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)

Leucine aminopeptidase (LAP) activity and creatinine concentration was estimated in serum of twenty five normal adult subjects, twenty four cases with active urinary bilharziasis, eleven cases with active intestinal bilharziasis, ten cases with mixed bilharzial infection (urinary and intestinal), fourteen bilharzial cases with clinical hepato-splenomegaly of bilharzial etiology, thirteen bilharzial cases with clinical hepatosplenomegaly and ascites, and twelve cases with cancer bladder of bilharzial etiology. Significant elevation in the serum enzyme level was found in all bilharzial cases which generally ran parallel to the course of the disease, being more marked in hepatosplenomegalic cases than in cases which showed no clinical signs of liver or spleen involvement. However, it was observed that the enzyme level was lower ascitic than in nonascitic cases. For serum creatinine concentration, no significant variation from normal value was observed in the group of patients with active urinary, active intestinal, mixed infections of bilharziasis and bilharzial hepatosplenomegalic cases. However, a very highly significant decrease in serum creatinine concentration was observed in the group of patients with bilharzial hepatosplenomegaly and ascites. Serum LAP activity and creatinine concentration in the group of patients with cancer bladder of bilharzial etiology showed no statistical variation from normal values.
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PMID:Leucine aminopeptidase, Significance of serum elevation in bilharziasis. 103 91

Simian hemorrhagic fever (SHF) virus and a new strain of Ebola virus were isolated concurrently in recently imported cynomolgus monkeys (Macaca fascicularis) being maintained in a quarantine facility. Ebola virus had never been isolated in the U.S. previously and was presumed to be highly pathogenic for humans. A chronology of events including measures taken to address the public health concerns is presented. The clinicopathologic features of the disease were abrupt anorexia, splenomegaly, marked elevations of lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase, with less prominent elevations of blood urea nitrogen, creatinine, and other serum chemistry parameters. Histologically, fibrin deposition, hemorrhage, and necrosis of lymphoid cells and reticular mononuclear phagocytes were present in the spleens of SHF and of Ebola virus-infected animals. Intravascular fibrin thrombi and hemorrhage were also present in the renal medulla and multifocally in the gastrointestinal tract. Necrosis of lymphoid and epithelial cells was occasionally noted in the gastrointestinal tract. The histopathologic findings considered specific for Ebola virus infection include hepatocellular necrosis, necrosis of the zona glomerulosa of the adrenal cortex, and interstitial pneumonia, all of which were generally associated with the presence of 1 to 4 mu intracytoplasmic amphophilic inclusion bodies. The disease spread within rooms despite discontinuation of all direct contact with animals, and droplet or aerosol transmission was suspected. Antibody to Ebola virus developed in animal handlers but no clinical disease was noted, suggesting a less virulent strain of virus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Combined simian hemorrhagic fever and Ebola virus infection in cynomolgus monkeys. 131 46

Castrate yearling male sheep were treated for 8 weeks with either 50 micrograms/kg body wt/8 hourly sc insulin-like growth factor-I (IGF-I) (n = 10) or with saline (n = 9). IGF-I treatment increased plasma IGF-I from 235 +/- 17 to 347 +/- 16 ng/ml (P less than 0.001). There was a gradual divergence in body wt (P less than 0.10) between treatment groups. Food intake did not change significantly. The weight of the spleen corrected for body wt increased by 40% (P less than 0.001) and there was a marginal increase in adjusted kidney wt (P less than 0.1). There was no effect of IGF-I on carcass weight or dimensions, or on long bone length, although the weight per unit length of the tibia (P less than 0.05) and femur (P less than 0.10) were increased. There was no effect on wool growth. Plasma IGF binding proteins (IGFBPs) were quantified by ligand blot analysis. In the IGF-I treated group, IGFBP-1 showed a transient increase (P less than 0.05) at day 3 but was similar in both groups at day 55 of treatment. IGFBP-2 was suppressed (P less than 0.05) by day 55 and IGFBP-3 and 4 did not change. Plasma glucose was elevated (P less than 0.05) and plasma insulin was suppressed (P less than 0.01) from 280 +/- 32 pg/ml to 124 +/- 30.4 pg/ml, plasma urea (P less than 0.01) and creatinine (P less than 0.05) were reduced in the IGF-I treated group. The somatogenic effect of IGF-I in this study was minimal suggesting that in the well fed animal with an intact somatotropic axis IGF-I treatment at doses which double plasma IGF-I does not enhance somatic growth performance. However, the marked splenomegaly shows the sensitivity of splenic growth to systemic IGF-I. The suppression of insulin with chronic IGF-I treatment was accompanied by hyperglycaemia--this may explain in part the lack of a significant anabolic response and may limit the utility of IGF-I therapy unless higher doses with insulin-like effects are used.
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PMID:Body growth, carcass composition, and endocrine changes in lambs chronically treated with recombinantly derived insulin-like growth factor-I. 137 17

