Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 94-year-old male with a history of atrial fibrillation, aortic stenosis, heart failure, apical thrombus, arterial hypertension, aneurysm of the abdominal aorta, and a urinary bladder carcinoma, cardiologic investigations revealed pulmonary rales, enlarged heart, absolute arrhythmia, and positive troponin-, myocardial thickening, enlarged cardiac cavities, hypocontractility, aortic stenosis, slight aortic insufficiency, severe mitral insufficiency, and surprisingly left ventricular hypertrabeculation. Upon neurological investigations, a polyneuropathy was suspected but a myopathy not completely excluded. The presented case shows that LVHT occurs also in nonagenarians and is associated with neuromuscular disease and positive troponin-T, in the absence of ischemic heart disease or severe renal failure. The cause of troponin-T-positivity remains multi-factorial.
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PMID:Noncompaction and neuromuscular disease with positive troponin-T in a nonagenerian. 1792 84

At least one of four diabetic patients is affected by distal symmetric polyneuropathy, which represents a major health problem, since it may present with partly excruciating neuropathic pain and is responsible for substantial morbidity, increased mortality, and impaired quality of life. Treatment is based on four cornerstones: 1) causal treatment aimed at (near)-normoglycemia, 2) treatment based on pathogenetic mechanisms, 3) symptomatic treatment, and 4) avoidance of risk factors and complications. Recent experimental studies suggest a multifactorial pathogenesis of diabetic neuropathy. From the clinical point of view, it is important to note that, based on these pathogenetic mechanisms, therapeutic approaches could be derived, some of which are currently being evaluated in clinical trials. Among these agents, only alpha-lipoic acid is available for treatment in several countries and epalrestat in Japan. Although several novel analgesic drugs such as duloxetine and pregabalin have recently been introduced into clinical practice, the pharmacologic treatment of chronic painful diabetic neuropathy remains a challenge for the physician. Individual tolerability remains a major aspect in any treatment decision. Epidemiological data indicate that not only increased alcohol consumption but also the traditional cardiovascular risk factors such as hypertension, smoking, and cholesterol play a role in development and progression of diabetic neuropathy and hence need to be prevented or treated.
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PMID:Treatment of diabetic neuropathy and neuropathic pain: how far have we come? 2227 45

Type 2 diabetes mellitus is a disease that affects a rapidly increasing number of patients. Most patients with Type 2 diabetes will develop vascular complications. This may be microvascular disease, such as nephropathy, retinopathy or polyneuropathy, and also macrovascular disease, such as coronary heart disease, stroke or peripheral artery disease. Optimal control of elevated blood glucose levels will reduce the symptoms of hyperglycemia and help to prevent the development of complications. In addition, treatment of hypertension and lipid disturbances has been shown to reduce the incidence and severity of vascular complications significantly. The current treatment goals focus on adequate and aggressive treatment of these three risk factors. The central dogma for treatment of blood glucose, blood pressure and cholesterol levels is 'the lower the better'. Ongoing trials evaluate the effect of further lowering these treatment goals and of specific types of medication on cardiovascular events.
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PMID:Type 2 diabetes mellitus: prevention of macrovascular complications. 1832 94

Glycemic control and diabetes duration are believed to be the most important risk factors for the development of diabetic microangiopathy; however, the rate of progression of nephropathy, retinopathy and polyneuropathy varies considerably among patients. Besides the presence of risk factors such as hypertension, dyslipidaemia and smoking, there is evidence suggesting that genetic predisposition plays a role in the susceptibility to microvascular complications. Based on underlying pathogenesis, polymorphisms of several candidate genes belonging to multiple pathways have been investigated, like the genes related to mechanisms of hyperglycaemia-induced damage (such as advanced glycation end-products and reactive oxygen species increased formation, augmented activity of the aldose reductase pathway); genes related to the renin-angiotensin system; genes coding for cytokines, growth factors and its receptors, glucose transporter; among many others. This article reviews some studies that corroborate the importance of the genetic background in the development of diabetic microangiopathy.
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PMID:[Genetic susceptibility to microangiopathy development in Type 1 diabetes mellitus]. 1843 49

Neurological crises do not occur in patients with tyrosinaemia type I treated with NTBC. We report an 8 month-old boy with severe neurological crisis after interruption of NTBC treatment including progressive ascending polyneuropathy and diaphragmatic paralysis, arterial hypertension, respiratory distress requiring mechanical ventilation who later also developed impaired liver function and tubulopathy. After re-introduction of NTBC the patient slowly regained normal neurological functions and recovered completely.
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PMID:Severe neurological crisis in a patient with hereditary tyrosinaemia type I after interruption of NTBC treatment. 1850 May 74

