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)

Copper poisoning developed in 1 adult and 3 juvenile llamas after excessive dietary intake of copper resulted in an incorrect copper:molybdenum ratio. Total dietary copper was determined to be 36 mg/kg of feed, with a copper:molybdenum ratio of 16.6:1. Clinical signs associated with the toxicosis included acute onset of anorexia and lethargy. Liver enzyme activities (aspartate amino transaminase, lactate dehydrogenase, gamma-glutamyl transferase) and serum copper concentration were high in specimens obtained within 48 hours before death. Gross necropsy findings were limited to mild hepatomegaly. Histologically, hepatic lesions included acute massive necrosis of hepatocytes with and without bile duct proliferation, double hepatic plates with loss of orientation, anisocytosis, anisokaryosis, and an intralobular mosaic pattern of necrosis involving half of the hepatocytes. Analysis of hepatic copper concentrations suggested that juvenile llamas develop signs of poisoning at lower hepatic copper concentrations, compared with adults.
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PMID:Copper poisoning in four llamas. 279 84

We analysed the clinical and pathologic features of 42 patients with immunologically confirmed peripheral T-cell lymphoma. The median age was 60 years and the male to female ratio was 1:1. A prior lymphoproliferative or autoimmune disorder was present in 14 per cent of the patients. Signs of advanced disease were usually present from the onset, such as B symptoms (55 per cent), generalized lymphadenopathy (57 per cent), stage III/IV disease (62 per cent), and elevated levels of serum lactate dehydrogenase (68 per cent). Primary extranodal disease (14 per cent), hepatomegaly (12 per cent), splenomegaly (12 per cent), lung/pleural involvement (12 per cent), skin involvement (21 per cent), and bone marrow involvement (28 per cent) were uncommon. Lymphocytopenia was present in 64 per cent of the patients, and none of nine patients tested were serologically positive for human T-cell leukemia/lymphoma virus (HTLV-I) infection. Among 38 patients receiving combination chemotherapy, 20 (53 per cent) achieved a complete remission. The actuarial median survival of all patients was 17 months. Age greater than 60 years and stage III/IV disease predicted a poor clinical outcome, whereas the large cell histological subtype predicted a favourable outcome. Prospective clinical studies using uniform treatments and a uniform histologic classification scheme are needed to confirm these findings.
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PMID:Peripheral T-cell lymphoma: a clinicopathologic study of 42 cases. 288 15

Twenty cows from a dairy herd consisting of 60 healthy, lactating Holsteins developed clinical signs of anorexia, mental derangement, dehydration, recumbency, and ruminal atony after ingesting water containing blue-green algae. Of the 20 cows, 9 died. The algal bloom, which developed in a stagnant pond during hot, dry weather, was identified as the cyanobacterium Microcystis aeruginosa, a potentially hepatotoxic algae. One week after the onset of toxicosis, affected cows seemed healthy, although liver-associated enzyme activities (alkaline phosphatase, gamma-glutamyl transferase, aspartate transaminase, and lactate dehydrogenase) were increased. Intraruminal administration of the intact wet bloom to a healthy 125-kg Angus heifer was followed by hepatic necrosis and death. The liver was large, friable, and gun-metal blue, with microscopically evident hepatocyte dissociation, degeneration, and necrosis. The ingesta of the heifer contained typical clumps of cells that were identified as M aeruginosa. The intraperitoneal administration of lyophilized cell material from that bloom to 18 mice caused marked hepatic enlargement. The intraperitoneal median lethal dose of the dried bloom was estimated to be 10 mg/kg of body weight. A cyclic peptide toxin purified from the algae seems to be similar structurally to toxins from other characterized hepatotoxic blooms of M aeruginosa.
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PMID:Blue-green algae (Microcystis aeruginosa) hepatotoxicosis in dairy cows. 311 92

Sixty-one patients with essential thrombocythemia (ET) were followed from 1974 through 1987 at the Medizinische Poliklinik. Fifty-one patients (84%) presented with thromboembolic complications, and eight patients (13%) with hemorrhages. In seven patients (12%), a thrombocytosis was detected accidentally. Disturbances of the microcirculation (67%), mainly of the fingers and toes (53%), were the most frequent thromboembolic symptoms. The mean age of all patients was 58 years (male patients, 61 years; female patients, 56 years). The average platelet count at diagnosis was 897,000/microliter. The average maximal platelet count was 1.231 X 10(6)/microliter (range, 500,000/microliter to 4 X 10(6)/microliter). Seventy-two percent had a moderate leukocytosis (average, 12,400/microliter), 34% a splenomegaly, 29% a hepatomegaly. Signs of hypermetabolism were infrequent, lactate dehydrogenase (LDH) and uric acid elevations, if present, were moderate. Bleeding time and viscosity were normal in most patients. Spontaneous platelet aggregation was increased in 81% of patients (n = 40). Platelet aggregation studies with the aggregation inducing substances adenosine diphosphonate (ADP), platelet activating factor (PAF), thrombin, collagen, and adrenalin showed hypoaggregation in most patients. Adrenalin-induced aggregation distinguished best between ET-patients and reactive thrombocytosis showing hypoaggregation in all ET-patients tested (n = 16) and in none of 22 controls. Bone marrow studies were performed in 57 patients. The histologic studies (done in 49 patients) were consistent with a chronic myeloproliferative disorder in all cases. In 41 cases (84%) the picture of a megakaryocytic myelosis was found, in 12 of these a granulocyte-rich form of megakaryocytic myelosis. Cytologic studies only (eight patients) did not differentiate ET well from reactive thrombocytosis. Platelet aggregation studies and bone marrow histology may be of help in the diagnosis of difficult cases of thrombocytosis. The Philadelphia status was negative in all cases studied (14 patients). Fourteen patients died. The causes of death were thromboembolic complications in probably 11 and acute leukemia in two patients. The probability of 10-year survival is 64% after a mean follow-up time of approximately 5 years. It appears that considering the average age of ET patients at diagnosis, life expectancy is close to normal.
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PMID:Essential thrombocythemia. Clinical characteristics and course of 61 cases. 336 70

