Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Colestipol hydrochloride is an insoluble, nonabsorbable copolymer with bile-acid-binding capacity. It prevents reabsorption of cholates from the intestinal tract into the enterohepatic circulation causing a net loss of bile acids, and therefore of cholesterol. Sixty subjects with cholesterol levels over 250 mg/100 ml were studied for 104 weeks. Patients with normal phenotypes, types 2,3, and 4, were given 5 gm three times daily and experienced an average drop of 40 mg/100 ml (14%). While patients with types 2,3, and 4 hyperlipidemia responded effectively, cholesterol levels in type 2 patients dropped earliest and most consistently with an average decrease of 58 mg/100 ml (19%). A comparable group of patients with hyperlipidemia taking placebo showed on average no change in serum cholesterol. Serum triglyceride values were not altered significantly. The resin is not absorbed from the gastrointestinal tract and produces a slight increase in fecal volume. Results of chemistries, enzyme assays, prothrombin times, hematology, and urinalysis and body weights wer unaltered. There was no evidence of lithogenic bile production. Colestipol is a tasteless and ordorless copolymer with high acceptability. Side effects were limited to occasional bloating, gas, and constipation. The drug is a safe, effective, palatable hypolipedmic agent.
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PMID:Colestipol hydrochloride, a new hypolipidemic drug: a two-year study. 109 Oct 1

Scanning and transmission electron microscopic examinations of the coronary vessels were performed on rats, and the findings compared. Both procedures demonstrated a tightly meshed network of arterial endothelium orientated to the direction of flow, thereby allowing optimal adaptation to changes in direction of blood flow, high intervascular pressure, structures of the remaining intima components and variable states of arterial wall tension. Venous endothelium proved to possess a markedly less uniform constitution, the texture of the inner surfaces being strongly determined by the surrounding perivascular tissue. Induction of arterial hypertension in rats (via GOLDBLATT-hypertension) and in Cynomolgus monkeys (via aortic constriction), and hyperlipidemia in hypertensive rats through a fatty diet enabled the study of a wide spectrum of coronary artery endothelium disease, primarily at early stages. Both species demonstrated hypertensive endothelial dehiscence (gaps), basically passive in nature and due to increased endothelial mobility. Occasionally, peculiar cytoplasma deformations could be found surrounded by circumscribed, consecutive endothelial gaps, allowing speculation of increased contraction-like states of intraendothelial filament tension due to hypertension. Areas of intima damage were usually focal and demonstrated numerous degenerative endothelial changes, endothelium necrosis and defects. Small endothelial gaps were covered by a film of thombocytes, though this finding was seen only in monkeys. Attempts at endothelium regeneration and reparation were manifest in increased endothelial mitosis, pseudoendotheliums, endothelial giant cells and films of leucocyte aggregations covering endothelium defects. Migration of leucocytes into the intima was actively furthered through small leaks in the endothelium. Hyperlipidemic and hypertensive rats showed endothelial bloating, due in part to vacuolar intracytoplasmatic lipid deposits with phagocytosis of fine particles of cholesterin crystals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Scanning and transmission electron microscopy findings in the coronary vessels in physiologic and pathologic states]. 409 May 89

Recent cohort and case control studies of low-dose combined oral contraceptives (COCs) containing the new generation of progestogens have allowed classification of adverse effects into those which are rare but serious and should be considered risks and those which are more frequent but are less of a threat to health. Low-dose COCs continue to affect coagulation in a complex way, but the risk is less than with the older preparations, and it can be minimized by screening women for a personal or familial history of early or unusual thrombosis and for levels of protein C, S, and antithrombin III. Women with true migraine with focal signs should also avoid using COCs. The relative risk of myocardial infarction (MI) may increase from 4:1 in women with one risk factor (age, smoking, hypertension, hyperlipidemia, and diabetes) to 20:1 with two risk factors and 128:1 with three or more risk factors. In the absence of all risk factors, a recent study indicated that the relative risk of MI with COC use was 1.9 for current and past use. COC use also causes a slight increase in hypertension in most women, especially those who are older or have a family history of hypertension. While the COC can affect carbohydrate and lipid metabolism, the new generation of progestogens has reduced these effects. The COC may accelerate presentation of gallbladder disease in predisposed women. The COC protects against benign breast disease but may increase the risk of breast cancer and cervical cancer slightly. There is a strong link between hepatocellular adenoma and COC use, but the incidence is low. Return to fertility after use has not been a problem. Both estrogenic adverse effects (nausea, dizziness, irritability, weight gain, bloating) and progestogenic adverse effects (vaginal dryness, acne, hirsutism, weight gain, depression, loss of libido) can occur in 50% of women, but these generally disappear after a few months of use. In conclusion, the low-dose, third generation COCs are associated with minimal risks in the absence of other risk factors and have many beneficial effects such as the prevention of ovarian and endometrial cancer; a decrease in pelvic inflammatory disease and ectopic pregnancies; and protection from anemia, primary dysmenorrhea, functional ovarian cysts, and benign breast disease as well as from the morbidity and mortality associated with pregnancy.
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PMID:The combined oral contraceptive. Risks and adverse effects in perspective. 776 40

