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)

Sixteen patients with different kinds of hyperlipidemia were treated with Atroplex (Mg-Chlorphenoxyisobutyrate 350 mg, Mesoinositol-Hexanicotinate 250 mg), a new serum lipid decreasing drug. Within an interval of 60 days' standard treatment of 3 tablets of Atroplex, the serum level of cholesterol was reduced by 16-20% and that of triglycerides by 36-49%. This significant effect was obvious over the whole period of treatment. According to the compound of Clofibrate, Atroplex interfered with the anticoagulant treatment with phenprocoumon. In spite of this an AC-therapy is possible during the Atroplex medication, if the AC doses are reduced by 30-50%.
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PMID:[New drug combination for medical management of hyperlipemia: clinical study]. 34 Mar 91

In this research, 74 patients with coronary heart disease (CHD) were grouped in matched-pair, one group took orally Inositol and Mai Tong as the control group, the other group took orally Yi Xin Decoction as the tested group. Indices, i. e. serum levels of apolipoprotein A-1 (Apo A-1), apolipoprotein B (Apo-B), high density lipoprotein cholesterol (HDL-c), high density lipoprotein subcomponent cholesterol (HDL2-c), B-lipoprotein (B-LP), total cholesterol (Tch), triglyceride (TG) were measured before and after treatment for 28 days; the results showed that the patients with CHD have prominent derangement of lipid metabolism, which is similar to previous reports. Yi Xin Decoction modified according to Syndrome Differentiation, produced the effect of decreasing the serum Apo-B levels and TG. It also increased Apo-A-1, HDL-c and HDL2-c respectively. Moreover the effect of lowering Apo-B and raising HDL-c in the Yi Xin Decoction group was better than that in the control group. There was no side effect at all; all these indicated that Yi Xin Decoction has a remarkable function of regulating the disturbance of lipid metabolism in CHD patients. In order to further investigate the curative effect of Yi Xin Decoction and elucidate its mechanism, the authors have also investigated Yi Xin Decoction on the experimental mice with hyperlipemia. The result Showed that Tch and TG in atromid and Yi Xin Decoction group reduced after medication, P < 0.01. In comparing with control group, the HDL-c and acidic cholesterol in stool Yi Xin Decoction group rose, P < 0.05. The above study has provided reliable basis for the clinical application of Yi Xin Decoction and also a new medicine to regulate disturbance of lipid metabolism for CHD patients.
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PMID:[Clinical and experimental study on its regulatory function of yi xin decoction (heart-nourishing decoction) to lipids metabolic disturbance in coronary heart disease]. 139 90

