Sturge-Weber disease with subarachnoid hemorrhage.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to F H Anderson.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In a prospective study of 59 patients receiving total parenteral nutrition we found that patients with low serum albumin were more likely to develop cholestasis than patients with normal serum albumin. Only 25% of patients with a normal serum albumin developed cholestasis. Seventy-nine percent of patients with low serum albumin (less than 3.5 g/dl) developed cholestasis (p less than 0.01). In those patients who developed cholestasis, there was a significant correlation (r = 0.63, p less than 0.01) between the serum albumin and the number of days after onset of total parenteral nutrition when cholestasis appeared. The role of hypoalbuminemia in the development of total parenteral nutrition-associated cholestasis deserves further study.
We carried out a study to determine which of the liver function tests was the most sensitive and/or specific in detecting parenteral nutrition associated cholestasis. The tests utilized were alkaline phosphatase, gamma-glutamyl transpeptidase, cholylglycine, sulfolithocholylglycine, and bilirubin. Fifty-nine patients with no prior evidence of liver dysfunction were studied. We found gamma-glutamyl transpeptidase to be the most sensitive (89.5%) and also the least specific (61.9% specificity). Specificity of gamma-glutamyl transpeptidase was improved when it was combined with alkaline phosphatase. We recommend the combination of these two enzymes as the most cost effective way of detecting parenteral nutrition-associated cholestasis.
Rats were fed liquid diets for 7 days containing either triolein or Liposyn, which is rich in linoleic acid, as fat sources, and liver cell suspensions were prepared following collagenase perfusion. The release from isolated cells of alkaline phosphatase and aspartate transaminase during a 3-hr incubation did not differ. The uptake and release of 14C-taurocholate during a brief incubation was lower but not significantly in Liposyn-fed rats (0.1 greater than p greater than 0.05): the uptake was 9.74 +/- 1.58 vs 16.7 +/- 3.3 nmol/mg protein in triolein-fed rats; the release was 3.17 +/- 0.65 vs 5.35 +/- 1.01 nmol/mg protein in triolein-fed rats. The uptake of 14C-aminolevulinic acid was similar in both groups, but release of 14C-bilirubin during a 30-min incubation was 5,420 +/- 1010 in the Liposyn group vs 12,030 +/- 2,200 dpm/mg protein in the triolein group (p = 0.02). It is concluded that a diet high in linoleic acid decreases bilirubin release in isolated liver cells consistent with the ability of this diet to cause cholestasis in vivo.
Mice were fed a liquid diet containing different fat sources for 6 days and several biochemical parameters in the liver were examined. Mice fed diets containing Nutralipid or Liposyn as 45% of total calories had 30.5 +/- 2.5 and 25.8 +/- 3.7 nmol cholesteryl esters per milligram liver protein, respectively, as compared with 13.14 +/- 2.4 for those fed regular mouse food and 13.7 +/- 2.45 for those fed an emulsion containing mostly triolein as fat source. A similar increase in liver cholesteryl esters resulting from estrogen treatment has been proposed as the basis for changes resulting in decreased bile flow in the rat. It is suggested that the high content of polyunsaturated fatty acids in nutrient emulsions might be responsible for cholestasis sometimes observed in patients receiving these preparations. This is further supported by the observation that, as in the case of estrogen treatment, the cholesteryl ester level returned to normal when mice were treated with the detergent Triton WR-1339.
Osteoporosis in men is a common cause of morbidity, mortality and health care expenditure throughout the Western world. Most cases are secondary to disease or to drug therapy, but in 30-45% of affected individuals no cause can be identified. Research into the factors underlying 'idiopathic' male osteoporosis is limited, but is gradually moving more patients into the 'secondary' category. Recently, attention has focused on interactions between sex hormones and bone: there is evidence that male bone requires both androgens and oestrogens for normal health. Many conditions predispose to osteoporosis in men: hypogonadism, alcohol abuse and the use of corticosteroids are the most frequently identified factors. Osteoporosis following organ transplantation attracts interest despite its relative rarity. Treatment for osteoporotic men is poorly researched and remains largely unsupported by experimental evidence, although clinical experience suggests a useful role for bisphosphonates, testosterone and perhaps fluorides. Symptom control and explanation remain the most important therapeutic interventions.