Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of a 61-year-old woman with large granular lymphocytosis associated with pulmonary tuberculosis. She was admitted to our hospital because of high fever, anemia and splenomegaly. On admission, the leukocyte count was 6,890/microliters with 52% of large granular lymphocytes. Immunophenotypical analysis of the increased cells showed following results; CD2+, CD3-, CD16+, CD57+. These cells had natural killer (NK) activity. Molecular genetical analysis showed these cells had germline configuration of the T cell receptor beta chain genes. About four months after admission, chest X-P revealed multiple mass shadow and the diagnosis of pulmonary tuberculosis was made by the examination of gastric juice. Anti-tuberculosis therapy was started, and soon after clinical symptom and pancytopenia were improved. For about one year, anti-tuberculosis therapy was continued, and now hematological abnormality is not found. We considered that this case was reactive large granular lymphocytosis of NK cells to lung tuberculosis.
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PMID:[Transient large granular lymphocytosis associated with pulmonary tuberculosis: a case report]. 207 32

The patient is a 39 year-old Japanese male who had traveled to Southeast Asia from March 14, 1987 and returned on April 2. On April 3 and 5, he had a high fever with chills and he was admitted to our hospital. Despite initial treatment with antibiotics, a high fever over 39 degrees C appeared with a 48 hour periodicity. On the 8th day after admission, malarial parasites were identified on the peripheral blood smear after repeated trials. Combined with a raised serum antibody titer, Plasmodium vivax malaria was diagnosed. He was successfully treated with the sulfadoxine 500 mg and pyrimethamine 25 mg (Fansidar) and body temperature was normalized after the 12th day. More interestingly, the patient showed pancytopenia without splenomegaly. The bone marrow aspiration revealed hypoplasia of erythroblasts, granulocytes and megakaryocytes. Because of this pancytopenia in the peripheral blood and hypoplasia of the bone marrow which improved after recovery from malarial infection, it was indicated that they were caused by the malarial infection. Generally, it is considered that anemia in malarial patients is caused by destruction of the blood cells by parasites and/or hypersplenism and compensatory hyperplasia of the bone marrow is seen. On the contrary, this case showed pancytopenia accompanied with hypoplasia of the bone marrow probably due to the malarial infection suggesting a new aspect of pathogenesis in the hematological abnormality of the malarial infection.
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PMID:[A case of Plasmodium vivax malaria complicated with pancytopenia due to hypoplasia of the bone marrow]. 250 94

Thrombocytopenia is an important and common hematological abnormality in patients with HIV-1/HCV coinfection. Splenomegaly is a frequent finding in these patients and usually causes hypersplenism and thrombocytopenia. We analyzed the clinical results of a minimal invasive treatment (splenic artery embolization) for thrombocytopenia secondary to hypersplenism and refractory to other therapies in two hemophiliac patients, HIV seropositive and with cirrhosis due to chronic HCV infection. The results suggest that splenic artery embolization is a safe, relatively atraumatic and effective method for the treatment of splenomegaly and hypersplenism in selected patients with HIV-1/HCV coinfection.
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PMID:[Splenic artery embolization for the treatment of hypersplenism in hemophilic, HIV-1 and HCV seropositive patients]. 1287 7

