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)

The prevalence of immunologic and coagulation disorders in 75 schizophrenic patients treated with chlorpromazine or other antipsychotic drugs was evaluated. Four groups were studied: Group A, chlorpromazine treatment for more than 2 1/2 years; Group B, chlorpromazine and other antipsychotic drug treatment for more than 2 1/2 years; Group C, chlorpromazine treatment for less than 2 1/2 years; Group D, no chlorpromazine, but other antipsychotic drug treatment. Significant elevation of serum IgM and prolongation of partial thromboplastin time were noted in patients who had long-term chlorpromazine treatment. The latter was caused by a circulating inhibitor resembling that seen with systemic lupus erythematosus. There was a significant correlation between the IgM level versus chlorpromazine dose or duration of treatment and the partial thromboplastin time versus chlorpromazine dose or duration of treatment. In Groups A and B, 63% had a positive antinuclear antibody test (greater than or equal to 1:80), 40% had antibodies to native DNA, and 58% had antibodies to nucleoprotein. These antibodies were negative in the other groups. The percentages of T lymphocytes were below normal in 13 of 41 patients treated with chlopromazine. Twenty of 42 patients in Groups A and B, and none of 28 in Groups C and D had splenomegaly. This study indicates that most patients on long-term chlorpromazine treatment develop one or more immunologic abnormalities.
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PMID:Immunologic and coagulation disorders in chlorpromazine-treated patients. 31 32

A variant strain of Rauscher leukemia virus (RLV-A) obtained from a transplantable murine monomyelocytic leukemia causes a disease characterized by frank anemia, wasting, hepatosplenomegaly and erythroblastosis. The involvement of platelets in this disease are reported here. The RLV-A induced a severe thrombocytopenia (25 percent of control level) at the terminal stage of disease. This thrombocytopenia was not associated with disseminated intravascular coagulopathy since the prothrombin times were always within normal limits. The partial thromboplastin time was elevated in the terminal stages of disease and was found to be associated with factor deficiencies, possibly owing to the presence of anti-factor antibodies, in the intrinsic coagulation pathway, especially factor VIII. Further, splenectomy did not abolish the thrombocytopenia, since splenectomized, virally infected animals also developed severe thrombocytopenia (29 percent of control levels). The ensuing splenomegaly during progression of disease was not the cause of the thrombocytopenia. A physiological response to the severe thrombocytopenia was the production of larger size platelets. At terminal stages of the disease, platelet volume increased to 4.2 mu 3 (normal is 3.0 mu 3). An increase in platelet volume was also observed in splenectomized, virally infected animals. Electron microscopy indicated that these circulating platelets contained c-type viral particles. Viral infection was associated with decreased life span of circulating platelets, as measured by 75Se-methionine at mid and terminal stages of the disease. Our results suggest that direct viral infection of platelets and/or megakaryocytes with subsequent cell lysis is a possible cause of the observed thrombocytopenia observed in RLVA-induced disease and may also occur in other retrovirally-induced diseases.
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PMID:Thrombocytopenia in a retrovirally-induced murine erythroleukemia. 145 28

Primary lymphoma of the spleen is characterized by predominant splenomegaly. Lymphoplasmacytic malignant lymphoma of the spleen, of low malignancy in the Kiel classification, low and intermediate grade in the National Cancer Institute Working Formulation (NCIWF), is rare. It is often associated with a monoclonal immunoglobulin M (IgM). Four patients presenting with primary splenic lymphoma of plasmacytic type associated with a high level of monoclonal IgM and a lupus anticoagulant (LA) are described. This association has not previously been reported. In contrast with the usual heterogeneity of LA, this LA is relatively homogeneous with an important prolongation of the prothrombin time (greater than 18 sec for a control of 12), more prolonged partial thromboplastin time (PTT) of the mixture patient + control plasma than PTT of the patient plasma. Despite the important coagulation abnormalities, none of these four patients has presented any hemorrhagic or thrombotic complications, even during major surgery such as splenectomy. The lupus-like anticoagulant effect ran parallel with the monoclonal IgM. Survival, after splenectomy and chemotherapy, appears to be favourable: three patients are alive with survivals of greater than or equal to 7 years. The follow-up is as yet too short for the last patient.
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PMID:Lupus anticoagulant associated with primary malignant lymphoplasmacytic lymphoma of the spleen: a report of four patients. 174 35

