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At least 397 records · Page 22Linked to original sources
PubMed1981

Pseudomembranous (antibiotic-associated) colitis.

We have come to understand the cause of antibiotic-associated pseudomembranous colitis (PMC) only in the last decade. Clostridium difficile produces the intestinal dysfunction and the characteristic finding of exudative plaques on the mucosa by elaborating a toxin in the colon. This report reviews the development of our knowledge of this disease and the rapid adoption of a rational therapy once the cause was specified. C. difficile or its toxin can be cultured or isolated from the stools of 90% of the patients with PMC. This organism is almost never found in healthy people or in any other conditions except inflammatory bowel disease, where its significance is not yet known. The detection of pseudomembranes by sigmoidoscopy establishes the diagnosis. The laboratory technics that confirm the presence of C. difficile and its toxin are being incorporated into many laboratories around the country. Treatment of diagnosed PMC is relatively simple and usually completely effective. The offending antibiotic is stopped, a proper fluid and electrolyte balance maintained, and oral vancomycin begun, 125 to 500 mg four times a day. Cholestyramine can also be used as an adjunct to this regimen. Relapse can occur in patients treated with oral vancomycin, necessitating a repeat course of therapy.

Anti-Bacterial Agents↗
PubMed1985

Xanthomas and hyperlipidemias.

The ability to recognize diverse clinical forms of xanthomas, such as tuberous, planar, eruptive and tendinous, is important in the detection of underlying systemic disease. A variety of primary genetic disorders, as well as numerous secondary conditions such as diabetes, obstructive liver disease, thyroid disease, renal disease, and pancreatitis, can lead to hyperlipoproteinemia that results in the formation not only of xanthomas but also of life-threatening vascular atherosclerosis. An understanding of the pathogenesis of the underlying lipoprotein alterations provides a rational approach to therapy utilizing dietary manipulations and drugs. Such treatment is capable of correcting most disorders of lipid metabolism, and, if appropriate therapy is initiated at the first sign of xanthoma evolution, it may prevent progression of atherosclerosis, provide resolution of xanthomas, and in some instances prevent serious pancreatitis.

Apoproteins↗
PubMed1991

Heterogeneity of rat liver parenchyma in cholesterol 7 alpha-hydroxylase and bile acid synthesis.

Periportal and perivenous hepatocytes were isolated from rat liver by digitonin/collagenase perfusion for investigating the acinar distribution of bile acid synthesis. The specific activity of cholesterol 7 alpha-hydroxylase (EC 1.14.13.17) was 7.9-fold higher in perivenous cells than in periportal hepatocytes. Mass production of bile acids differed 4.4-fold between cultured perivenous and periportal hepatocytes. In contrast, the levels of free cholesterol in homogenates and microsomes derived from both subfractions were similar. Feeding of rats with the bile-acid-sequestering anion-exchange resin colestid resulted in a pronounced stimulation of cholesterol 7 alpha-hydroxylase activity and bile acid mass production, but decreased the perivenous/periportal ratio of both parameters. These results demonstrate that bile acid mass production, but decreased the perivenous hepatocytes, possibly owing to feedback suppression by bile acids from the enterohepatic circulation. Furthermore, the opposite acinar localization of cholesterol and bile acid biosynthesis provides an interesting alternative to current views of the regulation of their metabolic pathways.

Animals↗
PubMed2005

Liver X receptor alpha interferes with SREBP1c-mediated Abcd2 expression. Novel cross-talk in gene regulation.

The peroxisomal ATP binding cassette (ABC) transporter adrenoleukodystrophy-related protein, encoded by ABCD2, displays functional redundancy with the X-linked adrenoleukodystrophy-associated protein, making ABCD2 up-regulation of therapeutic value. Cholesterol lowering activates human ABCD2 in cultured cells. To investigate in vivo regulation by sterols, we first characterized a sterol regulatory element (SRE) in the murine Abcd2 promoter that is directly bound by SRE-binding proteins (SREBPs). Intriguingly, this element overlaps with a direct repeat 4, which serves as binding site for liver X receptor (LXR)/retinoid X receptor heterodimers, suggesting novel cross-talk between SREBP and LXR/retinoid X receptor in gene regulation. Using fasting-refeeding and cholesterol loading, SREBP accessibility to the SRE/direct repeat 4 was tested. Results suggest that adipose Abcd2 is induced by SREBP1c, whereas hepatic Abcd2 expression is down-regulated by concurrent activation of LXRalpha and SREBP1c. In cell culture, SREBP1c-mediated Abcd2 induction is counteracted by ligand-activated LXRalpha. Finally, hepatic Abcd2 expression in LXRalpha,beta-deficient mice is inducible to levels vastly exceeding wild type. Together, we identify LXRalpha as negative modulator of Abcd2, acting through a novel regulatory mechanism involving overlapping SREBP and LXRalpha binding sites.

ATP Binding Cassette Transporter, Subfamily D↗
PubMed1983

Gemfibrozil in combination with other drugs for severe hyperlipidemia. Preliminary study comprising four cases.

In this very early report, Dr Nash shares his insights into a newly developing approach to hyperlipidemia therapy. Four severely hyperlipidemic patients in whom maximum dietary therapy had proved ineffective showed a dramatic reduction in cholesterol and triglyceride levels when treated with multiple drugs, including gemfibrozil. These cases demonstrate that maximally effective polypharmacy can have striking results in selected patients. These provocative findings should encourage other investigators to verify or refute them.

Adult↗
PubMed1990

Elevated cholesterol levels. How to individualize treatment.

Each of the three case studies represents a common presentation of a patient with elevated lipid levels. By categorizing patients using the guidelines of the National Cholesterol Education Program and considering the high-density lipoprotein cholesterol level, clinicians can more reliably assess response to treatment. An elevated total cholesterol level is only one of several important risk factors for coronary artery disease that must be confronted.

Adult↗
PubMed1978

Comparison of five regimens for treatment of experimental clindamycin-associated colitis.

The hamster model of clindamycin-induced enterocolitis was studied to determine the natural course of the disease and the response to five therapeutic regimens. Tissue culture assays of stools from untreated animals showed that colitis toxin is present at low titers within 24--36 hr after challenge with clindamycin; titers of toxin in subsequent specimens of stool increased progressively until the animals died on days 2--4 after challenge. Therapeutic regimens tested in this model were initiated 24 hr after clindamycin challenge when the majority of the animals had evidence of colitis toxin. Methylprednisilone, an anion exchange resin, and gas gangrene polyvalent antitoxin had a minimal effect on toxin titers in stool and failed to delay substantially death due to enterocolitis. Vancomycin and tetracycline eliminated toxin in stools and delayed death. However, the salutary effects of these antibiotics were noted only during the course of their administration since all animals died of enterocolitis and had high titers of toxin when treatment was discontinued.

Animals↗