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)

Intensive care patients receiving prolonged total parenteral nutrition (TPN) developed alterations of liver function tests, seen in the activity of certain serum enzymes. Hepatomegaly and jaundice sometimes appeared. The changes in chemical pathology were in serum transaminases activity (GOT, GPT, GDH); alkaline phosphatase and gamma-glutamyltranspeptidase as indices of cholestasis; lactate dehydrogenase, hydroxybutyrate dehydrogenase and creatine phosphokinase, as enzymes related to energy metabolism; pseudocholinesterase, as a protein metabolism-related enzyme. The possible causes of these alterations in critically ill patients undergoing TPN are considered and a functional final metabolic interpretation is proposed.
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PMID:Metabolic changes during prolonged total parenteral nutrition in intensive care. 3 24

The results of liver, bone, and brain scans in 84 patients with recurrent or metastatic malignant melanoma were reviewed. The liver scan was initially positive in 18% (14/78) and ultimately in 32% (25/78). Serum alkaline phosphatase and lactic dehydrogenase were elevated in 92%. These patients ultimately developed positive liver scans, while convincing hepatomegaly was noted in only 44%. Bone scans were eventually positive in 33% (16/49), all of whom had pain. Brain scans were positive in 15% (10/65), all of whom had CNS symptoms. In asymptomatic patients, bone and brain scans only rarely disclosed occult lesions.
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PMID:Radionuclide scanning in patients with advanced malignant melanoma. 52 90

Lysinuric protein intolerance (LPI), an autosomal recessive defect of diamino acid transport, is characterized chemically by renal hyperdiaminoaciduria, especially lysinuria, and by impaired formation of urea with hyperammonemia after protein ingestion. Our 20 patients thrived during breast-feeding, but ingestion of cow's milk caused diarrhea and vomiting. When able to select their diet, they rejected all protein-rich foods. They were short staturated and had weak atrophic muscles, osteoporosis, hepatomegaly and often splenomegaly. Four patients were mentally retarded. Fifteen patients had leukocyte counts below 4,000/mm3, and 17 patients had platelet counts below 150,000/mm3. Serum lactate dehydrogenase activity was constantly increased, and transaminase and aldolase activities were often increased. In the infants' livers, changes were only revealed by electron microscopy: increased and vesicular smooth endoplasmic reticulum, and abundance of glycogen particles in the hepatocytes. In the older patients, light microscopy demonstrated clearly limited areas where hepatocytes had large pale cytoplasm and small pyknotic nuclei. The diamino acids lysine, arginine and ornithine had plasma concentrations only one-third to one-half the normal mean; the renal clearances were clearly increased. Oral diamino acid loading tests suggested impaired intestinal absorption. Urea is built in the liver through transformation of ornithine to arginine, and cleavage of arginine to ornithine and urea. The addition of ornithine to an intravenous I-alanine loading prevented the hyperammonemia and normalized the urea production. Therefore, the diet has been supplemented with arginine, and more protein has been added. This therapy has lead to a remarkable catch-up growth in some patients. The pathophysiology of LPI is explained. Because of defective intestinal absorption and incrased renal loss, the diamino acids have a low plasma concentration. Their transport from plasma to hepatocytes is also impaired, and the liver becomes deficient in ornithine. This retards the urea cycle, and leads to postprandial hyperammonemia and protein aversion. The presence of the transport defect in the hepatocytes distinguishes LPI from other hyperdibasicaminoacidurias.
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PMID:Lysinuric protein intolerance. 115 80