The univariate analysis of prognostic factors showed the value of clinical variables (age, symptoms, lymph node enlargement, splenomegaly, hepatomegaly, clinical stage), haematological variables (haemoglobin, platelet count, leucocyte count, lymphocyte count, bone marrow involvement and biopsy pattern, cleaved lymphocytes, prolymphocytes, LDT) and biochemical variables (BUN, creatinine, calcium, phosphorus, uric acid and albumin). The multivariate analysis chose the combination of Rai's stage, age, cervical lymph node involvement, phosphorus and BUN. Two predictive models capable of separating appropriately low, intermediate and high risk groups were developed and validated. The results were compared with others in the literature. The interest of predictive models arising from multivariate analysis is stressed.
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PMID:[Chronic lymphatic leukemia. II. Analysis of prognostic factors and development of survival predicting models. Study of 187 patients]. 177 7

Treating MRL/1pr mice, which spontaneously develop systemic lupus erythematosus and rheumatoid arthritis, with 15-DOS resulted in a decrease in the amount of autoantibodies and inhibited proteinuria of the developing glomerulonephritis with an improved survival rate of these autoimmune mice. 15-DOS treatment also lowered the percentage of animals with swollen lymph nodes and inhibited the development of splenomegaly. In the established disease 15-DOS returned urine-protein values and renal function (serum urea and creatinine) to normal levels. Circulating rheumatoid factor and autoantibodies to double-stranded DNA were reduced and the increase in paw volume (signs of a polyarthritis) was inhibited.
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PMID:15-Deoxyspergualin (15-DOS) has a curative effect on the development of SLE-like autoimmune disease in MRL/1 mice. 179 21

Vasculitis may accompany rheumatoid arthritis. One must distinguish between vascular involvement associated with the pathogenesis of rheumatoid arthritis, isolated digital vasculitis, and the syndrome of clinical rheumatoid vasculitis. The cause of clinical rheumatoid vasculitis is unknown. High titers of rheumatoid factor, cryoglobulins, diminished circulating complement, an increased prevalence of HLA-DR4, and the pathologic findings suggest an immune etiology. However, similar, but perhaps less pronounced, abnormalities occur in uncomplicated rheumatoid arthritis, and these findings are not universal in complicating vasculitis. Classic cutaneous clinical manifestations include ischemic ulcers, digital gangrene, and palpable purpura. Mononeuritis multiplex is another classic presentation of rheumatoid vasculitis. Small digital infarctions may accompany other manifestations in clinical vasculitis or may occur alone as isolated digital arteritis, in which case the prognosis is relatively favorable. Weight loss, pleuritis, pericarditis, ocular inflammation, splenomegaly, hepatomegaly, and Felty's syndrome have also been reported in association with rheumatoid vasculitis. Although renal involvement has been considered unusual in rheumatoid vasculitis, several studies suggest that this may be more common than previously recognized. Ideally, a biopsy or an angiogram confirms the diagnosis of rheumatoid vasculitis, but often the diagnosis rests upon the clinical picture. In general, blind biopsies are not helpful, although one series indicated that a blind rectal biopsy may be an exception to this rule. An elevated erythrocyte sedimentation rate, increased C-reactive protein level, anemia, thrombocytosis, hypoalbuminemia, and a positive rheumatoid factor are common laboratory findings. Leukocytosis, hypergammaglobinemia, leukocytopenia, an elevated creatinine level, and minimal abnormalities of the urinary sediment also occur in patients with rheumatoid vasculitis. However, these abnormalities overlap in patients with uncomplicated rheumatoid arthritis, and their role in distinguishing rheumatoid vasculitis from uncomplicated rheumatoid arthritis is limited. Other immunologic tests have no established clinical role in diagnosing rheumatoid vasculitis. Therapy depends upon the clinical manifestation of rheumatoid vasculitis. Uncomplicated rheumatoid arthritis deserves appropriate therapy, and general attention to nutrition, cessation of tobacco, and control of blood pressure are indicated for all patients. Isolated digital vasculitis generally requires no more than the usual treatment for uncomplicated rheumatoid arthritis. Appropriate dermatologic management is indicated for ischemic ulcers. Most clinical experience in managing more symptomatic rheumatoid vasculitis has focused on glucocorticosteroids, D-penicillamine, and cytotoxic immunosuppressive drugs.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Vasculitis associated with rheumatoid arthritis. 218 61