We studied the effectiveness of and compliance with the use of cholestyramine in children with heterozygous familial hypercholesterolemia (FH) and familial combined hyperlipidemia (FCHL). During a 10-year period, 673 children (aged 10.5 +/- 4.0 years) were referred for evaluation of hyperlipidemia, of whom 87 (36 with FH; 51 with FCHL) were treated with cholestyramine (8 to 24 gm/day). In both groups, total cholesterol, low-density lipoprotein (LDL)-cholesterol, and apolipoprotein B levels were significantly reduced after cholestyramine use. In those with FH, plasma LDL-cholesterol levels decreased from 258 +/- 35 mg/dl (6.67 +/- 0.90 mmol/L) to 190 +/- 31 mg/dl (4.91 +/- 0.80 mmol/L); in those with FCHL, LDL-cholesterol levels dropped from 207 +/- 40 mg/dl (5.35 +/- 1.03 mmol/L) to 141 +/- 35 mg/dl (3.64 +/- 0.90 mmol/L). High-density lipoprotein-cholesterol levels were not significantly changed after cholestyramine use in either group. In the FCHL group, plasma triglyceride levels increased significantly from 81 +/- 35 mg/dl (0.92 +/- 0.40 mmol/L) to 134 +/- 42 mg/dl (1.52 +/- 0.48 mmol/L). Seven patients were lost to follow-up; 18 discontinued the medication within 1 month. Of the remaining 62 children, 59 had a good response to the drug. Of the 62 patients, 52 discontinued the medication after 21.9 +/- 10 months. Adverse effects included foul taste (73%), nausea with bloating (18%), and constipation. Cholestyramine is effective in reducing LDL-cholesterol levels in children with inherited hyperlipidemia, but the majority of children will not comply with its long-term use.
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PMID:Use of cholestyramine in the treatment of children with familial combined hyperlipidemia. 844 Nov 9

One of the many challenges for any physician is determining the correct course of treatment for patients with more than 1 area of complaint. Should the physician treat the symptoms or the underlying cause of a condition? If treating the cause, what and who determines the cause? Further complicating the issue, doctors must succeed in getting patients to follow the prescribed treatment, which has always been and will continue to be an issue in reaching therapeutic goals. In late 2009, a 49-year-old Caucasian woman visited the Natural Health Center of Medical Lake (NHCML) in Medical Lake, WA, complaining of multiple symptoms. One symptom was a goiter that had not been relieved with a prescription for 0.375 mg of Synthroid daily. Her comorbidities included mixed hyperlipidemia; multiple joint pains; alopecia; fatigue; bilateral, lower-extremity edema; and severe gastric disruption with bloating and acid reflux. After initial success from treatment, with a complete reduction of her presenting goiter and most of her other symptoms, the patient withdrew herself from her prescription medication and her nutritional supplementation. After 4 wk, the patient visited NHCML with indications of severe hypothyroidism, including a severely enlarged goiter of the right wing. After 6 wk of treatment with iodine and a glandular nutritional supplement (GTA Forte), her symptoms of severe hypothyroidism abated. Subsequent treatment for adrenal insufficiency, which was diagnosed at NHCML using salivary adrenal stress-index testing for cortisol rhythm and load, allowed complete resolution of her presenting complaints. This result persisted even at the 3-y follow-up to a greater degree than did the results from the use of thyroid nutritional supplementation and Synthroid, both alone and combined. The hypothalamus-pituitary-adrenal (HPA) axis may contribute to the existence of thyroid-type symptoms, particularly for those individuals with subclinical thyroid conditions. The treatment of the feedback mechanisms for the HPA axis may provide a valuable framework for treatment of mixed hyperlipidemia because normalizing or improving thyroid stimulating hormone (TSH) levels can reduce serum cholesterol levels.
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PMID:Adrenal and Thyroid Supplementation Outperforms Nutritional Supplementation and Medications for Autoimmune Thyroiditis. 2677 99