An attempt was made to estimate noninvasively portal pressure (PP) in patients with chronic liver disease, using the theory of quantification, a kind of multivariate analysis. Forty-one patients with liver cirrhosis and 22 patients with chronic hepatitis in whom hepatic venous catheterization had been performed were studied. Seventeen parameters (age, sex, mean blood pressure, red blood cell count, platelet count, prothrombin time, lactate dehydrogenase, alkaline phosphatase, total bilirubin, albumin, gamma-globulin, indocyanine green retention at 15 min, blood urea nitrogen, hepatomegaly, splenomegaly, ascites and edema) were selected for the estimation of PP. The estimated PP correlated significantly with the data obtained by hepatic venous catheterization with a high correlation coefficient of 0.835 (p less than 0.01). An investigation using the theory of quantification was also undertaken to determine which of the 17 parameters selected above was most useful in estimating PP. Among the 17 parameters indocyanine green retention at 15 min, red blood cell count, prothrombin time, hepatomegaly and splenomegaly seemed to contribute significantly to the estimation of PP. When the formula was applied to 31 successive patients with chronic liver disease (external samples), the correlation between the estimated and measured PP was 0.455 (p less than 0.01). These results indicate that the formula is clinically useful in estimating PP in patients with chronic liver disease.
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PMID:[Estimation of portal pressure using the theory of quantification]. 201 41

We report the diagnostic, prognostic and therapeutic features of non-Hodgkin's lymphoma in eight patients in whom the disease was seen as a primary tumor of the liver. This series illustrates the variety of situations in which lymphoma might be diagnosed: (a) abdominal pain and hepatomegaly (three cases), (b) incidental finding at evaluation of a patient with cirrhosis (two cases), (c) secondary neoplasm after treatment for Hodgkin's disease (one case) and (d) complication of AIDS (two cases). In most cases, clinical and/or radiological features were nonspecific. However, the combination of the following features must be considered as suggestive: occurrence of an apparently primary hepatic tumor in an immunocompromised patient, absence of the usual serum tumor markers and increased serum lactic dehydrogenase activity. The final diagnosis was based on histological examination of specimens obtained by ultrasonically guided liver biopsies or at surgery. All cases belonged to unfavorable histological subtypes. Immunohistochemical findings on paraffin-embedded sections demonstrated the B-lymphocyte lineage of the seven tumors available for study. In the three patients without coexisting disease, complete remission was obtained by surgery alone or combined with chemotherapy. In the two patients with coexisting cirrhosis, outcome was rapidly unfavorable, with death occurring less than 3 mo after diagnosis. Among the three immunocompromised patients, two experienced a rapid unfavorable outcome, and the remaining one was in complete remission after surgery and chemotherapy. In conclusion, primary non-Hodgkin's lymphoma of the liver arising in patients without coexisting disease has a slow progression and might be successfully treated by surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Non-Hodgkin's lymphoma presenting as a primary tumor of the liver: presentation, diagnosis and outcome in eight patients. 202 91

Phenytoin hepatotoxicity is a serious idiosyncratic reaction that occurs in less than one percent of patients. The onset of symptoms occurs early in therapy, usually within the first six weeks. Presenting symptoms often include fever, rash, lymphadenopathy, hepatomegaly, anorexia, and myalgias or arthralgias. Other significant findings that may develop throughout hospitalization are jaundice, periorbital or facial edema, and splenomegaly. The following alterations in liver function tests are associated with phenytoin hepatotoxicity: elevations in serum aminotransferases, lactic dehydrogenase, alkaline phosphatase, bilirubin, and prothrombin time. Rechallenges, lymphocyte stimulation test, and liver biopsy have been used to aid in the diagnosis. Rechallenge is the most definitive diagnostic approach; however, its use is limited by the potential of a fatal reaction. Although the exact mechanism of phenytoin hepatotoxicity is unknown, the majority of literature supports a hypersensitivity mechanism. The severity of this adverse effect ranges from self-limiting to fatal. Since 1965 six fatal cases have been reported. To date, sufficient evidence is not available to establish treatment guidelines. Discontinuation of phenytoin therapy is warranted.
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PMID:Phenytoin hepatotoxicity: a review of the literature. 265 93

Of twelve patients with malignant histiocytosis admitted between 1974 and 1987, clinical symptoms, diagnostic procedures and the course of the disease were retrospectively evaluated. Predominant findings at physical examination were fever (11/12), splenomegaly (12/12), hepatomegaly (8/12), and lymphadenopathy (8/12). Laboratory findings included anaemia, leukocytopenia, thrombocytopenia, high lactate dehydrogenase, and jaundice. Positive diagnostic procedures included biopsies or aspirates of bone marrow (11/12), spleen (6/10), liver (7/9), lymph node (4/4), skin (1/2), lung (1/1) and blood (2/12). In seven patients treated with combination chemotherapy an average survival of 540 days was observed, while two long-term disease-free survivals were accomplished.
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PMID:[Diagnosis and treatment of malignant histiocytosis]. 271 Feb 32