To investigate the hematological abnormality and clinical characteristics in systemic lupus erythematosus (SLE), the hematological data of 58 SLE and the curative effects of corticosteroid and immunosuppressive agents on SLE were retrospectively analysed by using SPSS/PC software. The results showed that the incidence of hematological abnormalities in 58 cases was as follows: 50 cases of hemogram abnormality (86.2%), 41 of anemia (70.7%), 34 of thrombocytopenia (58.7%), 37 of leukopenia (63.8%). Peripheral cytopenia of every cell lineage was common in SLE. The cell abnormalities of two or three lineages were seen in 41 cases (70.7%). The initial symptoms with hematological abnormality were found in 12 cases (20.7%), 7 out of 12 cases were erroneously diagnosed as hematology diseases (12.1%). In 30 out of 58 patients, the results of bone marrow examination showed that 23 had hyperplasia (76.7%) and 7 were hypoplasia. In 25 out of 38 cases, splenomegaly (65.8%) was found by B ultrasonography. In 25 patients with SLE receiving Coombs test, 3 were positive (12.0%). PAIg increased in 16 out of 22 cases of thrombocytopenia (72.7%). 26 cases of SLE with two or three lineage cytopenia in peripheral blood were treated by corticosteroid and immunosuppressive agent. The hemogram improved in all patients including 6 cases of bone marrow hypoplasia. It is concluded that the hematological abnormalities are frequent in SLE patients, which are short of specialty. The cytopenia of two or more lineage in peripheral blood is most common when bone marrow shows hyperplastic. The therapy with corticosteroid and immunosuppressive agents is efficacious.
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PMID:[Hematological abnormality and clinical characteristics in systemic lupus erythematosus]. 1515 27

Thrombocytopenia is the most common hematological abnormality encountered in patients with chronic liver disease (CLD). In addition to being an indicator of advanced disease and poor prognosis, it frequently prevents crucial interventions. Historically, thrombocytopenia has been attributed to hypersplenism, which is the increased pooling of platelets in a spleen enlarged by congestive splenomegaly secondary to portal hypertension. Over the past decade, however, there have been significant advances in the understanding of thrombopoiesis, which, in turn, has led to an improved understanding of thrombocytopenia in cirrhosis. Multiple factors contribute to the development of thrombocytopenia and these can broadly be divided into those that cause decreased production, splenic sequestration, and increased destruction. Depressed thrombopoietin levels in CLD, together with direct bone marrow suppression, result in a reduced rate of platelet production. Thrombopoietin regulates both platelet production and maturation and is impaired in CLD. Bone marrow suppression can be caused by viruses, alcohol, iron overload, and medications. Splenic sequestration results from hypersplenism. The increased rate of platelet destruction in cirrhosis also occurs through a number of pathways: increased shear stress, increased fibrinolysis, bacterial translocation, and infection result in an increased rate of platelet aggregation, while autoimmune disease and raised titers of antiplatelet immunoglobulin result in the immunologic destruction of platelets. An in-depth understanding of the complex pathophysiology of the thrombocytopenia of CLD is crucial when considering treatment strategies. This review outlines the recent advances in our understanding of thrombocytopenia in cirrhosis and CLD.
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PMID:The pathophysiology of thrombocytopenia in chronic liver disease. 2718 44

Thrombocytopenia may be caused by diseases of various organ systems, especially the blood system. Certain drugs may also cause thrombocytopenia. In addition, it can result from various causes of pseudo-reduction. Therefore, a correct understanding of the causes of thrombocytopenia and their underlying mechanisms has important significance for clinical diagnosis and treatment. This study aimed to report a case of a 68-year-old woman with left upper abdominal mass and loss of appetite. The auxiliary examination showed splenomegaly and thrombocytopenia. The clinician planned to perform splenectomy. However, the laboratory physician considered that thrombocytopenia might be ethylenediaminetetraacetic acid-dependent pseudothrombocytopenia (EDTA-PTCP). After effective communication between laboratory physicians and clinicians, the patient was diagnosed with splenic hyperfunction and pseudothrombocytopenia, and finally saved from undergoing splenectomy. The patient has a good prognosis after oral medication. Thrombocytopenia in this patient is caused by both hypersplenism and EDTA antagonism which is different from a single factor in other reports. The diagnosis of hematological abnormality may be challenging for physicians, especially thrombocytopenia. Therefore, medical staff should possess a rigorous working style and a high sense of responsibility besides maintaining high professional quality. Further, they should actively, timely, and effectively communicate with auxiliary departments to avoid misdiagnosis and missed diagnosis.
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PMID:Ineffective communication equals no communication: a case report of splenic hyperfunction combined with pseudothrombocytopenia. 3281 17