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)

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

Young rats were force-fed a lysine + arginine-devoid diet or a complete diet for 3 days, and selected biochemical and morphologic studies were conducted. Rats force-fed the experimental diet in comparison with those force-fed the control diet for 3 days showed decreased body weight gain, hepatomegaly with periportal fatty liver, pancreatic and splenic atrophy, and enhanced 14C-leucine incorporation into hepatic proteins. Differences in the experimental animals were observed in the free amino acid levels of serum (decreased lysine, arginine, and ornithine) and liver (decreased ornithine), in blood chemistries (decreased levels of ammonia N2, uric acid, cholesterol, protein, albumin, alkaline phosphatase, LDH and SGOT) and in hematologic findings (leukocytopenia and thrombocytopenia after a morning feeding). The experimental findings in young rats force-fed the lysine + arginine-devoid diet were compared with those reported to develop in children with lysinuric protein intolerance (LPI), an autosomal recessive defect in diamino acid transport. Children with LPI as described by others reveal a number of similarities as well as a number of differences in comparison to the findings in the experimental animals. The comparison suggests that some of the pathological manifestations of LPI may be related to a deficiency of diamino acids but others must be due to different alterations in this complex human disease.
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PMID:Chemical pathology of diamino acid deficiency: considerations in relation to lysinuric protein intolerance. 393 96

Acetaminophen-induced (750 mg per kg p.o.) hepatotoxicity in mice is characterized by hepatomegaly and massive centrilobular congestion which precede the appearance of necrosis. The vascular changes are correlated with the morphologic features using liver hemoglobin content to quantitate erythrocyte sequestration, and hematocrit measurements and 125I-albumin injections to determine plasma and blood volume. The initial increase in liver size was a result of plasma accumulation due to endocytic vacuolation of hepatocytes and Disse space enlargement in centrilobular regions. Further increases in liver size after 3 hr were a consequence of erythrocyte and additional plasma sequestration within the damaged liver. These events occurred without any increase in intrahepatic or portal venous pressure. Hepatic hemoglobin and plasma levels increased 10- and 5-fold, respectively, by 4.5 to 6 hr after administration of acetaminophen. There are two major consequences of acetaminophen-induced hepatotoxic congestion. First, blood and plasma volumes fell significantly, and we suggest that hypovolemic shock contributes to early mortality after acetaminophen. Second, impaired circulation within the congested liver, as manifested by reduced 125I-albumin entry into the liver when 125I-albumin was injected after congestion had developed, probably aggravates the initial injury. Early lesions were always evenly distributed around central veins. However, the pattern of damage at 24 hr could be variable. Occasional large confluent areas of necrosis were always congested, which is consistent with the concept that secondary ischemic damage can develop. Congestion and hypovolemia are reversible and can be largely prevented by administration of the protective compound N-acetylcysteine (1,200 mg per kg p.o.) 3 hr after acetaminophen.
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PMID:Acetaminophen-induced hepatotoxic congestion in mice. 397 55

Primary biliary cirrhosis (PBC) is a chronic nonsuppurative, destructive cholangitis, whose etiology is unknown. Morbidity arises early from pruritus and later from hypercholesterolemia with xanthoma formation. Therapy is supportive and directed at the complications of cholestasis. Plasmapheresis has been reported to benefit patients with hyperlipidemia and PBC; thus a pilot study of plasmapheresis utilizing the Haemonetics Model 30 with replacement by albumin and saline was conducted. Five patients (four female and one male) with a mean age of 43 (range 29-58) and a mean duration of illness of 9.5 years (range 6-21) with marked jaundice, xanthomas, xanthelasma, hepatomegaly, fatigability, anorexia, and pruritus, as well as mild nausea were studied. Peripheral neuropathy was present in two patients. Two patients had splenomegaly. Two patients had an associated Sjogren syndrome. All patients had high serum bilirubin, alkaline phosphatase, and cholesterol levels and mild elevations in aspartate amino transferase and alanine amino transferase activities. Immune complexes measured in four patients were present. Antimitochondrial antibody titers were significant in all patients. Patients underwent a mean of 63 plasmapheresis procedures over a mean of 112 weeks removing a mean of 94.7 liters of plasma. No serious toxicity was seen. All patients showed a reduction in pruritus, xanthomas, xanthelasmas, and serum cholesterol values. The two patients who had evidence of Sjogren syndrome noted subjective improvement. All patients who had fatigue, anorexia and nausea also noted moderate improvement. There was no change in hepatomegaly or splenomegaly in patients demonstrating such organomegaly. Liver function did not change significantly. Overall, four patients had improvement in their condition and one patient achieved stability.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The clinical effectiveness and safety of chronic plasmapheresis in patients with primary biliary cirrhosis. 403 Jul 9

