[A case of adult T-cell leukemia with pulmonary cryptococcosis, cryptococcal meningitis and Pneumocystis carinii pneumonia].

A 66-year-old woman was admitted to the Medical College Hospital of Oita on February 23, 1988, because of headache and fever. Chest X-P and chest CT findings showed a coin lesion in r-S4. Cryptococcus neoformans was isolated from the CSF. Abnormal lymphocytes with lobulated nuclei were found in 0-5% of peripheral leukocytes. The ATLA-antibody was positive and bone marrow smear showed normal myelogram. According to these data, we diagnosed the patient as smouldering adult T-cell leukemia accompanied with pulmonary cryptococcosis and cryptococcal meningitis. C. neoformans disappeared from the CSF and cryptococcal antigen was not detectable after Amphotericin B and Flucytosine treatment. On April 1, the patient complained of a dry cough, high fever and dyspnea. A chest X-ray showed bilateral patchy infiltrations. By the methenamine silver staining, cysts of Pneumocystis carinii were found in the specimens of transbronchial lung biopsy and bronchoalveolar lavage fluid. The abnormal shadow on chest X-ray disappeared after TMP-SMX and aerosolised pentamidine treatment.

IgE-induced blood coagulation alterations in the rabbit: consumption of coagulation factors XII, XI, and IX in vivo.

Intravenous administration of BSA into 3-month-old rabbits producing detectable anti-BSA antibody only of the IgE class of immunoglobulin induced a variety of intravascular blood coagulation alterations observed in the plasma 15 min after antigen challenge included: a) the intravascular consumption of intrinsic blood coagulation factors XII, XI, and IX and possibly the reduction in clottable fibrinogen; b) a significant prolongation of the activated partial thromboplastin time but not the prothrombin time; and c) the production of an inhibitor affecting the last stage of blood coagulation. The observed blood coagulation alterations were not caused by the manipulative procedures utilized, the presence of anti-BSA, IgG or IgM antibody, histamine-induced alterations in the vascular endothelium or the development of hypotensive shock. It is proposed that specific IgE antibody can induce directly or indirectly the activation of intrinsic blood coagulation in vivo.