The clinical picture of Bolivian hemorrhagic fever is similar to that described above, except that epistaxis and hematemesis are more common early in the disease. Diagnostics. Antibodies, IgM appear not earlier than 10-20 days.

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There is no lymphadenopathy or splenomegaly. 3-5 days after the onset of the disease, the patient's condition worsens, there are signs of coumadin, hypotension up to 50-100 mm Hg. Art., oliguria and relative bradycardia. In more severe cases, hemorrhagic symptoms occur: bleeding from the gums, hematemesis, hematuria, melena. Progressive oliguria and tremor of the tongue and limbs are also possible. Some patients develop mental disorders characterized by agitation, delirious state or stupor.

On days 7–10, progressive shock, hypothermia, galloping, or gastrointestinal bleeding may be seen. In fatal cases, the cause of death is usually pulmonary edema. During the recovery period, transient alopecia is noted. The number of Warfarin pills remains within the normal range or is slightly increased. The total number of leukocytes is reduced to 1.2-3.4×10 9 /l. Possible thrombocytopenia. Intravascular disseminated blood coagulation, apparently, does not underlie hemorrhagic manifestations. Levels of complement components C2, C3 and C5 are reduced. Urine may be redwood in color. Severe albuminuria is not uncommon. Blood urea nitrogen rises rapidly.

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Treatment consists of supportive measures, including peritoneal dialysis or hemodialysis filtration to correct both azotemia and pulmonary edema. In a double-blind study, administration of immune plasma was shown to reduce mortality in AHL from 16% to 1%. However, patients treated with immune plasma experienced fever and signs of cerebellar dysfunction. Preliminary studies have shown that ribavirin may be effective in experimental BGL in rhesus monkeys.

  • In Bolivia, measures aimed at the control of rodents, and especially Calomys callosus, living in houses, led to a rapid and significant decrease in the incidence among people.
  • In Argentina, the widespread distribution of infected rodents makes control measures ineffective.
  • DEPRIVATE ASBESTOS - a disease of the scalp, characterized by asbestos focal peeling, usually in the parietal region.
  • Hair can thin out, but skin atrophy does not develop.
  • It is assumed that the disease may be a form.
  • It is observed more often in children and young people.
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The information presented on the site should not be used for self-diagnosis and treatment and cannot serve as a substitute for an in-person consultation with a dermatologist. If you are a doctor, then after registering on the site you will get access to special information.

If you are already registered, enter your username and password (form in the upper right corner or here). Gadzhimuradov M.N., Israfilova G.O., Asadulaeva Z.G. Republican Dermatovenerological Dispensary of the Ministry of Health of the Republic of Dagestan, Makhachkala.

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Asbestos lichen (tinea amiantacea; syn: asbestos pitiriasis, asbestos follicular keratosis, psoriasiform seborrhea) is a disease of unclear etiopathogenesis. Currently point to several possible causes of asbestos lichen. It is believed that this disease is based on a severe form of seborrhea.

coumadin to other opinions, the disease is considered as one of the clinical forms of seborrheic eczema of the scalp or lichen simplex caused by pyococcal microflora. Sometimes it develops against the background of psoriasis, eczema, follicular keratosis and other dermatoses. Even asbestos lichen is considered as an eczematous reaction of the scalp to the influence of infection or the impact of trauma. The disease can occur for no apparent reason.

It is observed more often in children and young people in the region of warfarin pills, less often in the back of the head and temples. The scales resemble asbestos fibers, which are difficult to separate. Asbestos lichen is accompanied by itching of varying intensity. The hair is close to the skin, dry, shrouded in small whitish scales.

The histological picture of asbestos lichen is characterized by hyperkeratosis, parakeratosis and slight lymphocytic infiltration around the hair follicles, as well as degenerative changes in the sebaceous glands. The diagnosis is based on clinical data. The course of the disease is chronic, long-term. Differential diagnosis is carried out with mycosis of the scalp, seborrhea, psoriasis, eczema.

In therapy, general strengthening agents are shown, locally 3-5% salicylic ointment (on OL. Vaselini), sulfur-tar, sulfur-salicylic ointment. Long-term ingestion of warfarin sulfur, aevit and vitamins of group B is useful. Local applications of antifungal ointment (clotrimazole) on the scalp after its preliminary cleansing of scales are effective.

A 6-year-old boy with massive asbestos-like scales of coumadin pills was hospitalized to the hospital of the RKVD RD. Sick for about a month, when whitish scales appeared on the scalp. In the affected areas, intense itching is disturbing. Past illnesses: suffers from intracranial hypertension.