Biomedical subjects
Publications and source records attributed to T B Reynolds.
Endometriosis is only rarely the cause of massive bloody ascites. This entity simulates gynecological malignancy and is seldom recognized before surgical exploration of the abdomen. It is more commonly seen in black nulliparous females. Hormonal modulation has obviated the need for surgical resection, in some cases. We report a case of such an entity and review the medical literature.
Primary biliary cirrhosis (PBC) is one of the few nonalcohol-induced liver pathologies that causes false positives in assays of carbohydrate-deficient transferrin (CDT) for diagnosing alcohol abuse. CDT was quantified by isoelectric focusing-immunoblotting-laser densitometry (IEF-IB-LD) analysis of serum from 117 women: 57 PBC patients, 20 alcohol abusers, and 40 healthy donors. Only 5% (3 of 57) of PBC patients were positive at the densitometric cutoff value chosen (> 90% specificity). Serum samples from 15 PBC patients were further evaluated by IEF-IB-LD and CDTect chromatography-RIA. Receiver-operating characteristic (ROC) analysis showed that IEF-IB-LD better discriminated between PBC and alcohol abuse than CDTect did. By ROC analysis, mitochondrial autoantibodies to pyruvate dehydrogenase antigen M2 detected by enzyme immunoassay yielded optimal test performance for diagnosing PBC. Of six patients falsely positive for CDT by CDTect, five (83%) tested M2-positive. Thus, abnormal CDT results should be further evaluated by mitochondrial antibody testing in patients with findings compatible with PBC.
Acute hepatocellular injury, whether due to viral hepatitis, hepatic ischemia, or drug hepatotoxicity, results in elevated levels of serum aminotransferases (AST and ALT). Serum lactate dehydrogenase (LD) is reported to be markedly elevated in ischemic hepatitis. Thus, comparisons of the degree of elevation of serum levels of LD, ALT, and AST may be helpful in the differential diagnosis of acute liver injury. To study this, we reviewed serum enzyme patterns early in the course of acute liver injury in patients with acute viral hepatitis A and B (n = 51), ischemic hepatitis (n = 20), and acetaminophen injury (n = 26). All patients had serum ALT and/or AST at least five times the upper limit of normal. For a given ALT and AST level, LD was higher in ischemic hepatitis and acetaminophen injury than in viral hepatitis. The mean ALT/LD ratio for acute viral hepatitis was 4.65, for ischemic hepatitis 0.87, and for acetaminophen injury 1.46. Mean ALT/LD ratio for viral hepatitis was significantly higher (p < 0.0001) than for the other two groups combined. An ALT/LD ratio of 1.5 differentiated acute viral hepatitis from ischemic hepatitis and acetaminophen injury with a sensitivity of 94% and a specificity of 84%.
BACKGROUND: In an ultrasound pilot study of acute alcoholic hepatitis (AAH), parallel tubular structures within the liver subsegments were observed. Pulse-Doppler flowmetry revealed that these structures were formed by a dilated hepatic arterial branch and an adjacent portal venous branch. This finding was termed the "pseudoparallel channel sign" (PPCS). The aims of this study were to assess the significance of this sign and show the characteristic ultrasound findings of AAH. METHODS: PPCS was specifically searched for on ultrasonography by two physician operators in consecutive patients (77 AAH, 119 other alcoholic liver disease, 49 nonalcoholic liver disease, and 15 healthy patients). RESULTS: PPCS was observed in 90% of patients with AAH and in 23% of patients with other alcoholic liver disease. This sign was not detected in nonalcoholic liver disease or healthy patients. Biopsy specimens were available in 100 patients, 51 of whom were patients with alcoholism. In those 51 patients, PPCS gave a sensitivity of 82%, a specificity of 87%, and an accuracy of 84% in diagnosing AAH. Patients with criteria of AAH had more segments involved with PPCS than patients without. CONCLUSIONS: PPCS may be an important diagnostic finding in AAH.
Liver dysfunction in hyperthyroid patients has not been well characterized. We analyzed the clinical records of 43 patients with hyperthyroidism to define the spectrum of clinical and liver test abnormalities. The patients were divided into three categories: (a) 18 patients with uncomplicated hyperthyroidism (HT) (b) 19 with hyperthyroidism and congestive heart failure (HT/CHF), and (c) 6 with hyperthyroidism and concomitant unrelated liver disease (HT/ULD). Hepatomegaly and/or spenomegaly were noted in 15 of 19 (79%) patients with HT/CHF as compared to 6 of 18 (33%) patients with HT and 3 of 6 (50%) patients with HT/ULD. Four patients with HT/CHF had ascites. Serum aminotransferase levels greater than 250 IU/L were noted in only 1 of 37 (3%) patients without unrelated liver disease. Patients with HT/ULD or HT/CHF had markedly low prothrombin time. Serum bilirubin levels as high as 323 microM were noted in patients with HT. No characteristic liver histology due to hyperthyroidism was noted. Severe liver test abnormalities, including deep jaundice and prolonged prothrombin time, can occur in patients with hyperthyroidism alone or with HT/CHF. This makes the diagnosis of concomitant, unrelated liver disease difficult until the hyperthyroidism has been controlled.