The administration of 1.5 g/kg of di-(2-ethylhexyl)phthalate (DEHP), 50 or 10 micrograms/kg of luteinizing hormone-releasing hormone (LRH) to male Crj:Wistar rats for 1 week did not affect their testicular and prostatic gland weights. Co-administration of DEHP and LRH, however, induced testicular atrophy coincident with decreases in zinc and sulfhydryl concentration in the testis and reduction of the activity of testicular specific lactate dehydrogenase isozyme. These changes were similar to the results of high-dose administration of DEHP alone. Liver enlargement and hypolipidemia (reduction of serum cholesterol, triglycerides and phospholipids) occurred sometimes after co-administration of DEHP and LRH.
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PMID:Enhancing effects of luteinizing hormone-releasing hormone on testicular damage induced by di-(2-ethylhexyl)phthalate in rats. 274 71

The proband, a 17-year-old boy, was admitted to our department because of the difficulty in standing on heel. Physical examination revealed a marked weakness and atrophy of bilateral lower legs, especially anterior tibial muscles. Patellar and Achilles tendon reflexes were abolished. Marked hepatomegaly and moderate splenomegaly were noted on abdominal echogram and CT scanning. Serum creatine kinase, lactate dehydrogenase, GOT and GPT were markedly increased. There were no abnormal findings in thyroid function, serum lipid analysis and serum lactate level after ischemic forearm exercise test. EMG of anterior tibial and calf muscles showed a mixture of myogenic and neurogenic patterns and biopsy specimen of calf muscle was compatible with a dystrophic change. Liver biopsy specimen revealed no noticeable change except a slight ballooning of hepatocytes in light microscopy. However, electron microscopic examination showed a marked increase of intracellular vesicles and enlarged smooth ER in which low-density, cotton-like materials were contained. In family study, both his father and paternal uncle were also affected with advanced scapuloperoneal-type myopathy associated with a marked elevation of serum creatine kinase and hepatomegaly. The disorder differs from Miyoshi's distal muscular dystrophy, which shows an early involvement of flexor muscles in lower extremities and is inherited as an autosomal-recessive trait. Although the etiology of hepatomegaly in this case remains to be elucidated, the special findings on electron microscopic study imply the possibility of some unknown metabolic disorder involving both muscle and liver. This disease seems to be a new type of scapuloperoneal-type myopathy, probably having an autosomal-dominant inheritance.
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PMID:[Familial scapuloperoneal-type myopathy associated with a marked elevation of serum creatine kinase and hepatomegaly]. 275 61

The frequency, pattern, extent and clinical features of bone marrow involvement in 94 cases of non-Hodgkin's lymphoma, classified according to the International Working Formulation, were reviewed. In 30% of cases there was bone marrow involvement by lymphoma at the time of diagnosis. Marrow involvement was most frequently found in the follicular small cleaved cell (57%), diffuse mixed small and large cell (56%), and lymphoblastic (56%) lymphomas. A paratrabecular pattern of marrow involvement tended to occur in low or intermediate grade lymphomas. High grade lymphomas tended to show an interstitial or diffuse pattern of marrow involvement. The results of marrow aspiration and biopsy were of equal value and complementary to each other. In 43% of cases with marrow lymphoma there was peripheral blood involvement at the time of diagnosis. Blood involvement was most frequently found in the lymphoblastic lymphoma (70%). In general, the degree of blood involvement was related to the extent of marrow involvement. Patients with marrow involvement often presented with "B" symptoms and hepatomegaly. Abnormalities in at least one of the blood counts were quite common (93%). A normal blood count made marrow involvement unlikely but not impossible. Other common laboratory findings included hyperimmunoglobulinemia (47%) and elevated serum levels of lactate dehydrogenase (56%). Patients with marrow involvement showed a significantly higher frequency of hepatomegaly and abnormal blood counts, as compared to those with negative marrows (p less than 0.05 and less than 0.001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bone marrow involvement in non-Hodgkin's lymphoma. 276 11


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