Drugs online research references
J Lab Clin Med. 1987 Sep;110(3):279-86.
Effects of gemfibrozil on plasma lipoprotein-apolipoprotein distribution and platelet reactivity in patients with hypertriglyceridemia.
Sirtori CR, Franceschini G, Gianfranceschi G, Sirtori M, Montanari G, Tremoli E, Maderna P, Colli S, Zoppi F.
The effects of gemfibrozil on plasma lipoprotein distribution and composition and on platelet function were investigated in 11 patients with stable hypertriglyceridemia, six belonging to Fredrickson type IIb and five to type IV. Gemfibrozil (600 mg twice a day) significantly reduced total and very low density lipoprotein (VLDL)--associated triglyceridemia (respectively-32.4% and -40.4%, after 6 weeks of treatment). No significant variations were noted in the lipid components of low-density lipoproteins; by contrast, a marked increase (18%) was detected in high-density lipoprotein (HDL)--associated cholesterol. Comparison of the two patient groups (type IIb and type IV) showed that those with type IIb had both a more significant reduction of triglyceridemia and a more marked increase of HDL-cholesterol. Apolipoprotein B levels were reduced in both groups (-12%) with no change in apolipoprotein AI. The cholesterol content in the HDL subfractions, separated by rate zonal ultracentrifugation, was raised in HDL3 (18%) and in HDL2 (14%). Both particles also showed significant increases of the cholesterol/protein and the cholesterol/phospholipid ratios. A non-statistically significant decrease in collagen-induced aggregation and in the release of thromboxane B2 was noted after treatment. These findings suggest that, similar to what was recently reported in normal individuals and in laboratory animals, the probable mode of action of gemfibrozil is in reducing the secretion of atherogenic lipoproteins, particularly VLDL, while stimulating the production of small HDL particles.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3475394&dopt=Abstract
le.ac.uk
A histological method utilizing the optical dissector principle has been developed for determining the contribution of hypertrophy and hyperplasia to the hepatomegaly induced by the peroxisome proliferator gemfibrozil. The optical dissector is a technique derived from the 'new stereology' and has been used to estimate the number of hepatocyte nuclear profiles, that are present in a reference volume of tissue. The overall changes due to hypertrophy and hyperplasia in the rat liver after gemfibrozil treatment, did not reach significance, although the zonal hypertrophy change did. This indicated that although there was a 20% increase in liver weight with treatment, the hepatomegaly was caused by a combination of hypertrophy and hyperplasia, neither of which, on its own, was significantly different from the control values. The distinction of hyperplasia from hypertrophy, using a purely histological method, will be useful in assessing whether treatment related sustained hyperplasia is occurring in the liver.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10022288&dopt=Abstract
Int J Dermatol. 1999 Jan;38(1):65-9.
Effects of gemfibrozil on in vitro cultured normal human skin explants.
Wolf R, Lo Schiavo A, Russo A, de Angelis F, Ruocco V.
Macabbi Health Care Outpatient Clinic and the Sackler Faculty of Medicine, Tel-Aviv University, Israel.
BACKGROUND: Several lipid-lowering agents, when given topically, show a profound effect on skin morphology. Because of low bioavailability of these drugs for keratinocytes, the incidence is extremely low clinically. The most appropriate way to study the effect of hypolipidemic drugs on keratinocytes is by artificial exposure of the skin to high drug concentrations. OBJECTIVE: To study the effects of gemfibrozil on the morphology of in vitro cultured normal human skin explants. As gemfibrozil induces barrier disruption by inhibiting epidermal sterologenesis, essential for a competent permeability barrier, it is interesting to investigate the morphologic changes associated with this phenomenon. Studying the epidermal changes induced by lipid-lowering agents is important, not only because it might lead to a better understanding of the effects of these drugs on keratinocytes, but as it might also unlock the door to a wider knowledge of the pathomechanism of disorders of cornification. METHODS: Normal human skin from patients undergoing mastectomy was cultured in the presence of 2, 5, and 10 mM of gemfibrozil for 4 days The morphologic changes were evaluated by three blinded observers. Their reports were matched and collated. RESULTS: The cultured skin in the presence of gemfibrozil showed cell crowding of keratinocytes in the lower part of the epidermis, indicating epidermal hyperplasia and increased proliferation. Intercellular edema with the formation of small cavities in the epidermis, intracellular edema, and vacuolar alteration of keratinocytes in the upper portion of the epidermis were also observed. The intensity of these changes tended to parallel the gemfibrozil concentration. Some dermo-epidermal detachments did not correlate with the gemfibrozil concentration, but rather with tissue characteristics peculiar to each explant. CONCLUSIONS: The morphologic changes caused by gemfibrozil to normal human skin were not characteristic of psoriasis, and included intracellular and intercellular edema in the upper portion of the epidermis and cell crowding, indicating epidermal hyperplasia in the lower portion of the epidermis. The present experimental study gives further support to the hypothesis that hypolipidemic drugs cause an initial break in the barrier function of the epidermis, followed by a physiologic epidermal response, aimed at barrier restoration. This rather nonspecific stimulus to epidermal proliferation may trigger psoriasis in predisposed patients.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10065615&dopt=Abstract
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