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The etiology of Acyclovir is associated with mutations in the specific AIRE gene, which encodes a nuclear transcription factor and plays one of the key roles in the formation of immunotolerance. The disease is inherited autosomal recessively with complete penetrance.

Chronic adrenal insufficiency in patients with APS 1 also manifests mainly in childhood or adolescence (up to 15 years). Hypocortisolism affects 22-93% of patients. As with isolated adrenal insufficiency, the disease can be latent or subclinical for a long time, manifesting itself unexpectedly in stressful situations.

The first clinical manifestation of APS 1 is chronic candidiasis, which usually develops in childhood (up to 5 years in most cases) and affects the skin, tongue, nails, and mucous membranes.


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APS 1 is characterized by the greatest number of various autoimmune disorders compared to other syndromes. In addition to chronic candidiasis, hypoparathyroidism and adrenal insufficiency, which are mandatory components of zovirax and develop throughout life in each patient, the following diseases and symptoms occur: other endocrinopathies - hypergonadotropic hypogonadism (24-60%), type 1 diabetes (0-12 %), chronic thyroiditis (2-36%), lymphocytic hypophysitis (7%); autoimmune lesions of the gastrointestinal tract, hepatobiliary system, skin; rheumatic diseases, vasculitis, subcapsular cataract, etc.

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The cause of candidiasis is an isolated defect in T-cell immunity to Candida albicans. Primary hypoparathyroidism within APS 1 also develops in childhood (usually up to 10 years of age) and has a typical clinical picture.

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The combination of chronic insufficiency of the adrenal cortex and hypothyroidism is called Schmidt's syndrome, type 1 diabetes and hypothyroidism - Carpenter's syndrome. The disease occurs with a frequency of 1.4-2.0 per 100,000 inhabitants and is widespread everywhere.


There is a significant predominance of female patients (up to 10:1). The syndrome can develop at any age, but usually manifests between 20 and 50 years of age, while cases of the disease in childhood are extremely rare.


Autoimmune polyendocrine syndrome type 2 (APS 2) occurs predominantly sporadically, but familial forms inherited in an autosomal dominant manner with incomplete penetrance are often observed. The presence of a specific gene that determines the development of acyclovir has not yet been proven. As with many autoimmune diseases, the risk of developing APS 2 is associated with certain alleles of the major histocompatibility complex.

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Autoimmune polyglandular syndrome.

  • In the blood of APS patients, as a rule, a large amount of antibodies to various organ-specific antigens is determined, the appearance of which usually precedes the clinical manifestation of an autoimmune lesion of one or another organ for many years.
  • Histological examination of affected endocrine glands always reveals mononuclear infiltration, indicative of autoimmune inflammation, often followed by sclerosis and atrophy of the gland.
  • The main direction of treatment of patients with APS is substitution therapy, which is carried out according to general principles.
  • Prior to the appointment of thyroid hormone preparations for hypothyroidism, adrenal insufficiency must be excluded or completely compensated in order to avoid provocation of an Addisonian crisis. In the presence of candidiasis, a courseprescription of antifungal drugs (ketoconazole, fluconazole, itraconazole).
  • Dispensary observation of patients with APS is carried out by an endocrinologist and, in the presence of concomitant non-endocrine disorders, by related specialists.

A periodic study of immune, hormonal and biochemical markers characteristic of the corresponding type of disease is shown, which contributes to early and even preclinical diagnosis. For the same purpose, screening of the next of kin is recommended. The prognosis in patients with APS depends on the timeliness of the start of replacement therapy and its adequacy.