L1 was given to eight patients with beta-thalassaemia major who had previously been treated with deferoxamine (DF) for 4-10 years. The patients' ages ranged from 11 to 27 years. Serum ferritin values ranged from 1.3 to 11.5 x 10(3) micrograms/l. L1 was given twice daily at a daily dose of 55-80 mg/kg body weight and was continued for 10 months in two patients, 9 months in three, 7 months in two patients and 4 months in one patient. As previously observed with DF, each patient's urinary iron excretion (UIE) varied greatly from day to day. The mean UIE of the eight patients ranged from 11 to 49 mg/d (0.2-0.87 mmol/d) on subcutaneous DF and from 16 to 53 mg/d (0.28-0.95 mmol/d) on L1. Two patients excreted significantly more and one patient significantly less iron while on L1. If the UIE was calculated as mmol Fe/mmol creatinine there was no statistically significant difference. Serum ferritin values fluctuated widely in all, with a consistent downward trend in three, no change in four and an increase in one of two non-splenectomized patients. This patient's splenomegaly and need for transfusions continued to increase while on L1. No toxicities attributable to the drug were detected during the period of study and tolerance of the drug was excellent.
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PMID:L1 (1,2-dimethyl-3-hydroxypyrid-4-one) for oral iron chelation in patients with beta-thalassaemia major. 226 18

The association between glomerular disease and hepatosplenic schistosomiasis is well documented in reports from South America. During the present hospital investigation in Sudan, 58 patients admitted for intercurrent complications of advanced hepatosplenic schistosomiasis were studied. The patients, median age 35 years, had no concurrent Schistosoma haematobium infection. Diagnostic criteria included an enlarged spleen (n = 58), at least 1 episode of hematemesis (n = 55) and/or melena (n = 36), endoscopical demonstration of gastroesophageal varices (29/29 studied), ultrasonographical imaging of hepatic periportal fibrosis (18/18 studied), and intraoperative liver biopsy with characteristic histological findings (11/16 biopsied). Serum creatinine, urea, electrolytes, cholesterol, total protein, and electrophoresis were within normal limits. Median urinary protein/creatinine ratio was 0.06 and thereby not significantly different from European reference values. Only 1 patient had proteinuria of 1.7 g/l. Minimal hematuria was found in 5 patients. Ten kidney biopsies were taken intraoperatively during a portal decompression procedure (Hassab operation). Light, immunofluorescence, and electron microscopy produced no evidence of glomerulonephritis. These findings indicate that S. mansoni induced nephrotic syndrome may be less frequent in Sudan than in South America. Renal involvement due to S. mansoni infection may therefore encompass geographical variances.
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PMID:Renal function and morphology in Sudanese patients with advanced hepatosplenic schistosomiasis and portal hypertension. 249 2

Twelve evaluable patients with progressive hairy cell leukemia were treated with deoxycoformycin at a dose of 4 mg/m2 every 2 weeks. Five patients had not been splenectomized, and one had failed to respond to interferon-alpha. Complete remission, as defined by absence of hairy cells in the bone marrow and normalization of the peripheral blood and regression of splenomegaly, was obtained in 11 of 12 patients (92%). These patients have remained in unmaintained remission for 1+ to 13 months with an average of 7.5 months. Two of these patients had a bone marrow relapse at 8 and 12 months, respectively. During treatment the monocytopenia corrected, and, after complete remission was obtained, marrow was aspirable. Toxicity was mild and reversible. There were no significant infections associated with this treatment. It was of interest that we could treat two patients with creatinine clearance of 50 and 60 ml/min using lower doses (and 2-3 mg/m2) than our conventional therapy of 4 mg/m2 every 2 weeks. They obtained a complete remission after 6 and 10 treatments, respectively. Low-dose deoxycoformycin has proven to be an excellent treatment for hairy cell leukemia.
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PMID:Treatment of hairy cell leukemia: the Ohio State University experience with deoxycoformycin. 349 42

Hepatic metabolism is the primary process of elimination of propafenone. It therefore is important to understand the effect of altered liver function on the disposition and elimination kinetics of this drug. Patients with abnormal liver function probably will require treatment with propafenone for cardiac arrhythmias; an understanding of the relationship between liver function and the pharmacokinetics of propafenone will provide a rational basis for optimal dosage adjustments in these individuals. Our results demonstrate that both systemic clearance and bioavailability of propafenone are sensitive to variability in liver function. The bioavailability of propafenone is inversely related to the clearance of indocyanine green (ICG), whereas a direct relationship exists between systemic clearance of propafenone and ICG clearance. Comparisons of clinical parameters with the propafenone data yielded interesting results. An overall clinical grading of severity of liver disease based on the presence or absence of portal hypertension (i.e., varices and/or splenomegaly), prior encephalopathy, and ascites did not correlate well with propafenone results. However, albumin, total bilirubin, serum glutamic oxaloacetic transaminase (SGOT) concentrations and prothrombin time values correlated strongly with the overall results. No definite relationships with subjects' age; weight; and hemoglobin, alkaline phosphatase, lactic acid dehydrogenose, cholesterol, blood urea nitrogen, or creatinine levels were detected. These results demonstrate that moderate to severe liver disease significantly affects the absorption and disposition of propafenone. In patients with cirrhosis, and presumably other forms of hepatic dysfunction, careful adjustments of propafenone doses are needed to optimize therapy.
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PMID:Influence of hepatic dysfunction on the pharmacokinetics of propafenone. 369 82


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