Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma beta-thromboglobulin (beta-TG), a platelet-specific protein, is a marker of intravascular platelet degranulation. We measured plasma beta-thromboglobulin by radioimmunoassay in 13 patients with thrombocytopenia of various etiologies to determine whether or not the test is clinically useful in the differential diagnosis of thrombocytopenia. Four patients with intravascular platelet consumption (three with thrombotic thrombocytopenic purpura and one with vasculitis) had significantly higher plasma beta-thromboglobulin levels than four patients with extravascular platelet destruction due to idiopathic thrombocytopenic purpura. Five patients with thrombocytopenia and decreased numbers of megakaryocytes in the bone marrow also had beta-thromboglobulin levels that were not elevated. Two patients with thrombotic thrombocytopenic purpura achieved clinical remission associated with a decrease in beta-TG level to the normal range. Plasma beta-thromboglobulin determination can be useful in determining the mechanism of thrombocytopenia when bone marrow examination demonstrates adequate megakaryocyte numbers.
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PMID:Clinical use of beta-thromboglobulin levels in diagnosing and treating consumptive and immune thrombocytopenia. 616 92

A 52-year-old female was admitted to our hospital in August 1988, for evaluation of purpura and gingival bleeding. Hematologic examination showed mild leukocytosis (12,400/microliter) and severe thrombocytopenia (1,000/microliter). On bone marrow examination, megakaryocyte count was normal and the number of myeloblasts was increased (7.2%). Serological examination was positive for anti-nuclear antibody and anti-DNA antibody. She was diagnosed as having idiopathic or autoimmune thrombocytopenia, and received thrombocyte transfusion and gamma-globulin administration. Hematologic values improved temporarily, but leukocytosis and thrombocytopenia recurred. On the 22nd hospital day, leukocytes increased to 49,300/microliter and thrombocytes decreased to 10,000/microliter. Bone marrow myeloblasts were also increased to 18.8%, and she was suspected of having myelodysplastic syndrome. Then, hematologic values improved simultaneously, and she was discharged in November 1988. After the discharge, leukocyte count ranged from 6,000 to 16,500/microliter, but the number of bone marrow myeloblasts was normal. However, transient thrombocytopenia appeared in association with decrease or absence of bone marrow megakaryocytes and rise of platelet associated-IgG, (PA-IgG) to 99.6 ng/10(7) cells. From September to December 1989, she complained of fever, morning stiffness, multiple arthralgia, and oral ulcer. On serological findings, she was positive for LE cell. Therefore, she was diagnosed as having systemic lupus erythematosus (SLE). In January 1990, she had a high grade fever and dyspnea. Bilateral pleuritis and interstitial pneumonitis were shown on the chest roentgenogram. She received gamma-globulin administration, methylprednisolone pulse therapy, and mechanical ventilation. However, hypoxia developed rapidly, and she died of respiratory failure. Autopsy revealed severe interstitial pneumonitis, fibrinous pleuritis, fibrinous pericarditis, and vasculitis in the arcuate artery of the kidney. This is the first report of SLE complicating thrombocytopenia associated with decrease of megakaryocytes and rise of the PA-IgG, and severe leukocytosis associated with increased bone marrow myeloblasts.
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PMID:[An autopsy case of systemic lupus erythematosus complicating leukocytosis, amegakaryocytic thrombocytopenia, interstitial pneumonitis, and pleulitis]. 881 May 48