How many autoimmune disease are there

Certain treatments can slow or stop the discoloration, including medications and UV light therapy. Scleroderma causes an abnormal growth of connective tissue in the skin and blood vessels, leading to skin that is hard and thick. In some people, the condition is mild, but in some others, scleroderma can affect internal organs and be life threatening. Symptoms include :.

There is currently no cure for scleroderma , but a person can treat the symptoms using medications for heartburn and bowel discomfort. Sometimes, a doctor may also recommend immunosuppressants, especially for fibrosing scarring lung disease. This causes an oxygen deficiency, leading to symptoms such as:. Doctors treat hemolytic anemia with corticosteroids, which reduce inflammation, and immunosuppressant drugs, which lower immune system activity.

A doctor might also consider a splenectomy, which refers to the surgical removal of the spleen. The spleen removes damaged red blood cells from circulation, so by removing it, a person is less likely to have low red blood cell levels. However, autoimmune processes can also affect other blood cells. When they affect platelets, it can lead to thrombocytopenia. When they affect white blood cells, it can give rise to leukopenia, lymphopenia, and neutropenia.

Repeated exposure to gluten may damage the intestinal lining. However, most people with celiac disease can prevent these symptoms by removing sources of gluten from their diet. Inflammatory bowel disease IBD causes chronic inflammation of the digestive tract, giving rise to pain and irritation. The symptoms of IBD can include:. IBD does not currently have a cure, but people may see an improvement in symptoms and their quality of life by changing their eating habits.

Medications such as aminosalicylates, corticosteroids, and immunosuppressants — including biologics — can also help. In type 1 diabetes , the immune system attacks the cells in the pancreas that make insulin. Insulin is a hormone that controls blood sugar levels. People with type 1 diabetes can manage the condition with daily insulin injections to balance out the amount of carbohydrates they eat.

Unlike type 2 diabetes , a person cannot prevent type 1 diabetes by making diet or lifestyle changes. However, monitoring diet and exercise levels can help reduce symptoms. This can cause a range of symptoms , including:. Antithyroid medications can lower thyroid hormone levels, and radioactive iodine damages the thyroid cells so that they do not produce as much hormone. In severe cases, a doctor may recommend removing part or all of the thyroid gland. In multiple sclerosis MS , the immune system mistakenly attacks the myelin sheath that protects the nerves.

This causes damage, affecting the transmission of information to and from the brain and spinal cord and the nerves they connect with. The fetus, containing foreign antigens, relies on the mother to serve as its host, resulting in immune changes that tend to cause a suppression of the maternal immune system [ 26 ]. This is believed to be carried out in order to prevent rejection of the fetus but leads to a suppressed immune system, which can certainly trigger the onset of autoimmune diseases.

Hormonal changes will also occur during the post-partum period leading to an increased incidence of certain autoimmune diseases, such as rheumatoid arthritis. A study found that in the post-partum, there is a significant rise in the incidence of rheumatoid arthritis cases having an incidence rate ratio of in the 24 months after delivery [ 27 ].

The changes in hormone levels in females going through puberty increases their risk of developing autoimmune diseases. A study was conducted in Taiwan to indicate the vast difference in the likelihood of developing an autoimmune disease such as SLE for girls rather than boys. This epidemiological study had indicated a substantial increase in the prevalence of juvenile SLE amongst Taiwanese girls in comparison to boys who were of the same age [ 30 ].

The prevalence of SLE in girls at the age of one was 0. For boys, the prevalence was almost zero per , at ages 1 and 7, and to 7. After the onset of puberty, there is an increase in incidence with pubertal girls found to be at a greater risk for developing multiple sclerosis than pre-pubertal girls [ 32 ]. Such reports suggest that the hormonal changes which occur during pubertal development could be an underlying factor in the gender disparity of autoimmune diseases.

Evidence has shown that the changing hormonal climate which occurs during the menopausal transition plays a role in the increased susceptibility of peri- and post-menopausal women to autoimmune diseases due to its effect on inflammatory processes. For instance, in women around 50 years of age, the neutrophil percentage dropped, whereas lymphocyte percentage rose [ 33 ], thereby subjecting perimenopausal women to an increased risk of lymphocyte-mediated autoimmune diseases.

