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PubMed2002

Leflunomide induced fevers, thrombocytosis, and leukocytosis in a patient with relapsing polychondritis.

The most common adverse events reported with the use of leflunomide are hypertension, infections, alopecia, and various gastrointestinal complaints. No fatal adverse hematologic events have been reported in humans, although anemia and leukopenia have been described in animals receiving 20 mg/kg/day. We describe a patient with relapsing polychondritis, in whom treatment failure with glucocorticoids, methotrexate, hydroxychloroquine, and azathioprine led to the institution of therapy with leflunomide at a maintenance dose of 20 mg/day. Two months after the dose of leflunomide had been increased to 30 mg daily, the patient developed high fevers, photophobia, thrombocytosis, and leukocytosis that returned to normal following treatment with cholestyramine and discontinuation of leflunomide. Rechallenge with leflunomide was not attempted and the syndrome did not recur during 14 month followup.

Anti-Inflammatory Agents↗
PubMed2002

LDL cholesterol lowering by bile acid malabsorption during inhibited synthesis and absorption of cholesterol in hypercholesterolemic coronary subjects.

BACKGROUND AND AIMS: Recent large-scale trials have consistently documented the fact that a 25-35% reduction in low-density lipoprotein cholesterol (LDL-C) can delay the progression of atherosclerosis. This raises the question as to how much it is possible to reduce serum cholesterol using feasible therapies. The aim of this study was to investigate the cholesterol-lowering efficacy of a triple therapy combining bile acid malabsorption with the inhibition of cholesterol synthesis and absorption. METHODS AND RESULTS: Eleven consecutive hypercholesterolemic coronary patients from Lipid Clinics on a low-fat, low-cholesterol baseline diet added simvastatin (20 mg/day) for three months, and then dietary plant stanol ester margarine (2.25 g of stanols/day) for eight weeks; finally, cholestyramine 8 g/day was added for another eight weeks. This was a before-after trial, in which the results of each period were compared with baseline and those of the previous period. Serum lipids were quantitated using commercial kits, and serum sterols by means of gas-liquid chromatography. Simvastatin lowered LDL-C by 39% (p < 0.001), and additional stanol ester margarine by a further 13% (p < 0.05). The triple treatment led to 67% reduction from baseline (p < 0.001), with all LDL-C values being < 2.6 mmol/L, and increased high-density lipoprotein cholesterol (HDL-C) by 15% (p < 0.01). It also increased the serum lathosterol/cholesterol ratio (p < 0.01), thus indicating an upregulation of cholesterol synthesis, and increased the serum sitosterol ratio (p < 0.01) despite the simultaneous consumption of plant stanols. CONCLUSIONS: The massive reduction in LDL and increase in HDL-C obtained using our triple therapy suggests that the combination of stanol ester with only moderate doses of statin and resin makes it possible to control LDL-C levels effectively in hypercholesterolemic subjects.

Aged↗
PubMed1992

[Familial hypercholesterolemia--intensive diet therapy combined with drug therapy].

The aim of the investigation was twofold: to study the effect of lovastatin, a potent inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, alone and in combination with other lipid lowering drugs in an open 48 week single centre study, and to study if lipid lowering drugs influence adherence to diet in adult patients with familial hypercholesterolemia. Lovastatin monotherapy (80 mg daily) for 12 weeks reduced serum cholesterol, LDL-cholesterol and triglycerides levels by 36%, 44% and 24% respectively. HDL-cholesterol level was increased by 12%. The addition of 16 g cholestyramine daily further increased the reduction of total cholesterol and LDL-cholesterol levels by 17% and 24% respectively. Addition of 1 g probucol daily decreased total cholesterol, LDL-cholesterol and HDL-cholesterol levels by 9%, 5% and 27% respectively. Addition of omega-3-fatty acids (3.6 g daily) reduced total cholesterol, LDL-cholesterol and triglycerides levels by 10%, 12% and 20% respectively. Administration of potent lipid lowering agents did not influence adherence to a diet with a mean daily fat energy of 21% (CI: 20-22), cholesterol of 177 mg (CI: 157-196) and P/S ratio of 0.75 (CI: 0.66-0.84). A significant increase in liver enzymes was recorded in only one patient. One patient was withdrawn from the study because of myositis.

