genetic factors that may also have a role in the conditions’ long-term prognosis. With time, Graves’ disease’s activity might fluctuate and at times patients might become euthyroid. Besides the variation, it has been established that hyperthyroidism therapy can have an influence on the activity on the disease’s activity (Peter Laurberg, et al., 2008). Autoimmune adrenal insufficiency results from the adrenal cortex being destroyed through immune activities that are cell-mediated.

Addison’s disease can also emerge as autoimmune polyendocrinopathy syndromes. Where type 1 diabetes mellitus and/or thyroid disease occur together with Addison’s disease, the condition is referred to as autoimmune polyglandular syndrome type 2 (APS-2. APS-2 rarely occurs in children and there is lack of enough data for a comprehensive study (Heves Kimizibekmez, Rahime Gul Yesiltepe Mutlu, Nafiye Demikiran Urganci & Ayse Oner, 2015).

2. Pathophysiological Changes

Diabetes is a condition of metabolic disorders involving a chronic hyperglycemia brought about by insufficient insulin action. Diabetes 2’s major pathophysiological features are increased resistance to insulin and impaired insulin secretion. Impairment of the function of the pancreatic cell shows progressively as time passes. Insulin resistance and impairment of insulin secretion jointly contribute to the body, giving rise to the pathophysiological conditions. Even in cases where over-response is noted among people with obesity, early-phase secretory response is noted to decrease. This decrease is key component of the condition and is very vital as one of the basic pathophysiological changes happening at the early stages of the disease. Impaired insulin action in key target organs kike the muscles and the liver is common in type 2 diabetes cases. Resistance to insulin develops and then expands before the onset of the disease (Kothei KAKU, 2010).

Initiating early intervention is vital if the progression of the pathophysiological conditions is to be curbed. To ensure effective management of diabetes in the long-term, an early effort to eliminate glucose toxicity effects to the extent possible is essential. Microvascular disease has a close association with long-term control of glucose. Treatment should be adopted from the standpoint of not just vascular complications control but also to prevent aggravation of pathophysiological conditions (Koheri KAKU, 2010).


While there are many aspects still not yet fully explored and understood, an ever increasing speed is evidence of a significant place epigenetically modified gene expression has in autoimmunity development. Research done in the past employed methods that have been surpassed by new technology which involve next generation sequencing able to increase information clarity and detail in data gotten from epigenetic modifications. Nonetheless, bettering out comprehension of what role epigenetic modifications has in autoimmunity development has the potential to bring closer the possibility of preventing or controlling autoimmune disease by the utilization of drugs targeting proteins that control DNA methylation, chromatin modifications and various other epigenetic mechanisms.


Aaron W. Michels, & George S. Eisenbarth. (2010). Immunologic Endocrine Disorders. Journal of Allergy, Clinical Immunology, 225-237.

Aleksandra Krzewska, & Iwona Ben-Skowronek. (2016). Effect of Associated Autoimmune Diseases on Type 1 Diabetes Mellitus Incidence and Metabolic Control in Children and Adolescents. Biomed Research International.

Heves Kirmizibekmez, Rahime Gul Yesiltepe Mutlu, Nafiye Demirkiran Urganci, & Ayse Oner. (2015). Autoimmune Polyglandular Syndrome Type 2: A Rare Condition in Childhood. Kirmizibekmez H, Yesiltepe Mutlu RG, Demirkiran Urganci N, Oner A. Autoimmune Polyglandular Syndrome Type 2: A Rare Condition in Childhood. Journal of Clinical Research in Pediatric Endocrinology. 2015;7(1):80-82. doi:10.4274/jcrpe.1394., 80-82.

Kohei KAKU. (2010). Pathophysiology of Type 2 Diabetes and its Treatment Policy. Japan Medical Association Journal, 41-46.

Mark S. Anderson. (2008). Update in Endocrine Autoimmunity. Journal of Clinical Endocrinology and Metabolism, 3663-3670.

Peter Laurberg, Goran Wallin, Leif Tallstedt, Mirna Abraham-Nordling, Goran Lundell, & Ove Torring. (2008). TSH-receptor autoimmunity in Graves’ disease after therapy with anti-thyroid drugs, surgery, or radioiodine: a 5-year prospective randomized study. European Journal of Endocrinology, 69-75.

Sean Zeelie. (2012). Understanding Autoimmune Disease — a review article for the layman. Research Centre for Autoimmune Disease.

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