vitamin-b-12 and Liver-Failure

Topics: Adult; Aged; Alcoholism; Anemia, Macrocytic; Female; Folic Acid; Folic Acid Deficiency; Humans; Hydroxocobalamin; Hypothyroidism; Infant, Newborn; Liver Failure; Male; Pregnancy; Risk Factors; Time Factors; Vitamin B 12; Vitamin B 12 Deficiency

Patients with liver disease frequently experience changes in their nutritional status.. To determine changes in vitamin B12 and folic acid plasma levels in patients with chronic cirrhosis and to assess whether these parameters may be useful in the etiologic diagnosis of this disease.. Thirty-nine patients admitted for decompensated cirrhosis (29 with alcoholic etiology and 10 with non-alcoholic etiology) and 35 controls were prospectively studied. Plasma levels of vitamin B(12), folate acid, mean corpuscular volume (MCV), aspartate aminotransferase (AST), alanine aminotransferase (ALT), AST/ALT ratio, and gamma-glutamyltransferase (GGT), among other parameters, were measured.. Vitamin B(12) levels were 1151+/-568pg/ml in patients with decompensated cirrhosis and 440+/-133pg/ml in controls (p<0.05). Plasma folate levels were 8.57+/-3.8ng/ml in controls and 6.68+/-2.74ng/ml in patients with cirrhosis (p<0.05). Folate levels were lower in patients with alcoholic cirrhosis (mean value, 5.7+/-2.1) than in those with non-alcoholic cirrhosis (9.3+/-2.6; p<0.0005). The vitamin B(12)/folate ratio discriminated alcoholic etiology better than other parameters such as AST, ALT, MCV, AST/ALT ratio and GGT.. Plasma levels of vitamin B12 in patients with decompensated chronic liver disease are high, whereas plasma folate levels are low. The ratio between vitamin B12 and folic acid may be useful in the differential diagnosis of the etiology of chronic liver disease.

Topics: Adolescent; Adult; Aged; Alanine Transaminase; Aspartate Aminotransferases; Diagnosis, Differential; Erythrocyte Indices; Female; Folic Acid; Folic Acid Deficiency; gamma-Glutamyltransferase; Homocysteine; Humans; Liver Cirrhosis; Liver Cirrhosis, Alcoholic; Liver Diseases, Alcoholic; Liver Failure; Liver Function Tests; Male; Middle Aged; Prognosis; Prospective Studies; Vitamin B 12; Young Adult

To determine whether oral cobalt supplements could modify the clinical onset of annual ryegrass toxicity, groups (n = 5) of sheep were dosed orally with 0, 4 or 16 mg cobalt/day. After 3 weeks on this treatment, toxic ryegrass seed was added to their feed to provide 0, 0.15 and 0.30 mg corynetoxins/kg body weight, daily. Sheep receiving cobalt ingested 30% more toxin than did unsupplemented sheep before clinical signs developed (P = 0.03). There was no significant difference between groups receiving 4 and 16 mg cobalt. The results showed that cobalt delayed, but did not prevent, the onset of clinical signs of annual ryegrass toxicity.

Topics: Administration, Oral; Animal Feed; Animals; Aspartate Aminotransferases; Brain Diseases; Cobalt; Drug Tolerance; Glutamate Dehydrogenase; Glycolipids; Liver Failure; Lolium; Male; Plant Poisoning; Seeds; Sheep; Sheep Diseases; Toxins, Biological; Vitamin B 12