Adolescent↗
PubMed1992

High protein diet complements resin therapy of familial hypercholesterolemia.

The intermediate-term effects on plasma lipoprotein lipids of substituting meat and dairy protein for carbohydrate in the diets of five subjects (three women, two men) with familial hypercholesterolemia receiving cholestyramine (mean dose, 18 g/d) were studied. Subjects were randomly allocated to either the high or low protein diets (mean 27 versus 10% of energy as protein, 25% as fat, and 48 versus 65% as carbohydrate) for 4 to 5 weeks and then switched to the other diet for another 4 to 5 weeks. Mean fasting plasma HDL cholesterol rose significantly by 17 +/- 3% (1.11 +/- 0.12 vs 0.95 +/- 0.11 mmol/L, p less than 0.005, n = 5), whereas total triglycerides fell by 23 +/- 2% (1.7 +/- 0.3 vs 2.2 +/- 0.3 mmol/L, p less than 0.005, n = 5), VLDL triglycerides fell by 28 +/- 5% (0.88 +/- 0.15 vs 1.18 +/- 0.19 mmol/L, p less than 0.02, n = 5), VLDL cholesterol fell by 32 +/- 7% (0.39 +/- 0.08 vs 0.56 +/- 0.09 mmol/L, p less than 0.01, n = 5), the ratio of LDL cholesterol: HDL cholesterol by 19 +/- 5% (4.7 +/- 0.7 vs 5.7 +/- 0.7, p less than 0.05) and that of total cholesterol: HDL cholesterol by 16 +/- 5% (6.6 +/- 0.5 vs 8.0 +/- 0.7, p less than 0.05) on the high versus low protein diet. Increasing dietary protein intake at the expense of carbohydrate may be useful in treating hypoalphalipoproteinemia and/or hypertriglyceridemia in patients with familial hypercholesterolemia.

Adult↗
PubMedDate not supplied

[Managing methotrexate toxicity: a case report].

High-dose methotrexate is included in chemotherapy regimens used to treat a number of malignant neoplasms. Methotrexate plasma concentration is considered the best toxicity predictor. Monitoring methotrexate plasma concentrations is standard practice in the identification of at-risk patients, the titration of folinic acid doses, and the establishment of corrective measures. Methotrexate is a kidney-cleared weak acid, and renal function impairment may retard methotrexate clearance. A case of severe methotrexate-induced toxicity secondary to renal failure is reported in a patient with non-Hodgkin s lymphoma receiving methotrexate at a dose of 1 g/m2. Corrective measures included folinic acid rescue therapy, cholestyramine resin administration, hydration and urine alkalinization, urine pH monitoring, and extracorporeal clearance techniques.

Acute Kidney Injury↗
PubMed2005

Microscopic colitis: a report of two cases.

Microscopic colitis is characterized by chronic, watery, secretory diarrhea, with a normal or near-normal gross appearance of the colonic mucosa. Biopsy is diagnostic and usually reveals either lymphocytic colitis or collagenous colitis. The symptoms of collagenous colitis appear most commonly in the sixth decade. With collagenous colitis, the major microscopic characteristic is a thickened collagen layer beneath the colonic mucosa, and with lymphocytic colitis, an increase number of intraepithelial lymphocytes. Clinically, collagenous colitis is characterized by long-standing diarrhea. In patients with lymphocytic colitis, the duration of diarrhea is usually shorter and female predominance is less apparent. We report two cases of lymphocytic colitis in elderly women. Both presented with watery diarrhea of two month duration and weight loss. Extensive investigations were done and several medications failed to stop their diarrhea. Biopsy revealed lymphocytic colitis. Their diarrhea responded well to cholestyramine.

Aged↗
PubMed2005

Leflunomide induced acute interstitial pneumonia.

We describe a 54-year-old woman with rheumatoid arthritis (RA), who developed acute respiratory failure 2 weeks after cessation of 6-week treatment with leflunomide. We diagnosed interstitial pneumonia, probably induced by leflunomide because acute respiratory failure was preceded by elevated serum liver enzyme concentration and hypertension. She showed dramatic improvement with prednisolone and cholestyramine. Prompt treatment may improve the prognosis. In Japan, leflunomide has been implicated as a possible cause to initiate or exacerbate interstitial pneumonia in patients with RA according to postmarketing surveillance. Clinicians should exclude pulmonary disease prior to initiating leflunomide treatment in patients with RA on the basis of a thorough history and physical examination, and chest radiograph.

