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OBJECTIVE -- To evaluate the within-trial effect of losartan and conventional antihypertensive therapy (CT) compared with placebo and CT on the economic cost associated with end-stage renal disease (ESRD). RESEARCH [...]

* Objective: To compare the low-density lipoprotein (LDL) cholesterol-lowering efficacy of low-dose combinations of cholestyramine and fluvastatin. * Design: Randomized, double-blind, parallel group, placebo-controlled trial with a 24-week double-blind treatment period divided into three phases. * Setting: Office-based clinics. * Patients: Hypercholesterolemic, with LDL cholesterol of 4.14 mmol/L or greater (greater than or equal to160 mg/dL) and plasma triglycerides of 3.39 mmol/L or less ([less than or equal to]300 mg/dL). Four hundred sixty patients were screened; 224 patients were randomized into a double-blind treatment period; 203 completed the study; 6 dropped out because of adverse events. * Intervention: Patients were treated with 10 mg or 20 mg of fluvastatin alone, 8 g or 16 g of cholestyramine alone, or combinations of these fluvastatin and cholestyramine dosages (six treatment groups). * Measurements: Changes in lipid variables, particularly LDL cholesterol. * Results: The 10-mg and 20-mg fluvastatin monotherapy groups showed considerable reductions in LDL cholesterol initially -20.1% [SD, 8.8%] and -20.2% [SD, 10.1%],respectively);these reductions were maintained. Reductions in LDL cholesterol that resulted from the addition of cholestyramine, 8 g/d, to 10 mg of fluvastatin and 20 mg of fluvastatin were greater than those observed with monotherapy (10-mg fluvastatin - [10-mg fluvastatin plus cholestyramine], 9.1%; 95% Cl, 3.8% to 14.4%) and 20-mg fluvastatin - [20-mg fluvastatin plus cholestyramine], 11.6%; Cl, 6.5% to 16.8%). The increase in cholestyramine dose to 16 g/d in the three combination groups provided only a modest additional response. * Conclusions: Low-density lipoprotein cholesterol reductions of about 25% to 30% can be achieved with low-dose combination therapy with fluvastatin and cholestyramine. The addition of low-dose resin appears to produce greater overall cholesterol reduction than does a simple doubling of the fluvastatin dosage. The low-dose combination treatment was highly successful in achieving the goals of the National Cholesterol Education Program guidelines., Low doses of fluvastatin used in combination with cholestyramine appear to effectively reduce low-density lipoprotein (LDL) cholesterol levels. The effects of various doses of fluvastatin or cholestyramine used alone or in combination were measured in a group of 203 people with elevated LDL cholesterol levels. Groups receiving either 10 milligrams (mg) or 20 mg of fluvastatin showed similarly lower cholesterol readings after 4 weeks of treatment. Each of these groups was then given an 8 gram daily dose of cholestyramine along with their 10 mg or 20 mg dose of fluvastatin. LDL cholesterol levels dropped even further. LDL cholesterol levels dropped by 25.2% in those taking 10 mg fluvastatin with 8 grams of cholestyramine compared with a 6.2% drop in LDL levels in those taking 20 mg fluvastatin only. This suggests the lower dose of fluvastatin, used in combination with cholestyramine is sufficient. Lower doses also decrease the risks of side effects.

Abstract An otherwise healthy 29-year-old woman presented with a complaint of odynophagia of several months' duration. On examination, she was found to have a broadly based, yellow, exophytic lesion on [...]

Angiotensin-converting enzyme (ACE) inhibitors may reduce the risk of kidney failure in patients suffering from diabetes. ACE inhibitors are a group of drugs used to treat hypertension. A survey of the medical literature found that treatment with ACE inhibitors reduces the level of protein in the urine of diabetes patients. This reduction occurred regardless of the effect of the ACE inhibitor on blood pressure, the type of diabetes or the stage of kidney disease. Treatment with ACE inhibitors also preserved normal kidney function regardless of their effect on blood pressure. Other antihypertensive drugs reduced the levels of protein in the urine in diabetes patients, but this change was dependent on reductions in blood pressure. Other antihypertensive drugs also impaired kidney function. Hypertension is a condition that can lead to the development of kidney failure in diabetes patients suffering from kidney disease.