Two-week oral administration of MDL-19,660, a triazole antidepressant compound, resulted in a dose-related thrombocytopenia in rats given 40-360 mg/kg/d and dogs treated with 5-50 mg/kg/d. Consumptive loss of platelets was not apparent since splenomegaly, hemorrhage, microscopic thrombi or prolonged coagulation times (prothrombin and activated partial thromboplastin) were not observed. Platelet production did not appear to be impaired since megakaryocytes in the bone marrow of treated animals were similar in number or slightly increased compared to control animals. Although the pathogenesis of this thrombocytopenia is presently unknown, intravascular destruction by immune mechanisms or direct drug-related effects seems most likely.
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PMID:Thrombocytopenia in rats and dogs administered the antidepressant compound MDL-19,660. 201 70

There have been many reports of cases in which chronic increases in the numbers of natural killer (NK) cells have been reported. Whether this is reactive or neoplastic in nature has been debated. We report the first case of an aggressive NK cell leukemia in an adult with establishment of an NK cell line. A 70-year-old man had two spontaneous episodes of jejunal perforation and one month later developed a severe febrile illness with moderate splenomegaly. Hemoglobin was 13.1 g/L, and WBC count was 1.8 X 10(9)/L with 2% large granular lymphocytes (LGLs). Platelet count was 143 X 10(9)/L; prothrombin time (PT) and partial thromboplastin time (PTT) were normal. Bone marrow was infiltrated with 25% to 30% LGLs; serum lysozyme was normal. Serum LDH was initially 1,191 U/L and rose to 6,408 (normal 240 to 525 U/L). Ten days later, the WBC count increased to 99.9 X 10(9)/L with 70% LGL cells; the PT and PTT increased, and the platelet count dropped. No bacterial or viral cause of fever was identified. The cells from peripheral blood were LGLs that stained positively for acid phosphatase. All of the LGLs reacted with a monoclonal antibody reactive with NK cells (LEU-11b). Functionally, the patient's peripheral blood mononuclear cells (PBMs) demonstrated 100 times more lytic activity against K562 tumor cell lines than did normal PBMs. The patient's PBMs were propagated in vitro. The cultured cells showed the morphological, cytochemical, immunological, and functional characteristics of NK cells. In addition, partial trisomy involving chromosome 1 q with duplication in regions of q21 through q31 was observed in all metaphases analyzed. The extra chromosome 1q with duplication in regions q21 through q31 was translocated to the p-terminal of chromosome 5. One percent to 5% of normal PBMs comprise NK cells; in most cases, leukemias arise from normal phenotypic counterparts. This case demonstrated that aggressive NK cell leukemia may occur in adults. In addition, the chromosomal abnormalities suggest that this is not a reactive process but a malignancy.
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PMID:Aggressive natural killer cell leukemia in an adult with establishment of an NK cell line. 395 37

Chronic administration of chlorpromazine is associated with the development of a lupus-like circulating anticoagulant and a variety of immunological abnormalities. The prevalence of these findings was studied in 123 psychiatric patients. The anticoagulant was present in 11 of 30 patients receiving chlorpromazine (CPZ), in none of 17 patients who had been off phenothiazine therapy for over a year and in none of 53 controls. It was also seen in 5 of 13 patients who had been switched from CPZ to another phenothiazine even after several years being off CPZ. The anticoagulant was characterized by prolongation of the partial thromboplastin time, thromboplastin dilution test, and Russell's viper venom time. Washed frozen platelets partially corrected the abnormality induced by the anticoagulant. In all but one case the anticoagulant was associated with positive antinuclear antibody test and/or increased serum IgM. Six of 16 patients also had decreased complement levels, and two had a positive direct Coombs' test. None of these patients manifested bleeding, hemolysis, splenomegaly, or other clinical features of systemic lupus erythematosus.
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PMID:Chlorpromazine-induced lupus anticoagulant and associated immunologic abnormalities. 681 43