Adjuvants, Immunologic↗
PubMed1975

3-hydroxy-3-methylglutaryl coenzyme A reductase activity in human hair roots.

The activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase (1.1.1.34) was measured in isolated human hair roots. In growing scalp hair roots, the amount of enzyme activity per cell was surprisingly high and was of the same order of magnitude as has been reported for human liver cells and for human fibroblasts cultured in the absence of low density lipoproteins. Hair root enzyme activity showed no diurnal variation, was unaffected by cholestyramine feeding, and was similar in 14 normal subjects, one patient with abetalipoproteinemia, and one homozygote and three heterozygotes with familial hypercholesterolemia. The activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase in human hair roots appears to be unrelated to the level of low density lipoproteins in the plasma.

Abetalipoproteinemia↗
PubMed1991

Therapeutic strategy for the irritable bowel syndrome.

The major aims of medical therapy in irritable bowel syndrome (IBS) are: a) to ameliorate symptoms (pain, bowel movement abnormalities, bloating) and b) to improve psychological problems of the patients. The first step of IBS therapy is the diet. In fact some forms of IBS can be ascribed to food intolerance. When abdominal pain, meteorism and constipation are the main symptoms, treatment with high-fiber diet, antispastic and antimuscarinic drugs is indicated. Sometimes amitriptyline, an antidepressant which also shows anticholinergic and analgesic properties, can be helpful. When diarrhoea is prevalent, the most effective drug is represented by loperamide. If diarrhoea is related to meal ingestion, antispastic or antimuscarinic drugs can be successfully used. In the case of diarrhoea related to documented cholorrhoea, cholestyramine can be of benefit. Furthermore, there are some resistant cases, secondary to striking psychological problems that require sedatives and antidepressant drugs and sometimes, psycho and/or hypnotherapy.

Amitriptyline↗
PubMed1977

Binding properties in vitro of antacids for conjugated bile acids.

The binding properties of various commercial antacids for pure conjugated bile acids in an aqueous solution or the bile acids present in human gallbladder bile were characterized. Aluminum hydroxide was a potent binding agent, similar in affinity and capacity to cholestyramine. With aluminum hydroxide, dihydroxy bile acid conjugates were bound more strongly than trihydroxy bile acid conjugates, and glycine conjugates were bound more strongly than taurine conjugates; pH had no effect per se on binding. Magnesium hydroxide and aluminum phosphate bound bile acids much more weakly. Aluminum hydroxide warrants exploration in therapeutic situations in which bile acid binding is sought.

Aluminum↗
PubMed1991

[Treatment of hypercholesterolemic patients of different age with simvastatin: 1-year study].

Nowadays there is no direct evidence that lowering cholesterol may reduce the CHD in the elderly; however, several evidences suggest the potential benefit of a dietetic and/or pharmacologic intervention in healthy young-old hypercholesterolemics. In this study we evaluated the efficacy and tolerability of simvastatin, alone or in combination with cholestyramine, in two groups of patients (group A: age 30-55 years and group B: age 60-75 years) with primary hypercholesterolemia, over a 48-week period. In both groups Simvastatin induced a significant reduction in total and LDL cholesterol (p less than 0.001 both), with a decrease of the total/HDL cholesterol ratio (p less than 0.001). A reduction of the apo-B100 levels was also observed (respectively p less than 0.01 and p less than 0.001) with a significant improvement of the apo-B100/apo-A1 ratio (p less than 0.01). Simvastatin was well tolerated and free of remarkable side effects in both groups.

Adult↗
PubMed1990

Therapeutic priorities of Canadian internists.