Explore the source record for details and available documents.
Although investigative research of animal models in cocaine metabolism and associated liver cell injury has been fairly extensive during the past 10 yr, little evidence of hepatotoxicity has been documented in man. We report a case of fulminant hepatic failure and acute rhabdomyolysis resulting from cocaine use. Coagulative-type perivenular and midzonal necrosis and periportal microvesicular fatty change were the predominant morphological features throughout all lobules of the liver, in contrast to periportal necrosis described in the only previous case report with biopsy. Differences in zonal necrosis caused by the same drug are not typically seen in man experiencing direct or indirect intrinsic hepatotoxicity. However, experimental models have shown cocaine to have this ability, dependent on enzyme induction or inhibition, sex and dose. Therapeutic approaches for prevention of possible liver cell injury by cocaine toxicity are discussed.
Explore the source record for details and available documents.
Colchicine treatment was used in this randomized placebo-controlled trial in patients with severe acute alcoholic hepatitis [serum bilirubin greater than or equal to 5 mg/dL (85.5 mumol/L) mean, 17.5 +/- 7.5 mg/dL (299.25 +/- 128.25 mumol/L)]. Hospitalization mortality and morbidity and the effect on biochemical test results were the end points of the treatment. Patients in the two groups were evenly matched by demographics and laboratory test results. Mean time to study entry was less than 7 days from admission. The duration of the trial was 30 days. Thirty-six patients (24 men, 12 women) received colchicine (1 mg orally every morning) and 36 (25 men, 11 women) received an identical placebo. Seven (19%) colchicine-treated and six (17%) control patients died during the index hospitalization after a mean of 17.4 +/- 10.8 and 17.8 +/- 5.3 days, respectively (NS). During a 4-month follow-up period from entry into the trial, there were two additional deaths in each group. No differences between placebo- and colchicine-treated patients were observed in any of the laboratory parameters (serum bilirubin, aspartate transaminase, alanine transaminase, prothrombin activity, albumin, white blood cell count, hemoglobin, and creatinine) that were followed up over the 30-day treatment period. The frequency of complications did not differ statistically between the two groups. This study showed no effect of colchicine treatment on mortality and morbidity of severe alcoholic hepatitis. Colchicine cannot be recommended for the treatment of patients with alcoholic hepatitis.
We investigated the effect of rifampin on pruritus in 12 patients with chronic liver disease: non-A, non-B hepatitis (n = 3), alcoholic cirrhosis (n = 4), primary biliary cirrhosis (n = 4), and primary sclerosing cholangitis (n = 1). The study was a crossover, randomized, double-blind trial where placebo and drug were given daily in identical capsules (300 mg) for 2 weeks each, with a 1 week washout before and after each cycle. Mean duration of pruritus was 1.6 years (range of 4 months-5 years). Blood tests were done weekly and patients used a visual analogue scale (VAS) from 0 to 100 to mark their level of itchiness daily. Only transaminases were significantly lower while the patients were on rifampin. VAS scores were minimally affected by either rifampin or placebo. At the end of the trial, four patients said they were less itchy on rifampin and three preferred placebo. Of these seven patients, small falls in VAS scores occurred in two patients on rifampin and two on placebo; there was no change in the remaining three. There was little change in serum bile salt levels during the trial. No patient became jaundiced and deepening of jaundice did not occur in the four patients with initially elevated bilirubin. We conclude that a daily 300 mg dose of rifampin was not effective in relieving pruritus in a variety of chronic liver diseases.
The dangers of large-volume paracentesis have been overemphasized in the past. Recent data fail to show hypovolemia or any other complications ascribable to 5-L paracentesis when it is accompanied by IV infusion of 40 gm of albumin. Other data question the need for albumin infusion. Large-volume paracentesis is now a therapeutic option for relief of symptomatic, tense ascites, and, in company with sodium restriction, for chronic management of ascites refractory to diuretics.