Of 39 captive whooping cranes (Grus americana), 7 died during a 7-week period (Sept 17 through Nov 4, 1984) at the Patuxent Wildlife Research Center, Laurel, Md. Before their deaths, 4 cranes did not develop clinical signs, whereas the other 3 cranes were lethargic and ataxic, with high aspartate transaminase, gamma-glutamyl transferase, and lactic acid dehydrogenase activities, and high uric acid concentrations. Necropsies indicated that the birds had ascites, intestinal mucosal discoloration, fat depletion, hepatomegaly, splenomegaly, and visceral gout. Microscopically, extensive necrosis and inflammation were seen in many visceral organs; the CNS was not affected. Eastern equine encephalitis (EEE) virus was isolated from specimens of the livers, kidneys, lungs, brains, and intestines of 4 of the 7 birds that died, and EEE virus-neutralizing antibody was detected in 14 (44%) of the 32 surviving birds. Other infectious or toxic agents were not found. Morbidity or mortality was not detected in 240 sandhill cranes (Grus canadensis) interspersed among the whooping cranes; however, 13 of the 32 sandhill cranes evaluated had EEE virus-neutralizing antibody. Of the 41 wild birds evaluated in the area, 3 (4%) had EEE virus-neutralizing antibody. Immature Culiseta melanura (the most probable mosquito vector) were found in scattered foci 5 km from the research center.
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PMID:Mortality of captive whooping cranes caused by eastern equine encephalitis virus. 350 15

The progression of aflatoxicosis was evaluated in young broiler chickens (Hubbard X Hubbard). The experimental design consisted of four dietary treatments of aflatoxin (0, 1.25, 2.5, and 5.0 micrograms of aflatoxin/g of feed, ppm) and 11 replicates of 10 broilers/replicate. The broilers were maintained in electrically heated batteries with feed and water available ad libitum from hatching to 3 weeks of age. The broilers were weighed, bled, killed by cervical dislocation, and necropzied at 3, 6, 9, 12, 15, 17, and 21 days of age. Body weights were significantly decreased by 5.0 ppm aflatoxin at 6 days of age and by 2.5 ppm at 17 days of age. Aflatoxin induced a significant increase in the relative weight of the proventriculus, gizzard, spleen, and kidney. Liver atrophy was indicated in the early stages of aflatoxicosis by a decrease in the relative weight of this organ. As aflatoxicosis progressed, hepatomegaly became apparent due to lipid accumulation in the liver. Packed-cell volume and hemoglobin levels were significantly decreased by 5.0 ppm aflatoxin at 12 days and by 2.5 ppm aflatoxin at 21 days of age. Serum levels of albumin and total protein were significantly reduced at 5.0 and 2.5 ppm aflatoxin by 3 and 6 days of age, respectively. Serum levels of uric acid, triglycerides, and cholesterol were significantly decreased from control values from 12 through 21 days of age by 5.0 ppm aflatoxin and, to a lesser extent, by 2.5 ppm aflatoxin. The activity of serum lactic dehydrogenase was significantly decreased at all aflatoxin treatment levels from 12 through 21 days of age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Progression of aflatoxicosis in broiler chickens. 379 71