We surveyed 175 members of the Canadian Society of Internal Medicine to determine how they would rank seven commonly used treatments as to their clinical usefulness. A total of 70% of the respondents judged that the treatment of severe hypertension was the most beneficial. Coronary artery bypass surgery and treatment with acetylsalicylic acid for transient ischemic attacks were ranked next most useful. Cholestyramine therapy for hypercholesterolemia, the treatment of mild hypertension, isoniazid therapy for inactive tuberculosis and carotid endarterectomy in patients with mild stroke formed the final cluster. Except for treatment of severe hypertension there was a wide variation in the physicians' enthusiasm for the various treatments. Possible explanations for this variation include physicians' lack of awareness of the results of clinical trials, the wide range of risk reductions found in various trials of the same therapy, an unwillingness by physicians to generalize from clinical trials to individual patients, individual physicians' placement of different values on the morbidity associated with various diseases, and the fact that physicians may rarely explicitly compare the usefulness of therapies. In general, the number of patients needed to be treated to save one life better reflected the physicians' judgements than did the relative risk reduction.

Attitude of Health Personnel↗
PubMed1990

Cloning and regulation of cholesterol 7 alpha-hydroxylase, the rate-limiting enzyme in bile acid biosynthesis.

The rate-limiting step in bile acid biosynthesis is catalyzed by the microsomal cytochrome P-450 cholesterol 7 alpha-hydroxylase (7 alpha-hydroxylase). The expression of this enzyme is subject to feedback regulation by sterols and is thought to be coordinately regulated with enzymes in the cholesterol supply pathways, including the low density lipoprotein receptor and 3-hydroxy-3-methylglutaryl-coenzyme A reductase and synthase. Here we report the purification of rat 7 alpha-hydroxylase and the determination of a partial amino acid sequence. Oligonucleotides derived from peptide sequence were used to clone a full-length cDNA encoding 7 alpha-hydroxylase. DNA sequence analysis of the cDNA revealed a 7 alpha-hydroxylase protein of 503 amino acids with a predicted molecular weight of 56,890 which represents a novel family of cytochrome P-450 enzymes. Transfection of a 7 alpha-hydroxylase cDNA into simian COS cells resulted in the synthesis of a functional enzyme whose activity was stimulated in vitro by the addition of rat microsomal cytochrome P-450 reductase protein. RNA blot hybridization experiments indicated that the mRNA for 7 alpha-hydroxylase is found only in the liver. The levels of this mRNA increased when bile acids were depleted by dietary cholestyramine and decreased when bile acids were consumed. Dietary cholesterol led to an increase in 7 alpha-hydroxylase mRNA levels. The enzymatic activity of 7 alpha-hydroxylase paralleled the observed changes in mRNA levels. These results suggest that bile acids and sterols are able to alter the transcription of the 7 alpha-hydroxylase gene and that this control explains the previously observed feedback regulation of bile acid synthesis.

Amino Acid Sequence↗
PubMed1990

Evidence for substrate channeling in the early steps of cholesterogenesis.

We have directly tested the ability of acetoacetate, upon activation to the CoA thioester, to channel into the cholesterogenic pathway prior to scrambling of its carbon skeleton with the acetate pool. The approach relies upon trapping [3-13C]acetoacetate-derived hydroxymethylglutaryl-CoA, hydrolyzing this metabolite, and esterifying the resulting hydroxymethylglutaric acid to allow gas chromatography/mass spectrometry analysis of the dimethyl esters for the 13C enrichment and labeling pattern. 99% enriched [3-13C] and [1,3,5-13C]hydroxymethylglutaric acid samples were synthesized, providing standards against which physiological samples could be compared. Cytosolic extracts from brain and liver of cholestyramine-fed rats were incubated with [3-13C]acetoacetate (2 mM) or with [1-13C]acetate (5 mM). In contrast to [13C]acetate-derived hydroxymethylglutarate, which shows the expected triple labeling pattern, [13C]acetoacetate-derived hydroxymethylglutarate from both liver and brain extracts is predominantly monolabeled. These data suggest that, after acetoacetate is activated to the CoA thioester, cytosolic hydroxymethylglutaryl-CoA synthase effectively commits much of this acetoacetyl-CoA to cholesterogenesis before thiolase can scramble the carbon skeleton of the acetoacetyl moiety into the acetate pool. This chemical approach represents an alternative method for testing the channeling of metabolites through sequential steps in a metabolic pathway. Such a method may be useful when physical or kinetic techniques prove to be unsuitable.