The purpose of this study has been to provide information on the mortality and morbidity rates for operation on nonbleeding cirrhotic patients and to identify factors that portend a grave prognosis. A review of 102 cirrhotic patients who underwent a variety of major therapeutic operations revealed a mortality rate of 19.6 percent. Mortality rates were significantly increased (p less than 0.05) by emergency operation (45.8 percent), gastrointestinal related operation (27.6 percent), ascites (37.5 percent), a bilirubin concentration greater than 3.5 mg (44.4 percent), a prothrombin time increase greater than 2 seconds (36.1 percent), a partial thromboplastin time increase greater than 2 seconds (50 percent), an alkaline phosphatase concentration greater than 70 units (40.9 percent), an operative blood loss greater than 1,000 ml (33.3 percent), and the presence of one or more postoperative complications (39.6 percent). Mortality rates were not increased after extremity, genitourinary, or gynecologic operations, an albumin concentration less than 3 g, a serum glutamic oxalacetic transaminase concentration greater than 40 units, hepatomegaly, and a history of previous gastrointestinal bleeding. When significant risk factors were added, mortality rates were significantly associated (p less than 0.001): zero to one factors 5.1 percent, two to three factors 19.4 percent, four to five factors 33.3 percent, and more than six factors 66.7 percent. The complication rate was 47.1 percent and included liver failure (42.2 percent), sepsis (18.6 percent), and bleeding (8.8 percent). Thus, in cirrhotic patients a clear need for operation must exist, liver function must be optimized preoperatively, and the most simple and expeditious procedure must be performed to avoid excessive blood loss and postoperative complications.
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PMID:Morbidity and mortality after operation in nonbleeding cirrhotic patients. 660 65

Both acute and chronic ethanol administration inhibit the secretion of albumin and glycoproteins from the liver. Impairment of posttranslational steps of the secretory process are mainly involved in this secretory defect, although in some instances altered synthesis of the protein moiety may be a factor. Decreased secretion following ethanol administration results in the intrahepatic retention of export proteins. The secretory defect is a consequence of the metabolism of ethanol and is likely mediated via acetaldehyde, although more conclusive proof is still required. The manner by which acetaldehyde impairs the secretory process is unknown, but may be related to its high reactivity with hepatocellular proteins. The specific posttranslational steps or processes involved in the secretory defect are still unclear; however, it appears that the final steps of secretion (post-Golgi events) may be the primary site of impairment. Impaired secretion of proteins from the liver could contribute to altered levels of plasma proteins and hepatomegaly as well as to the liver injury observed in the alcoholic.
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PMID:Effect of ethanol on hepatic secretory proteins. 672 60

Continuous supraventricular tachycardia was induced in 13 fetal sheep for 72 to 216 hours. The PaO2 decreased from 18.1 +/- 1.2 (SEM) to 15.4 +/- 0.9 mm Hg and the PaCO2 increased from 41.5 +/- 1.2 (SEM) to 46.0 +/- 1.0 (SEM) mm Hg with pacing. The hematocrit, total protein, albumin, serum [Na+] and [K+], and osmolality remained unchanged throughout the study. All study fetuses showed signs of ascites (mean = 88 +/- 67.5 [SD] ml), and one was grossly hydropic. Six fetuses, all of which had greater than or equal to 50 ml of ascites, died as the results of pacing. Gross pathologic findings in 13 fetuses included: cardiomegaly in seven, cyanotic myocardium in two, hepatomegaly in seven, pulmonary congestion in two, generalized edema in three, and massive edema (hydrops) in one. None of these conditions was found in the 14 control animals. There was no correlation of the severity of effects upon the fetus and the induced heart rate, the duration of tachycardia, or the site of implantation of the pacemaker. The conclusion was that organomegaly, generalized edema, and hydrops fetalis were the direct result of supraventricular tachycardia in utero; the exact mechanism of production and the reasons for the variable manifestations of tachycardia remain unclear.
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PMID:Supraventricular tachycardia with edema, ascites, and hydrops in fetal sheep. 706 22

