[Contribution to the malabsorption syndrome. 2. Vitamin A level in the blood and its absorption in gastrointestinal diseases].
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A quantitative immunoenzymatic assay has been developed for alpha-fetoprotein which is sensitive and specific. Seventy-eight percent of United States hepatoma patients have detectable serum alpha-fetoprotein elevations over 50 ng/ml, whereas only 2 of 93 other gastrointestinal tumors were positive. Thirteen percent of patients with acute viral hepatitis, 44% of patients with massive hepatic necrosis, and 23% of patients with chronic active hepatitis had measurable serum alpha-fetoprotein concentrations. However, patients with non-viral acute or chronic liver disease were largely alpha-fetoprotein negative and alpha-fetoprotein was undetectable on multiple postoperative samples from 6 patients after hepatic lobectomy in the rapidly regenerating phase. Therefore, alpha-fetoprotein elevations in nonmalignant liver diseases are not due solely to hepatic regeneration but appear to be related to viral injury. The immunoenzymatic assay does not require purified antigen or radioisotope equipment and can detect and quantitate clinically significant alpha-fetoprotein levels greater than 50 ng/ml.
A gram-negative bacteria designated DF-3 was cultured on multiple occasions from stool samples of a patient with common variable hypogammaglobulinemia and chronic diarrhea. Antibiotic therapy resulted in elimination of the organism and resolution of the patient's symptoms. DF-3 has not been linked previously to human disease; because of its fastidious growth characteristics and unique isolation requirements, it may be a rarely identified cause of diarrhea and other gastrointestinal symptoms in immunocompromised patients.
Domestic cats with small intestinal disease may develop cobalamin deficiency because of reduced small intestinal uptake of this vitamin. This study assessed the impact of cobalamin deficiency on biochemical and clinical findings in cats with intestinal disease. Nineteen pet cats, all with severe hypocobalaminemia (< or =100 ng/L) and histories of gastrointestinal signs, were studied. Cats received cobalamin, 250 microg SC once weekly, for 4 weeks. Biochemical indices of cobalamin availability (e.g., serum methylmalonic acid, homocysteine, and cysteine concentrations), serum feline trypsinlike immunoreactivity (fTLI) and serum folate concentrations, and clinical findings were recorded at the start of the study and after 4 weeks of cobalamin therapy. Serum methylmalonic acid (MMA) concentrations (median; range) decreased after cobalamin supplementation (5373.0; 708.5-29,329.0 versus 423.5; 214.0-7219.0 nmol/L, P < .0001). Serum homocysteine concentrations were not significantly altered (mean +/- SD 8.2 +/- 2.9 versus 10.3 +/- 4.5 micromol/L, P = .1198), whereas cysteine concentrations increased significantly (122.3 +/- 38.8 versus 191.5 +/- 29.4 micromol/L, P < .0001). Mean body weight increased significantly after cobalamin therapy (3.8 +/- 1.1 versus 4.1 +/- 1 kg, P < .01), and the average body weight gain was 8.2%. Significant linear relationships were observed between alterations in serum MMA and fTLI concentrations and the percentage body weight change (P < .05 for both, Pearson r2 = 0.26 and 0.245, respectively). Mean serum folate concentration decreased significantly (mean +/- SD 19 +/- 5 microg/L versus 15.4 +/- 6.2 microg/L, P < .001). Reduced vomiting and diarrhea were observed in 7 of 9 and 5 of 13 cats, respectively. These results suggest that cobalamin supplementation in cats with small intestinal disease and severe hypocobalaminemia is associated with normalization of biochemical test results and improvements in clinical findings in most affected cats.
Recent investigations of several authors on portal venous and systemic endotoxemia in healthy adults have shown that endotoxins absorbed from the intestinal mucosa are found in portal venous blood, cleared by the RES of the liver and usually cannot be determined in peripheral blood. In patients with liver disease, however, there was often a reduced endotoxin clearance with spillover of endotoxin resulting in systemic endotoxemia. Among the complications of systemic endotoxemia, hepatocytotoxicity, pyrogen reaction, disseminated intravascular coagulation, impaired renal function, and endotoxic shock are most hazardous. In addition, O-antibody titers and lipid-A-antibody titers were found to be higher in patients with liver disease and in patients with Crohn's disease than in control groups. The investigations indicate that intestinal endotoxins are of importance in the pathogenesis of liver disease and of Crohn's disease and that reduction of intestinal endotoxins by antibiotics may be of value in the therapy of these diseases.
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