Acetates↗
PubMedDate not supplied

Treatment of heterozygous familial hypercholesterolemia with lipid-lowering drugs.

Patients with heterozygous familial hypercholesterolemia (FH) constitute a unique population at high risk for the premature development of coronary artery disease (CAD) and in whom long-term hypocholesterolemic therapy to reduce elevated levels of low density lipoprotein (LDL) cholesterol is most clearly indicated. Optimal therapy invariably requires diet regulation plus hypolipidemic drug therapy. When used as single agents, the bile-acid sequestrants, cholestyramine and colestipol, lower LDL cholesterol concentrations by 20% to 35% in compliant patients, whereas decreases of 20% to 30% can be achieved with nicotinic acid in doses of 3 to 6 g/day. Bezafibrate, fenofibrate, and ciprofibrate have also been shown to lower LDL cholesterol levels by 20% to 30%, and these drugs are more effective than gemfibrozil and clofibrate. Probucol, neomycin, and D-thyroxine reduce LDL cholesterol concentrations by 10% to 15% in single-drug use. Clinical trials with a new class of drugs that inhibit the rate-limiting enzyme in cholesterol biosynthesis, 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, and that includes lovastatin, simvastatin, and pravastatin indicate that these drugs lower LDL cholesterol concentrations by 30% to 50% in patients with heterozygous FH. Combined drug therapy with a bile-acid sequestrant and nicotinic acid lowers LDL cholesterol by 40% to 55%, whereas fenofibrate, bezafibrate, or probucol plus a bile-acid sequestrant results in reductions varying from 25% to 50%. The combinations of an HMG CoA reductase inhibitor with either a bile-acid sequestrant or nicotinic acid appears to be the most promising, and these regimens reduce LDL cholesterol levels by 45% to 60%. With appropriate use, the currently available hypocholesterolemic drugs have the potential to markedly change the natural history of premature atherosclerosis that occurs in untreated patients with FH.

Butyrates↗
PubMed1989

Amiodarone overdose and its management.

A patient taking an overdose of 3.4 g of amiodarone is described. Consciousness and physical examination remained normal throughout. Continuous electrocardiographic monitoring for 48 hours after admission revealed only a self-limiting episode of ventricular tachycardia, despite high serum levels of the drug (serum desethylamiodarone levels 4.4 mg/l). The pharmacokinetic properties of amiodarone and treatment strategies for the overdose situation are discussed. It is suggested that there may be a role for the use of cholestyramine in the treatment of both acute and chronic amiodarone toxicity.

Acute Disease↗
PubMed1989

Receptor-mediated uptake of low density lipoprotein stimulates bile acid synthesis by cultured rat hepatocytes.

The cellular mechanisms responsible for the lipoprotein-mediated stimulation of bile acid synthesis in cultured rat hepatocytes were investigated. Adding 280 micrograms/ml of cholesterol in the form of human or rat low density lipoprotein (LDL) to the culture medium increased bile acid synthesis by 1.8- and 1.6-fold, respectively. As a result of the uptake of LDL, the synthesis of [14C]cholesterol from [2-14C]acetate was decreased and cellular cholesteryl ester mass was increased. Further studies demonstrated that rat apoE-free LDL and apoE-rich high density lipoprotein (HDL) both stimulated bile acid synthesis 1.5-fold, as well as inhibited the formation of [14C]cholesterol from [2-14C]acetate. Reductive methylation of LDL blocked the inhibition of cholesterol synthesis, as well as the stimulation of bile acid synthesis, suggesting that these processes require receptor-mediated uptake. To identify the receptors responsible, competitive binding studies using 125I-labeled apoE-free LDL and 125I-labeled apoE-rich HDL were performed. Both apoE-free LDL and apoE-rich HDL displayed an equal ability to compete for binding of the other, suggesting that a receptor or a group of receptors that recognizes both apolipoproteins is involved. Additional studies show that hepatocytes from cholestyramine-treated rats displayed 2.2- and 3.4-fold increases in the binding of apoE-free LDL and apoE-rich HDL, respectively. These data show for the first time that receptor-mediated uptake of LDL by the liver is intimately linked to processes activating bile acid synthesis.

Animals↗