Irasek-Zulzer-Wilson Syndrome

Irasek-Zulzer-Wilson diagnosis.

Jirasek-Zulenzer-Vilosun syndrome - (Jirasek A., 1890-1959, surgical practice in Czechoslovakia, Zulzer W.W., American pediatricians. J.L. Wilson, 1926 a/o - American pediatricians) - a combination of symptoms of vesiculitis (dilation of the bladder) and mucopurulent urine of men, leading to the development of prostate tumors. The main reason is chronic urethritis and stagnation of urine in the bladder, prolonged urinary congestion. In this regard, microbes are transferred from the bladder to the prostate gland through the catheter. Local inflammation of the prostate gland requires special treatment related to the effect on the urethra, which should be simultaneously treated for inflammation. Warm sitz baths are recommended. A blood test indicates the presence of β-hemolytic streptococci, Proteus, Weise-heller bacillus, Vogt-Colli rods, etc. Treatment with penicillin is carried out for one or two months. Surgical treatment is indicated for men with infiltration of the hypogastric region and tumor growth into the rectum or pelvic veins. Infection of the genital organs can cause tumors of the testicles or genitourinary system. Chronic and aggressive pharyngitis, tonsillitis, and sinusitis are often observed in young men. The absence of the pharyngeal reflex causes atrophy of the uvula, epiglottis and soft palate. Putrid breath, unpleasant taste, lockjaw, paralysis, and convulsions often appear. Other symptoms may include diarrhea or constipation, skin changes (flaking), tooth loss, voice changes and other problems associated with vitamin imbalance or inflammation. Spicy quiche

Iraseki-Zulzer-Wilson syndrome is a rare genetic disorder also known as Iraseki-Schuls disease. This syndrome is caused by three mutations in the SMAD4 gene, located on chromosome 3p. Depending on the type of mutation, there may be different manifestations of the disease, but in general it is characterized by severe mental retardation, facial abnormalities, and problems with organs and tissues.

Initially, the syndrome was described as a severe form of muscular dystrophy, often resulting in death before birth. With the development of genetics, it became clear that this form of the disease is actually another, milder form of dystrophic myotonia. Genotyping was determined and the gene responsible for the development of the syndrome was identified. Subsequent research showed that this disease develops as a result of mutations in three genes.

Today, there are several diagnostic methods that can detect the presence of the syndrome in a patient. The most effective of them is molecular genetic