Described here is an autopsy case of a 30-year-old woman with systemic hemangiomatosis accompanied by coagulopathy and microangiopathic hemolytic anemia. She had hepato-splenomegaly, anemia, thrombocytopenia, prolonged prothrombin time and partial thromboplastin time, and fibrinogenopenia. A splenectomy was performed and a diffuse angioma of the spleen was found. Postmortem examination revealed cavernous hemangiomas and hemangioendotheliomatous lesions in the liver, bone marrow, intestine, and lymph nodes. Coagulation studies suggested that exacerbation of coagulopathy occurred due to Liniac (10MV X-ray) irradiation. Our observation raised the possibility that the irradiation might lead to chronic localized consumption coagulopathy, which was confined to the hemangioma, to acute disseminated types of intravascular coagulation.
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PMID:Diffuse hemangiomatosis, coagulopathy and microangiopathic hemolytic anemia. 723 17

Acute intrinsic renal failure was diagnosed in a two-year-old, male, German shepherd dog following a Vipera aspis bite. Clinical signs included depression, hypersalivation, vomiting, tachypnoea, abdominal pain, splenomegaly, oliguria with haematuria and haemolysed serum. Leucocytosis with a shift to the left, thrombocytopenia, prolonged coagulation times (activated partial thromboplastin time, prothrombin time and thrombin time), hypofibrinogenaemia, azotaemia and hyposthenuria were the most prominent laboratory abnormalities. Histopathological evaluation of the kidneys showed a discrete glomerular hypercellularity, mesangial lysis and renal tubules filled with many hyaline casts and some necrotic cells.
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PMID:Acute intrinsic renal failure and blood coagulation disorders after a snakebite in a dog. 747 66

We compared lethal toxicity and potential for splenomegaly and disseminated intravascular coagulation (DIC) of the lipid A derivative DT-5461 with those of compound 506 (C506) and bacterial lipopolysaccharide (LPS). These agents were given intravenously, by either bolus intravenous injection (2 ml/min) or drip infusion (3 ml/4 h), into the tail vein of rats under various regimens. In naive rats, the lethal dose after bolus intravenous injection was clearly higher than that after drip infusion for C506 and LPS, but not for DT-5461. In partially hepatectomized or D-galactosamine-treated rats, a marked enhancement of the lethality was observed for all agents relative to that in naive rats. Splenomegaly was commonly seen in all surviving rats after treatment, and histopathological examination revealed lymphoid hyperplasia in the B-cell area of the white pulp zone and lympho-reticular cell proliferation of the red pulp zone. When administered intravenously by drip infusion to rats pretreated with 0.4 M lactic acid, both C506 and LPS provoked DIC. This was manifested by a decrease in platelet counts, prolongation of activated partial thromboplastin time (APTT), and an increase in fibrin-fibrinogen degradation products (FDP), with hepatocellular necrosis and glomercular fibrin thrombus formation. In contrast, DT-5461 showed no such toxic events with the same protocol. In14-day intravenous toxicity studies of DT-5461, rats were more susceptible to hepatocellular necrosis and splenomegaly than squirrel monkeys. These results demonstrate that DT-5461 is a promising compound, with antitumor activity dissociated from its toxic potential.
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PMID:Toxic characteristics of the synthetic lipid A derivative DT-5461 in rats and monkeys. 1041 79

Crimean-Congo hemorrhagic fever was for the first time recognized in Yugoslavia in 1971. In this paper were presented clinical and laboratory findings of a patient infected with Crimean-Congo hemorrhagic fever in Kosovo in 1999. The disease was manifested with fever, headache, vomiting, myalgia, abdominal pain, pharyngitis, conjuctival injection, diarrhoea, hypotension, gingival bleeding, skin hemorrhages, hematuria, hepatomegaly, splenomegaly, jaundice, thrombocytopenia, prolonged prothrombin and partial thromboplastin time, high serum fibrinogen degradation product, leukocytosis, mild anemia, elevated levels of bilirubin and serum aminotransferases. Diagnosis was set clinically, epidemiologically and supported by serological tests. Supportive management of hypotension, multi-organ failure, coagulation disturbances the patient was of the utmost in the treatment together with the isolation and prophylactic measures.
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PMID:[Crimean-Congo hemorrhagic fever]. 1152 72


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