Diabetic polyneuropathy is the most frequent neuropathy in western countries. In Germany, there are 3.5 to 4 million diabetic patients. Diagnosis should rule out other polyneuropathies and assess two out of the five diagnostic criteria: neuropathic symptoms, neuropathic deficits, pathological nerve conduction studies, pathological quantitative sensory testing and pathological quantitative autonomic testing. So far, the pathophysiology of diabetic neuropathy remains to be fully understood. Among the various pathophysiological concepts are the Sorbitol-Myo-Inositol hypothesis attributing Myo-Inositol depletion to the accumulation of Sorbitol and Fructose, the concept of deficiency of essential fatty acids with reduced availability of gamma-linolenic-acid and prostanoids, the pseudohypoxia- and hypoxia-hypothesis attributing endothelial and axonal dysfunction and structural lesions to increased oxidative stress and free radical production. Obviously, the hyperglycemia induced generation of advanced glycation end products (AGEs) also contributes to structural dysfunctions and lesions. Elevated levels of circulating immune complexes and activated T-lymphocytes as well the identification of autoantibodies against vagus nerve or sympathetic ganglia support the concept of an immune mediated neuropathy. The reduction of neurotrophic factors such as nerve growth factor, neurotrophin-3 or insulin-like growth factors also seems to further diabetic neuropathy. The symmetrical, distally pronounced and predominantly sensory neuropathy is far more frequent than the symmetrical neuropathy with predominant motor weakness or the asymmetrical neuropathy. The painless neuropathy manifests with impaired light touch sensation, position sense, vibratory perception and diminished or absent ankle deep tendon reflexes. The painful sensory diabetic neuropathy primarily affects small nerve fibers and accounts for decreased temperature perception and paresthesias. The proximal, diabetic amyotrophy evolves subacutely or acutely, induces motor weakness of the proximal thigh and buttock muscles and is painful. Cranial nerve III-neuropathy is also painful and has an acute onset. Truncal radiculopathy follows the distribution of truncal roots and frequently causes intense pain. Autonomic neuropathy occurs with and without somatic neuropathy. The most important therapy is to attempt optimal blood glucose control, to reduce body weight and hyperlipidemia. Symptomatic therapy includes alpha-lipoic acid treatment, as the antioxidant seems to improve neuropathic symptoms. Aldose reductase inhibitors might reduce sorbitol and fructose production and normalize myo-inositol levels. However, there are no aldose reductase inhibitors available in Europe as yet. Evening primrose oil, containing gamma-linolenic acid, might improve nerve conduction velocities, temperature perception, muscle strength, tendon reflexes and sensory function. Substitution of nerve growth factor showed promising results in pilot studies but failed in a large-scale multicenter study. Symptomatic pain treatment can be achieved with tricyclic antidepressants, selective serotonin reuptake inhibitors, anticonvulsants such as carbamazepine, gabapentin or lamotrigine, or anti-arrhythmic drugs such as mexiletine. Topical capsaicin application should reduce neuropathic pain but also induces local discomfort in the beginning of therapy. Vasoactive substances, so far have not proven to be of major benefit in diabetic neuropathy. Physical therapy and thorough footcare are of primary importance and allow prevention of secondary complications such as foot amputations.
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PMID:[Diabetic somatic polyneuropathy. Pathogenesis, clinical manifestations and therapeutic concepts]. 1092 53

Endothelial dysfunction (ED) is an early feature of cardiovascular risk and diabetes. Hyperglycemia and hyperlipidemia are causative factors. Excessive endothelial mitochondrial superoxide (ROS) production with hyperglycemia and hyperlipidemia is a key mechanism. Inositol components of an insulin inositol glycan mediator, d-chiro-inositol (DCI) and 3-O-methyl DCI (pinitol), decrease hyperglycemia and hyperlipidemia. We tested whether these, myoinositol and dibutyryl DCI (db-DCI), would prevent or reverse ED in diabetic rats and rabbits. Oral inositols reduced hyperglycemia and hypertriglyceridemia with different potencies and prevented ED in rat aortic rings and mesenteric beds. Inositols added in vitro to five diabetic tissues reversed ED. Relaxation by Ach, NO, and electrical field stimulation was potentiated by inositols in vitro in rabbit penile corpus cavernosa. Inositols in vitro restored impaired contraction by the eNOS inhibitor l-NAME and increased NO effectiveness. DCI and db-DCI decreased elevated ROS in endothelial cells in high glucose and db-DCI reduced PKC activation, hexosamine pathway activity, and advanced glycation end products to basal levels. Xanthine/xanthine oxidase generated superoxide was reduced by superoxide dismutase or inositols, with db-DCI efficacious in a mechanism requiring chelated Fe(3+). Histochemical examination of rat aortic rings for protein SNO demonstrated a decrease in diabetic rings with restoration by inositols. In summary, inositols prevented and reversed ED in rat and rabbit vessels, reduced elevated ROS in endothelial cells, potentiated nitrergic or vasculo-myogenic relaxations, and preserved NO signaling. These effects are related to their metabolic actions, direct superoxide scavenging, and enhancing and protecting NO signaling. Of the inositols tested, db-DCI was most effective.
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PMID:Inositols prevent and reverse endothelial dysfunction in diabetic rat and rabbit vasculature metabolically and by scavenging superoxide. 1637 99