* Background.--In recent years, several authors have noted that oral calcium treatment was associated with a reduction in serum cholesterol level. Methods.--Calcium carbonate was examined for its ability to lower serum cholesterol levels in hypercholesterolemic patients. Fifty-six patients with mild to moderate hypercholesterolemia were examined in this randomized, double-blind, placebo-controlled crossover study. Patients were treated with a low-fat, low-cholesterol diet targeted at the American Heart Association Step-1 diet for 8 weeks before and while receiving placebo or calcium carbonate (9.98 mmol [400 mg] of elemental calcium) three times daily with meals for 6 weeks. Patients were then crossed over to the alternate treatment for an additional 6-week period. Results.--Compared with placebo, calcium carbonate achieved a 4.4% reduction in the low-density lipoprotein cholesterol level, and a 4.1% increase in the high-density lipoprotein cholesterol level. The ratio of low-density lipoprotein cholesterol to high-density lipoprotein cholesterol significantly decreased by 6.5% with calcium carbonate treatment. Calcium carbonate treatment did not significantly affect blood pressure or serum levels of triglycerides, lipoprotein Apo B, or calcium. Relative urinary saturation ratios of calcium oxalate levels were unchanged during calcium carbonate therapy. Compliance with diet and treatment was excellent and no significant adverse effects were noted. Conclusions.--Thus, calcium carbonate was a modestly effective and well-tolerated adjunct to diet in the management of mild to moderate hypercholesterolemia in this clinical study. (Arch Intern Med. 1992;152:2441-2444)

Renal pathology and dyslipidemia commonly coexist. Treatments that lower albuminuria/ proteinuria may lower lipids, but it is not known whether lipid lowering independent of lessening albuminuria/proteinuria slows progression of kidney [...]

Nephron loss is a common progression of a diverse range of kidney diseases. Recent experimental models of chronic renal disease have suggested that hemodynamic and nonhemodynamic mechanisms play key roles in progressive renal injury. Extensive renal ablation in the rat was followed by development of altered glomerular hemodynamics. Albuminuria and histologic damage leading to focal glomerulosclerosis were preceded by the development of increased glomerular pressures and were prevented by interventions such as severe dietary protein restriction and angiotensin-converting enzyme (ACE) inhibitor therapy. Both experimental interventions ameliorated glomerular hypertension. It was therefore concluded that these interventions ameliorated injury by glomerular hemodynamic effect. Similar findings were obtained in a rat model of type I diabetes mellitus induced by streptozotocin in which glomerular hemodynamic factors appeared important to the development of progressive renal disease. Recent studies have suggested that nonhemodynamic factors have important roles in the progression of glomerular injury. For example, although the predominant effects of ACE inhibitor therapy appear to be hemodynamically mediated, data are emerging which suggest that these agents may also influence growth/proliferation of glomerular cells. Because hyperplasia/hypertrophy may influence glomerular susceptibility to injury, this may also be a potential mechanism whereby ACE inhibitor therapy influences glomerular damage. In addition, a variety of studies have suggested that hyperlipidemia, which is a frequent accompaniment of glomerular disease, is an important modulator of glomerular injury independent of glomerular hemodynamic effects. Coagulation factors, calcium phosphorus balance, as well as the genetic susceptibility of the glomerulus to injury, all appear to contribute to progressive nephron destruction. (Am J Cardiol 1990;6S:49 I-53 I), Various kidney diseases are associated with the loss of nephrons, the structural and functional units of the kidney consisting of the glomerulus, the filtering unit and attached tubule. Various mechanisms both related and unrelated to circulation contribute to the progression of kidney disease. Extensive destruction of the kidney in the experimental rat model is followed by the development of changes in the circulation of the glomerulus, which consists of small blood vessels called capillaries that filter blood through the kidney. Increased pressure within the glomeruli is followed by albuminuria (blood proteins in the urine), and structural damage leading to glomerulosclerosis, the thickening of the glomerulus. These disorders are prevented by restricting protein in the diet and use of angiotensin-converting enzyme (ACE) inhibitors, which prevent the formation of angiotensin, a factor that constricts blood vessels. Both dietary protein restriction and ACE inhibitors improve glomerular hypertension (high blood pressure) and injury through effects on circulation within the glomerular capillaries. In the rat model of type I diabetes mellitus, glomerular circulatory factors were also important in the progression of kidney disease. Other factors which contribute to glomerular damage include abnormal growth of glomerular cells, hyperlipidemia (increased lipids, factors that can clot the blood), the balance between calcium and phosphorus, and genetic predisposition. (Consumer Summary produced by Reliance Medical Information, Inc.)

