Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim in treatment of hypertension is normalization of blood pressure. The impact of treatment of hypertension on the development of IHD depends not only on the treatment of hypertension but also on influencing other basic risk factors, i.e. hyperlipoproteinaemia and smoking. Treatment of hypertension can be and should be individual and depends on a) age, b) the level of hypertension, c) complications of hypertension and d) the presence of other diseases, in particular hyperlipoproteinaemia and diabetes mellitus. The treatment of choice in hyperlipoproteinaemia are calcium antagonists, prazosin, ACE inhibitors and beta-blockers with ISA. There is experimental evidence suggesting that calcium antagonists (in particular isradipine) but also beta-blockers suppress the progression of atherosclerosis and AGE inhibitors prevent the development of cardiac and vascular hypertrophy. Effective treatment leads to a decline in the mortality from cerebrovascular attacks--in the USA in the course of 20 years a decline by 60%--in Czechoslovakia so far the mortality from cerebrovascular disease did not change which indicates unfortunately a very poor control of hypertension in the population.
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PMID:[Treatment of hypertension and cardiovascular complications]. 182 87

The pathological role of the non-enzymatic modification of proteins by reducing sugars has become increasingly evident in various disorders. It is now well established that early glycation products undergo progressive modification over time in vivo to the formation of irreversible cross-links, after which these molecules are termed "AGEs (advanced glycation end products)". AGEs have been implicated in the development of many of the pathological sequelae of diabetes and aging, such as diabetic microangiopathy, ischemic heart disease and neurodegenerative diseases. Recently, digested food-derived AGEs are also found to play an important role in the pathogenesis of AGE-related disorders. Diet is a major environmental source of pro-inflammatory AGEs. Indeed, restriction of dietary glycotoxins decreases excessive AGE levels and subsequently reduces the inflammatory responses in patients with diabetes. These observations suggest that inhibition of absorption of dietary AGEs may be a novel target for therapeutic intervention in the above-mentioned AGE-related disorders. AST-120 (Kremezin) is an oral adsorbent that attenuates the progression of chronic renal failure (CRF) by removing uremic toxins. We have recently found that AST-120 binds to carboxymethyllysine (CML), one of the well-characterized, digested food-derived AGEs in vitro and that administration of AST-120 decreases serum levels of AGEs in non-diabetic CRF patients. These findings suggest that digested food-derived AGEs such as CML may be a novel molecular target for oral adsorbent AST-120 and that AST-120 could exert beneficial effects on CRF patients by adsorbing diet-derived AGEs and subsequently decreasing serum AGE levels. If our speculation is correct, AST-120 may have therapeutic potentials for the treatment of patients with various AGE-related disorders as well. In this paper, we would like to propose the possible ways of testing our hypotheses. Does the long-term treatment of AST-120 decrease serum and tissue levels of AGEs in diabetic patients? Does this treatment also reduce the risk for the development and progression of diabetic vascular complications such as diabetic retinopathy or ischemic heart disease? If the answers are yes, do the serum and/or tissue levels of AGEs after AST-120 treatment predict its beneficial effects on diabetic vascular complications? How about the effects of AST-120 on Alzheimer's disease, another AGE-related neurodegenerative disorder? Does the treatment of AST-120 reduce the risk for Alzheimer's disease and/or improve the cognitive impairment of patients with this disorder? These prospective studies will provide further valuable information whether the inhibition of absorption of dietary AGEs by AST-120 could be clinically relevant.
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PMID:Oral administration of AST-120 (Kremezin) is a promising therapeutic strategy for advanced glycation end product (AGE)-related disorders. 1733 65

Cardiovascular diseases (CVD) may be mediated through increases in the cardiovascular risk factors. Hemoglobin A1c (HbA1c) also called glycated hemoglobin is presently used for the diagnosis and management of diabetes. It has adverse effects on cardiovascular system. This review deals with its synthesis and effects on the cardiovascular system. The serum levels of HbA1c have been reported to be affected by various factors including, the lifespan of erythrocytes, factors affecting erythropoiesis, agents interfering glycation of Hb, destruction of erythrocytes, drugs that shift the formation of Hb, statins, and drugs interfering the HbA1c assay. Levels of HbA1c are positively correlated with serum glucose and advanced glycation end products ( AGE), but no correlation between AGE and serum glucose. AGE cannot replace HbA1c for the diagnosis and management of diabetes because there is no correlation of AGE with serum glucose, and because the half-life of protein with which glucose combines is only 14-20 days as compared to erythrocytes which have a half-life of 90-120 days. HbA1c is positively associated with CVD such as the carotid and coronary artery atherosclerosis, ischemic heart disease, ischemic stroke and hypertension.HbA1c induces dyslipidemia, hyperhomocysteinemia, and hypertension, and increases C-reactive protein, oxidative stress and blood viscosity that would contribute to the development of cardiovascular diseases. In conclusion, HbA1c serves as a useful marker for the diagnosis and management of diabetes. AGE cannot replace HbA1c in the diagnosis and management of diabetes. There is an association of HbA1c with CVD which be mediated through modulation of CVD risk factors.
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PMID:Does HbA1cc Play a Role in the Development of Cardiovascular Diseases? 3017 23