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A Lanir

Publications and source records attributed to A Lanir.

58 records · Page 4Linked to original sources

Hepatic transplantation survival: correlation with adenine nucleotide level in donor liver.

The hypothesis was tested that human donor livers with higher ATP content and energy charge achieve better results after hepatic transplantation. Biopsies were obtained from 25 donor livers immediately prior to implantation and analyzed for adenine nucleotides using high-performance liquid chromatography. The results were correlated with organ histology, transplant function and outcome. Significantly higher concentrations of ATP (4.22 +/- 2.87 vs. 0.71 +/- 0.69 nmoles per mg protein, p less than 0.01), ADP (8.75 +/- 2.96 vs. 4.49 +/- 1.95 nmoles per mg protein, p less than 0.01) and energy charge (0.43 +/- 0.15 vs. 0.21 +/- 0.04, p less than 0.02) were found in successful (n = 20) relative to failed (n = 5) livers. No significant differences were found in AMP, xanthine or hypoxanthine for the two groups, although the average values were higher in failed livers. Fifteen recipients with liver ATP concentration above 2 nmoles per mg protein and energy charge above 0.3 recovered well. Five other successful patients with lower ATP concentration (0.70 +/- 0.39 nmoles per mg protein) and energy charge (0.20 +/- 0.03) had postoperative courses complicated by infection or prolonged hyperbilirubinemia. In five patients whose livers failed, all had low ATP content and energy charge. Of these, three received a replacement liver and two died shortly after the transplantation. The study demonstrates a direct correlation between high ATP content and good posttransplant outcome.

Adenine Nucleotides↗

Alcohol-induced changes in urinary aminolevulinic acid and porphyrins: unrelated to liver disease.

Urinary porphyrins and their metabolites aminolevulinic acid (ALA) and porphobilinogen (PBG) were determined in 15 normal volunteers and in 45 alcoholics, subdivided into three groups according to their liver function tests and histology: alcoholics exhibiting no evidence of hepatocellular damage; alcoholics with fatty liver and impaired function of liver enzymes; and alcoholics with proven liver cirrhosis. The dominant trend observed in those alcoholics devoid of any evidence of liver disease was increased ALA, PBG, and uroporphyrin. Coproporphyrinuria was shared by the patients exhibiting liver damage. The data shown enabled us to differentiate between the direct, primary effect of alcohol on the heme biosynthetic pathway and the secondary indirect effect, which is probably related to liver damage that follows alcohol consumption. Evaluation of the results led to the suggestion that urinary ALA could possibly serve as a marker of alcoholism. The specificity and sensitivity of the test were found to be 87% and 80%, respectively.

Adult↗

MR imaging in myelofibrosis.

Two patients with myelofibrosis demonstrated decreased signal intensity from the bone marrow due to replacement of marrow fat with fibrosis and cellular elements.

Aged↗

Treatment of severe, resistant familial combined hyperlipidemia with a bezafibrate-lovastatin combination.

Familial combined hyperlipidemia (FCHL) is a common lipid disorder characterized by high levels of cholesterol, triglycerides, or both. The basic metabolic abnormality is overproduction of apolipoprotein B-100. High atherogenicity has been attributed to all forms of FCHL. We evaluated combined bezafibrate-lovastatin therapy in 10 patients (9 men and 1 woman) with FCHL and markedly high cholesterol and triglyceride levels who were at high risk of coronary artery disease and who had not responded to diet and bezafibrate treatment alone. Eight patients had coronary artery disease, 6 had hypertension, and 3 had noninsulin-dependent diabetes mellitus. Lovastatin 20 mg/day was added to the bezafibrate 600 mg/day regimen for 6 weeks; the lovastatin dosage was then doubled to 40 mg/day for an additional 6 weeks. The addition of 20 mg of lovastatin resulted in decreases of 15%, 20%, and 13% in total cholesterol, low-density lipoprotein (LDL) cholesterol, and triglyceride levels, respectively. Increasing the dose of lovastatin to 40 mg resulted in further moderate decreases of 4%, 3%, and 8% in total cholesterol, LDL cholesterol, and triglycerides, respectively, compared with the 20 mg/day dosage. Although previous reports have emphasized the potential side effects of combination treatment with lovastatin and fibric acid derivatives, our patients tolerated the regimen well, with no significant subjective complaints or laboratory abnormalities. The bezafibrate-lovastatin combination is a possible therapeutic option for severe, resistant FCHL, but close medical supervision is needed because of potential side effects.

Adult↗