Screening takes on new meaning when percentage of kidney function, not creatinine clearance, is used for assessment. Treatment is boosted by new data supporting the efficacy of angiotensin receptor blockers, [...]

Abstract We conducted a study to investigate whether taste buds are present on the human adult uvula. Our impetus was to determine whether surgical procedures that involve removal of the [...]

Angiotensin converting enzyme (ACE) inhibitors prevent the formation of the natural factor angiotensin II, which constricts blood vessels. These ACE inhibitors are used to treat high blood pressure (hypertension). The rationale for using ACE inhibitors to treat kidney disease, and the effects of these agents in patients with hypertension and impaired kidney function were assessed. A review of the literature showed that ACE inhibitors decrease damage to the glomeruli, the units of small blood vessels that filter blood through the kidney, by reducing elevated pressures within the glomeruli and blood vessels throughout the body. ACE inhibitors have also been shown to reduce systemic blood pressure without affecting glomerular blood flow or filtration rate in hypertensive patients with kidney disease. These antihypertensive drugs improve proteinuria (the abnormal presence of blood proteins in the urine), but their effects on the progression of kidney disease unrelated to diabetes are not known. Because ACE inhibitors have not yet been approved by the Food and Drug Administration for treatment of kidney disease, their use is considered to be innovative. Review of the data shows that ACE inhibitors may reduce kidney function, particularly in patients with impaired function of both kidneys or heart disease, and may be associated with hyperkalemia (high blood potassium) in patients with diabetes or severely impaired kidney function. Thus, although ACE inhibitors reduce proteinuria in patients with kidney disease, their effects on the progression of kidney disease are still unknown. (Consumer Summary produced by Reliance Medical Information, Inc.)

Wegener's granulomatosis is a disease of unknown cause that is characterized by areas of necrosis, localized tissue death, and associated pathology of the blood vessels of the affected organs. The disease often affects lungs and kidneys. Treatment with immune blood must be started as soon as possible, and thus definitive diagnostic tests that can rapidly identify this disease are extremely important. The current study reports on a new laboratory diagnostic method that successfully identified 42 of 45 patients with active Wegener's granulomatosis, a sensitivity of 93 percent. The test was also found to be highly specific in that only two of 58 patients with a disease process similar to Wegener's tested positive, for a specificity of 97 percent. Patients with Wegener's have been found to have anticytoplasmic antibodies directed against their own white blood cells; the test makes use of this finding. The test uses blood obtained from patients suspected of having Wegener's granulomatosis and applies it to white blood cells obtained from normal donors. If the patient's blood contains the anticytoplasmic antibodies, it combines with the test cells and can be visualized by the addition of florescent dyes. Although the role of anticytoplasmic antibodies in the development of Wegener's granulomatosis remains unknown, detection of these factors can be of considerable diagnostic importance.

Rupture of the extracranial carotid arteries or their major branches is known as carotid blowout syndrome (CBS). CBS is a well-recognized complication of cancer of the head and neck.... Brian [...]

Rhabdomyosarcoma of the larynx is extremely rare in adults, as only 17 well-documented cases have been previously reported in the English-language literature. Of these, only 2 cases (both male) involved [...]

We sought to determine the prevalence and patterns of complementary and alternative medicine (CAM) use among head and neck cancer patients who were being treated at an academic otolaryngology practice [...]