Autoimmune diseases such as rheumatoid arthritis and SLE affect women over the age of 40 more frequently. It can be deduced that certain autoimmune conditions are more prevalent given the age and physiological state of the patient. For example, researchers are unsure as to why it has been shown that high levels of estrogen and progesterone are protective for disease activity in rheumatoid arthritis.

Therefore, pregnancy would be considered protective against the risk of disease development, due to the increase in estrogen and progesterone levels. On the contrary, menopause and post-partum are often associated with disease worsening due to a drop in estrogen and progesterone levels [ 34 ]. There is also a surge of female sex hormones during puberty such as estrogen. High levels of estrogen have been observed in the synovial fluid of patients who are affected by both SLE and rheumatoid arthritis.

This is due to the action of aromatase on peripheral tissues. Eighty percent of all individuals affected by autoimmune disorders tend to be women due to variation within the sex chromosomes and hormonal changes. Currently, there are no known cures to autoimmune disorders. Other triggers such as hormonal changes during puberty and pregnancy for women may often be inevitable. Autoimmune disorders can often be hereditary; thus, it is crucial for individuals who are potentially at risk to be aware of their full family history.

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Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus. The authors have declared that no competing interests exist. National Center for Biotechnology Information , U. Journal List Cureus v. Published online May Author information Article notes Copyright and License information Disclaimer.

Corresponding author. Fariha Angum moc. Received May 2; Accepted May This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

This article has been cited by other articles in PMC. Abstract Autoimmune disorders are characterized as a condition in which the host's immune system mistakenly attacks itself. Keywords: autoimmune disorders, lupus, sex chromosomes, systemic lupus erythema. Introduction and background Autoimmune disorders are conditions in which the immune system is unable to differentiate between healthy tissue and potentially harmful antigens.

Table 1 Autoimmune disorders and the average age of onset SLE, systemic lupus erythematosus. Open in a separate window. Review Sex chromosomes Men and women alike are born with 23 pairs of chromosomes, with 22 pairs of autosomes and one pair of sex chromosomes, the differentiating factor between the two genders. Figure 1. Conclusions Eighty percent of all individuals affected by autoimmune disorders tend to be women due to variation within the sex chromosomes and hormonal changes.

Footnotes The authors have declared that no competing interests exist. References 1. Female predominance and X chromosome defects in autoimmune diseases.

J Autoimmun. Talal N. Systemic lupus erythematosus in the community. Incidence, prevalence, outcome, and first symptoms; the high prevalence in black women. Fessel WJ. Arch Intern Med. The epidemiology of rheumatoid arthritis in Rochester, Minnesota: a study of incidence, prevalence, and mortality. Am J Epidemiol. Arthritis Rheum. A role for sex chromosome complement in the female bias in autoimmune disease. J Exp Med.

X-inactivation profile reveals extensive variability in X-linked gene expression in females. Carrel L, Willard HF. Tales of the Y chromosome. Willard HF. The X chromosome and sex-specific effects in infectious disease susceptibility. Hum Genomics. Mammalian X-chromosome inactivation. Annu Rev Genet. Dicer regulates Xist promoter methylation in ES cells indirectly through transcriptional control of Dnmt3a. Epigenetics Chromatin. The female X-inactivation mosaic in systemic lupus erythematosus. Stewart JJ.

Immunol Today. Role of histone H3 lysine 27 methylation in X inactivation. Altered X-chromosome inactivation in T cells may promote sex-biased autoimmune diseases. JCI Insight. A gene network regulated by the transcription factor VGLL3 as a promoter of sex-biased autoimmune diseases.

Autoimmune diseases are affecting more people for reasons unknown. Likewise, the causes of these diseases remain a mystery. Studies indicate these diseases likely result from interactions between genetic and environmental factors. Gender, race, and ethnicity characteristics are linked to a likelihood of developing an autoimmune disease.

Progress happens through multiple research efforts, such as:. Use the browser controls to adjust the font size, or print this page. Further Reading. Fact Sheets 2 pages. Last accessed July 19, Genetics of autoimmune diseases: insights from population genetics. J Hum Genet. Ultraviolet radiation exposure is associated with clinical and autoantibody phenotypes in juvenile myositis.