The purposes of this study were (a) to measure serially ascitic fluid polymorphonuclear cell response in treated spontaneous bacterial peritonitis and (b) to determine whether an ascitic fluid polymorphonuclear cell count of less than 250 per mm3 on serial paracenteses was a satisfactory endpoint for antibiotic therapy. Thirty of 33 patients showed an exponential fall in ascitic fluid polymorphonuclear cell count after 48 hr of antibiotic therapy; the magnitude of decrease correlated with survival (p less than 0.01). Among the patients whose antibiotic therapy was discontinued when the ascitic fluid polymorphonuclear cell count reached 250 per mm3 or less, the duration of therapy was considerably shorter than for the patients who received "conventional" therapy (p less than 0.01). Recurrence of spontaneous bacterial peritonitis was similar in the two groups. Mortality correlated with the severity of underlying liver disease but not with duration of antibiotic therapy.
Nonsteroidal anti-inflammatory drugs such as indomethacin induce a rapid reduction in renal perfusion and blunt the effects of diuretics in patients with cirrhosis and ascites. Nonacetylated salicylates reportedly cause less reduction in renal prostaglandins than do aspirin and other nonsteroidal anti-inflammatory drugs. To determine whether nonacetylated salicylates affect renal function, we compared diflunisal with indomethacin in nine patients with cirrhosis and ascites. One 50-mg dose of indomethacin reduced inulin clearance (91 +/- 11 to 76 +/- 11 ml/min) and blunted furosemide-stimulated natriuresis (58 +/- 12 to 36 +/- 9 mEq/h) and diuresis (1103 +/- 148 to 809 +/- 170 ml/h, all p less than 0.05). Three doses of diflunisal had no effect on inulin clearance (94 +/- 16 ml/min), natriuresis (60 +/- 12 ml/h), or diuresis (1041 +/- 112). Indomethacin caused greater reduction in urinary prostaglandin E2 (50% vs. 10%) and in serum thromboxane (94% vs. 80%) than diflunisal (p less than 0.05). Thus, nonacetylated salicylates avoid renal impairment and may be the preferred nonsteroidal anti-inflammatory drug in patients with cirrhosis and ascites.
Two cases of phenytoin toxicity in patients with chronic liver disease who were taking 300 mg phenytoin daily are described. Each patient developed encephalopathy, characterized by confusion, disturbed conscious state, asterixis, and nystagmus, which was resistant to treatment with protein restriction, lactulose, and neomycin, but responsive to withdrawal of phenytoin. We suggest that the phenytoin did not precipitate hepatic encephalopathy, but caused an encephalopathy that mimicked it. We recommend that phenytoin be used cautiously in patients with liver disease, and that the drug's unbound serum level be measured if encephalopathy occurs.
Explore the source record for details and available documents.
Serum bile acid levels were measured in eight patients with portal hypertension before and after portosystemic shunt surgery to see if the levels were useful for assessment of shunt patency. Both fasting and two-hour postprandial levels showed poor correlation with portosystemic shunting and could not be used to judge shunt patency.
Serial measurements of plasma volume and ascites volume were made during treatment with large doses of oral diuretics in 14 patients with stable chronic liver disease. Eight patients had pitting edema in addition to ascites. Reproducibility of ascites and plasma volume measurements was verified in 10 control subjects not receiving diuretics. Six patients without edema undergoing rapid diuresis lost a mean of 1.2 +/- 0.2 L of ascites and an equivalent amount of weight (1.3 +/- 0.4 kg) per day. All had a rise in blood urea nitrogen or creatinine, or both, and a fall in creatinine clearance. Eight patients with edema undergoing rapid diuresis lost more weight (1.8 +/- 0.5 kg/day, p = 0.06) but less ascites (0.7 +/- 0.35 L/day, p less than 0.05) than those without edema, and none developed renal insufficiency. After edema disappeared, ascites mobilization increased (1.4 +/- 0.7 L/day) and renal dysfunction occurred. Plasma volume fell an average of 24% +/- 9% in patients without edema but did not change in patients with edema (-0.4% +/- 3%). When edema disappeared, plasma volume fell significantly (28% +/- 8%, p less than 0.001). Electrolyte changes including hyponatremia, hyperkalemia, and hypochloremia were seen only in the group without edema. Patients with ascites and no edema are able to mobilize more than 1 L/day during rapid diuresis, but at the expense of plasma volume contraction and renal insufficiency. Patients with peripheral edema appear to be protected from these effects because of the preferential mobilization of edema and may safely undergo diuresis at a rapid rate (greater than 2 kg/day) until edema disappears.
Explore the source record for details and available documents.