Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the Australian/British IBP studies on KarKar Island and at Lufa in the Eastern Highlands, Papua New Guinea, information was collected on the epidemiology and genetic constitution of the same subjects. Advantage of this special situation has been taken to determine whether any associations exist between the genetic markers and the disease states. Those found and which appear real include Rhesus D(u) with proteinuria; MN with splenomegaly and hepatomegaly; Ss with parotid enlargement; acid phosphatase, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogense and haemoglobin J- Tongariki with presence of malarial parasites; phosphoglucomutase with proteinuria and parotid enlargement; haptoglobin with proteinuria and with splenomegaly and hepatomegaly. These associations are discussed in terms of the probabilities of their arising from heterogeneity in population structure, linkage disequilibrium and pleiotropy.
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PMID:Associations between polymorphic variety and disease susceptibility in two New Guinea populations. 82 72

Patients with chronic heart failure (CHF) can often develop such diseases as hepatitis of viral etiology, alcoholic hepatitis, drug affection of the liver and other diseases masked as congestive liver. In most cases CHF concomitant liver diseases have an atypical course with a tendency to a chronic course. CHF is one of the important pathogenetic mechanisms lying in the basis of chronicity of concomitant liver diseases. Refractory CHF, inconsistency of the hemodynamic indices of persistent hepatomegaly must lead a physician to the detection of probable independent liver diseases complicating the syndrome of heart failure. CHF is a factor causing an enhanced fibrosing liver reaction. An important diagnostic test of fibrinogenesis lying in the basis of chronicity of liver diseases, is the determination of enzymatic markers reflecting synthesis and catabolism of the main substance of connective tissue. Change in the levels of haptoglobin, ceruloplasmin and glutamic acid dehydrogenase is an indirect sign of damage of the liver parenchymal endoplasmic reticulum. These indices can serve as differential criteria of the prevalence of cardiovascular disorders in the liver or concomitant independent liver diseases.
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PMID:[Pathogenetic mechanisms of chronicity in liver diseases in patients with circulatory failure]. 361 41

A rare case of thrombotic microangiopathy in a patient with hemophagocytic syndrome is reported. An 18-year-old girl was admitted following prolonged fever, watery diarrhea, abdominal discomfort, and a 2-week history of rhinorrhea, cough, and painful cervical lymph nodes. Anemia, thrombocytopenia, jaundice, hepatomegaly, and mild azotemia developed within 2 weeks of admission. The diagnosis of a reactive hemophagocytic syndrome, probably secondary to infection, was made based on the findings of bone marrow examination. Extensive investigation failed to identify a causative agent. The disease initially responded rapidly to intravenous steroids and high-dose immunoglobulin therapy but relapsed soon after tapering of the steroids. Although her condition improved again on resumption of treatment with high-dose steroids, nephrotic range proteinuria and microscopic hematuria developed after the steroids were tapered. Fragmented erythrocytes were seen in peripheral blood with elevated serum lactate dehydrogenase and decreased serum haptoglobin concentrations. The results of subsequent renal pathology examination were also compatible with thrombotic microangiopathy. The disease course finally stabilized after a course of pulse methylprednisolone therapy. Immune hyperactivity, particularly hypercytokinemia and monocyte hyperactivity, could have accounted for the development of thrombotic microangiopathy in this case. Only strong immunosuppressive therapy can control such disease activity.
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PMID:Thrombotic microangiopathy in hemophagocytic syndrome: a case report. 1210 56

A 5-year-old girl developed acute lymphoblastic leukemia (T-ALL) 15 months after being diagnosed with autoimmune hemolytic anemia (AHA), while AHA was in partial remission. AHA was mediated by warm antibodies. Because AHA could not be controlled during the induction therapy of ALL, she was administered immunoglobulin G and plasmapheresis was performed. Hepatomegaly dissappeared in the 4th month. However, anemia requiring blood transfusion, positive direct Coombs' test, and splenomegaly dissappeared in the 13th month of the leukemia treatment; reticulocytosis and decreased haptoglobin level persisted. AHA exacerbated in the 24th month of the ALL therapy. Prednisolone was started but the family refused to continue the therapy. This case presents some features that were not reported before, such that ALL was preceded by AHA and involved T-cell lineage, AHA was mediated by warm antibodies, and the two disorders took place in childhood.
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PMID:Autoimmune hemolytic anemia preceding T-ALL in a five-year-old girl. 1602 Jan 3