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

Ethyl-N-bis (2,2-dimethylethylamidinophosphoro) carbamate (AB-132) has been shown to potentiate the effect of whole-body radiation on inhibition of splenomegaly induced by Friend leukemia virus in ICR/H Swiss mice. The combined effect of AB-132 and radiation does not appear to be related to Friend virus inhibition but seems to act on the proliferating tumor in the spleen. Nine children with advanced cancer were treated with combined administration of local radiation and systemic AB-132. Although regression of tumor was seem, no dramatic effect on survival was apparent. One case of metastatic Ewing's sarcoma showed systemic tumor response to AB-132 in addition to localized response to radiation. Bone marrow depression appeared to be the main side effect of combination therapy.
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PMID:Laboratory and clinical evaluation of the radiation-potentiating activity of ethyl-N-bis (2,2-dimethylethylamidinophosphoro) carbamate (AB-132). 105 39

Patients with HCL are subject to a variety of medical problems. Many of these complications are caused by the cytopenias and splenomegaly produced by proliferating neoplastic cells. Infection is a common cause of morbidity in HCL, but it is not clear whether there is an inherent defect in the immune system. The incidence of infection is related to neutropenia and is increased by the administration of cytotoxic drugs and corticosteroids; such drugs should be used cautiously in these patients. Opportunistic or unusual pathogens occur frequently in HCL, but recovery from such infections is the rule if the diagnosis is made early. Marrow hypoplasia is not infrequently seen and may present diagnostic difficulties. Such patients may have a lower tumor burden and clinically milder anemia. Hemorrhagic complications are unusual in HCL, though many patients have platelet function abnormalities. Other medical problems occur with increased frequency in HCL, and failure to recognize them leads to increased morbidity in this disease. Autoimmune disease is seen in up to one fourth of patients. It takes the form of self-limited skin and joint disease, or a more progressive, systemic of patients. It takes the form of self-limited skin and joint disease, or a more progressive, systemic vasculitis. Both forms can usually be treated with splenectomy or corticosteroids, but alkylating agents can also be used successfully. Bone disease is usually localized and responds well to radiotherapy. Other problems such as amyloidosis, multiple myeloma, and paraproteinemia are uncommon in HCL.
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PMID:Clinical problems in hairy cell leukemia: diagnosis and management. 639 Jun 85

Hematologic abnormalities were studied prospectively in 38 patients with brucellosis. Anemia was found in 74% of patients, leukopenia in 45%, neutropenia in 21%, lymphopenia in 63%, and thrombocytopenia in 39.5%. Eight patients (21%) were pancytopenic; seven of these individuals also had splenomegaly. Bone marrow hypoplasia was not found. Bleeding complications developed in 26% of patients and were significantly associated with clotting abnormalities (low platelet count, low fibrinogen level, and/or prolongation of thrombin clotting time); i.e., bleeding occurred in approximately 50% of patients with marked clotting abnormalities but in no patients with normal clotting. Determination of fibrinogen levels at different stages of brucellosis led to a redefinition of the normal level for patients with this infection. Patients without clotting abnormalities had fibrinogen levels of 233-711 mg/100 ml (mean, 384 mg/100 ml), whereas patients with thrombocytopenia and prolonged thrombin clotting time had levels of 122-360 mg/100 ml (mean, 216 mg/100 ml; P less than .001) that increased to 233-519 mg/100 (mean, 360 mg/100 ml) when clotting values returned to normal. Lymphopenia was significantly correlated with the severity of clinical manifestations (bleeding and hepatic involvement).
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PMID:Hematologic changes in brucellosis. 648 Nov 87

Symptomatic arsenic poisoning is not often seen in occupational exposure settings. Attempted homicide and deliberate long-term poisoning have resulted in chronic toxicity. Skin pigmentation changes, palmar and plantar hyperkeratoses, gastrointestinal symptoms, anemia, and liver disease are common. Noncirrhotic portal hypertension with bleeding esophageal varices, splenomegaly, and hypersplenism may occur. A metallic taste, gastrointestinal disturbances, and Mee's lines may be seen. Bone marrow depression is common. 'Blackfoot disease' has been associated with arsenic-contaminated drinking water in Taiwan; Raynaud's phenomenon and acrocyanosis also may occur. Large numbers of persons in areas of India, Pakistan, and several other countries have been chronically poisoned from naturally occurring arsenic in ground water. Toxic delirium and encephalopathy can be present. CCA-treated wood (chromated copper arsenate) is not a health risk unless burned in fireplaces or woodstoves. Peripheral neuropathy may also occur. Workplace exposure or chronic ingestion of arsenic-contaminated water or arsenical medications is associated with development of skin, lung, and other cancers. Treatment may incklude the use of chelating agents such as dimercaprol (BAL), dimercaptosuccinic acid (DMSA), and dimercaptopanesulfonic acid (DMPS).
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PMID:Chronic arsenic poisoning. 1186 18