Among 2175 patients seen over the last three years in a non-specialized department of internal medicine with no intensive care unit, 100 had supranormal serum lactic dehydrogenase activities. These patients' case-reports have been analyzed. Nearly half the patients (47/100) had a malignant disease (cancer or hemopathy). Among the remaining patients, 19 had a hepatic disorder (alcohol hepatitis in 10, viral hepatitis in 8, and isoniazide hepatitis in 1), 7 had a heart disease (heart failure with hepatomegaly in 5, myocardial infarction in 2), and 27 had various other conditions (including hemolysis in 6 and polymyositis en 3). The value of serum LDH assay is obvious in situations other than acute conditions such as myocardial infarction of pulmonary embolism; these are better known and have not been studied here as their prevalence was low among the patients enlisted in our study. In comparison to other enzymes (alkaline phosphatase (AP), gamma-glutamyl transpeptidase (GGT), transaminases (GOT, GPT) that were also routinely assayed in our patients, abnormal serum LDH activities are much less common and their significance is quite different. An increase in serum and their significance is quite different. An increase in serum LDH activity indicates a serious condition, often with a fatal outcome. The "various other conditions" group includes patients with hemolysis, hepatitis and myositis; the other patients in this group either had severe infectious diseases or died suddenly in the first few days of their hospitalization before diagnosis had been established. Each etiologic group has been analyzed to asses the characteristics of patients with increased LDH activity according to each etiology. Analysis of coincident abnormalities of the other enzymes listed above shows marked differences between etiologic groups; diagnostic accuracy can thus be enhanced in certain conditions. Most patients with malignancies had poorly differentiated tumors, with metastases: 28 had an epithelial tumor, with hepatic and/or bone metastases in 23 cases, 5 had cancer of the liver, 10 had a malignant hemopathy (2 lymphomas, 5 myeloproliferative syndromes, 3 acute leukemias), and 4 had a sarcoma. Cancer of the lung is the most common malignancy (10 cases) and may be responsible for increased serum LDH activity even in patients without metastases. Serum LDH assay is of value for monitoring the course in patients with initially increased activities as it falls under effective therapy and rises during exacerbations.
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PMID:[Value and diagnostic significance of serum lactic dehydrogenase in internal medicine (author's transl)]. 628 24

A 50-year-old black female developed hepatic dysfunction secondary to captopril therapy, 25 mg tid for one month. Liver biopsy showed primarily cholestasis, with secondary hepatocellular elements. Symptoms consisted of jaundice, pruritus, anorexia and weight loss, hepatomegaly, and abdominal tenderness. Total bilirubin, alkaline phosphatase, lactate dehydrogenase (LDH), and serum glutamic-oxaloacetic transaminase (SGOT), reached highs of 506 mumol/L, 737 U/L, 319 U/L, and 100 U/L, respectively. Recovery was slow, but complete, after discontinuation of the drug.
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PMID:Captopril-induced cholestatic jaundice. 636 96

We reviewed the records of 73 patients with primary melanoma of the choroid and ciliary body with metastasis treated at M. D. Anderson Hospital and Tumor Institute between 1973 and 1979. At time of diagnosis of primary melanoma 71 of 73 patients had tumor localized to the eye and were treated with enucleation of the affected eye. The interval from resection of primary tumor to detection of systemic metastases in the 71 patients ranged from one to 201 months (median 43.5 months). Weight loss and abdominal pain due to hepatomegaly were the most common symptoms, and hepatomegaly was the most common physical sign. The liver was the most common site of tumor recurrence, occurring in 44 of 71 patients. Among liver enzymes, serum lactic dehydrogenase was found to be the most sensitive indicator of liver metastasis and was elevated in 96% of patients with tumor in the liver. Liver involvement with tumor was associated with poor response to chemotherapy and significantly poorer survival than involvement of other extracranial sites. The survival duration from time of development of systemic metastasis ranged between one and 31 months (median seven months), with a one-year survival rate of 29%. The median survival of patients from diagnosis of ocular melanoma was 52 months, with a five-year survival rate of 43%.
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PMID:Prognosis in metastatic choroidal melanoma. 724 14

The serum levels of soluble intercellular adhesion molecule 1 (ICAM-1) were significantly elevated (P < .001) in patients with chronic B-lymphocytic leukemia (B-CLL, n = 113) compared with healthy controls (n = 31). sICAM-1 levels in B-CLL were positively correlated to the tumor mass as reflected by the modified Rai and the Binet staging systems, lymphocyte counts, and isolated spleno/hepatomegaly. During disease progression or regression on cytoreductive therapy, the circulating sICAM-1 levels changed accordingly. sICAM-1 was also correlated to a kinetic parameter such as the lymphocyte doubling time. Furthermore, the serum sICAM-1 levels were inversely correlated to hemoglobin levels in patients with early clinical stage, and this may turn out to be of prognostic value. sICAM-1 was compared with other serum markers said to reflect disease activity in B-CLL, ie, soluble CD23, thymidine kinase, lactate dehydrogenase (LDH), and beta 2-microglobulin. sICAM-1 was equally well or better correlated to clinical stage and lymphocyte doubling time. In univariate regression analysis, all serum markers but LDH correlated with survival, and in multivariate analysis, sICAM-1 was the only marker approaching significance for additional prognostic information when included after clinical stage and lymphocyte doubling time. Based on the present observations, it appears that prospective studies repeatedly monitoring serum sICAM-1 in B-CLL are justified.
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PMID:Serum levels of soluble intercellular adhesion molecule 1 are increased in chronic B-lymphocytic leukemia and correlate with clinical stage and prognostic markers. 777 31


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