A retrospective was designed to analyse the mode of presentation, clinical signs and haematological and biochemical abnormalities in 225 consecutive Black (Zulu) patients who were admitted to a general medical ward between the years 1970 and 1981 and in whom cirrhosis was later diagnosed. The most common presenting complaint was swelling of the body (60% of the patients), followed by abdominal pain (32%) and episodes of bleeding, mainly from the gastrointestinal tract (19%). On examination, hepatomegaly was encountered in 66% of the patients, with moderate to massive enlargement in 40%. Ascites was detected in 56%, with tense abdominal distension in 34%. Jaundice was present in 38% and emaciation, mental disturbance and splenomegaly in over 25%. Spider naevi (found in 2 patients) and Dupuytren's contracture (found in 1) were very rare. Thrombocytopenia and a high ESR were common. Over 90% of patients had low albumin and high globulin concentrations (albumin less than 20 g/dl and globulin greater than 60 g/dl in 25%). Bilirubin and alkaline phosphatase levels and the prothrombin index were found to be within normal limits in 32%, 24% and 52% of cases respectively. Histologically the lesion was most commonly micronodular (73%) with variable deposits of fat and iron. Peritoneoscopy was the most useful special investigation in the diagnosis of cirrhosis, leading to a correct diagnosis in 77% of cases. In conclusion, the clinical signs, biochemical abnormalities and histological features suggest that the factors causing cirrhosis in the community studied are mixed; it may result from the combined effects of alcohol abuse, malnutrition and chronic viral (e.g. hepatitis B) infections.
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PMID:Clinical presentation and biochemical abnormalities in black (Zulu) patients with cirrhosis in Durban. 707 88

The clinical and pathological features of 22 patients, 11 males and 11 females 17-70 years of age (48.0 +/- 16.0 years), with hepatic tuberculosis were reviewed. Five patients had no evidence of extrahepatic tuberculosis (local form), and 17 had the miliary form. The clinical features of the miliary and local forms were similar with pyrexia, abdominal pain, hepatomegaly and body weight loss as the main manifestations. The biochemical findings were also quite similar in reversed albumin and globulin (A/G) ratio (2.9/3.5 vs. 3.2/3.4 g/dl) and disproportionate elevation of alkaline phosphatase (ALP) in comparison with bilirubin values but lower levels of alanine aminotransferase (ALT) (40.4 +/- 51.0 vs. 170.8 +/- 209.4 U/l; p < 0.05) and ALP (208.5 +/- 138.9 vs. 389.5 +/- 271.1 U/l; p < 0.05) in the miliary form. Patients with the local form had higher albumin (3.2 +/- 0.8 vs. 2.9 +/- 0.7 g/dl), aspartate aminotransferase (AST) (160.4 +/- 221.7 vs. 65.9 +/- 69.7 U/l), and gamma glutamyl-transpeptidase (gamma GT) (217.0 +/- 144.0 vs. 136.0 +/- 92.1 U/l), although the differences were not significant. The histopathological features of the miliary form were also similar to the local form with granuloma, caseation, acid-fast bacilli, fatty change and portal fibrosis as the main findings. The local form revealed more severe signs of hepatocytic damage while the miliary form was more wasting. The results suggest that the miliary and local forms of hepatic tuberculosis had quite similar clinical presentations and pathological features. The biochemical tests suggesting hepatic tuberculosis were reversed A/G ratio and disproportionate elevation of ALP.
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PMID:Hepatic tuberculosis: comparison of miliary and local form. 774 92

In a prospective study, we investigated whether human immunodeficiency virus (HIV) infection alters the clinical presentation in patients with tuberculous pleuritis. One hundred twelve of 118 patients who presented with pleural effusion suffered from tuberculosis (TB); 65 patients (58%) were HIV seropositive. Evidence of disseminated TB was found more often in HIV-positive than in HIV-negative patients (30.8% vs 10.6%, p < 0.02). Dyspnea, fever, night sweat, fatigue, and diarrhea, severe tachypnea, hepatomegaly, splenomegaly, and lymphadenopathy were significantly more common in HIV-infected than in HIV-negative patients with TB. The same applied to a negative Mantoux reaction, lower hemoglobin, higher beta 2-microglobulin values, and in pleural fluid, lower albumin and higher gamma-globulin levels. Among HIV-infected patients, PPD skin test anergy was significantly associated with relative low albumin and gamma-globulin levels of pleural fluid. However, the radiographic features did not differ with respect to HIV status; they were predominantly those of primary pleuritis (78% in each group). We conclude that coexisting HIV infection affects clinical and laboratory features, but not the radiographic presentation of patients with TB pleuritis in Tanzania.
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PMID:Clinical features of HIV-seropositive and HIV-seronegative patients with tuberculous pleural effusion in Dar es Salaam, Tanzania. 795 5


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