Glucose-fed rat is a model of insulin resistance that displays sensory polyneuropathy and hypertension. This study aimed at comparing the beneficial effects of N-acetyl-L-cysteine (NAC, antioxidant) and ramipril (angiotensin-1 converting enzyme inhibitor) on tactile and cold allodynia induced by chronic glucose feeding. Impact of these treatments was also assessed on hypertension, plasma glucose and insulin concentrations, insulin resistance and kinin B(1) receptor expression. Male Wistar rats (50-75 g) were given 10% d-glucose in their drinking water for 11 weeks or tap water (controls). Glucose-fed rats were treated either with NAC (1 g/kg/day, gavage), ramipril (1 mg/kg/day in drinking water) or no drug during the last 5 weeks. Glucose feeding for 6 weeks induced a significant increase in systolic blood pressure and hyperglycaemia which was accompanied by tactile and cold allodynia. At 11 weeks, plasma insulin, insulin resistance (HOMA index), kinin B(1) receptor mRNA in spinal cord and renal cortex and B(1) receptor binding sites in spinal cord were enhanced in glucose-fed rats. NAC and ramipril caused a progressive to complete inhibition of tactile and cold allodynia from 6 to 11 weeks. High systolic blood pressure, hyperinsulinemia, insulin resistance and kinin B(1) receptor expression were also normalized or attenuated in glucose-fed rats by either treatment. Results suggest that chronic treatment with an antioxidant or an ACE inhibitor provides similar beneficial effects on sensory polyneuropathy, hypertension and insulin resistance in glucose-fed rats. Both therapies were associated with a reduction of the expression of the pro-nociceptive kinin B(1) receptor.
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PMID:Blockade of sensory abnormalities and kinin B(1) receptor expression by N-acetyl-L-cysteine and ramipril in a rat model of insulin resistance. 1855 89

Metabolic syndrome (MS) encompasses a series of diseases which, when combined, increase vascular risk more than the sum of their individual risks. Insulin resistance (IR) is one of the basic components of MS. - Abdominal fat distribution is an IR marker and is associated to factors increasing vascular risk such as dyslipidemia, high blood pressure, and hyperglycemia, components of the so-called metabolic syndrome. - IR is related to glomerular sclerosis and renal failure through several mechanisms, Including genetic and environmental factors, and stimulation of the renin-angiotensin-aldosterone system. - IR usually precedes development of DM, and therefore contributes to its early identification. MS increases the risk of chronic complications from DM and is associated to an increased prevalence of cardiovascular disease, particularly coronary heart disease, increasing mortality from this cause. - The presence of MS in DM2 is usually associated to a greater prevalence of microalbuminuria or proteinuria and peripheral polyneuropathy.
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PMID:[Metabolic syndrome and kidney disease]. 1901 36

We present a case report of a 59-year-old man with a history of arterial hypertension and excision of malignant melanoma. He was admitted to the hospital because of two months history of diarrhoea, weight loss and circulatory collapse. In addition, the patient suffered from marked vegetative instability with symptomatic hypotension, polyneuropathy and progression of renal insufficiency, without proteinuria. Complex examination did not reveal neoplasms, endocrine, autoimmune, infectious or neurodegenerative disorders. A serial biopsy of colon failed to provide a clue to the diagnosis. However, AA amyloidosis was found on the kidney biopsy. Neither chronic inflammation nor malignancy was revealed and, hence, no causal treatment could have been established. The patient died from multiple organ failure. The autopsy confirmed systemic AA amyloidosis. The triad consisting ofdiarrhoea, polyneuropathy and hypotension should rise the suspicion on amyloidosis.
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PMID:[Persistent diarrhoea, hypotension, polyneuropathy]. 1906 86

Chronic arsenic toxicity (arsenicosis) due to drinking of arsenic contaminated ground water is a major environmental health hazard throughout the world including India. A lot of new information is emerging from extensive research on health effects of chronic arsenic toxicity (CAT) in humans during the last two decades. Available literature has been reviewed to highlight the problem including its malignancies. Pigmentation and keratosis are the specific skin lesions characteristics of CAT. CAT also produces various systemic manifestations over and above skin lesions, important ones being chronic lung disease like chronic bronchitis, chronic obstructive pulmonary disease and bronchiectasis, liver disease like non-cirrhotic portal fibrosis and other diseases like polyneuropathy, peripheral vascular disease, hypertension and ischeamic heart disease, diabetes mellitus, non-pitting oedema of feet/hands, weakness and anaemia. Cancer of skin, lung and urinary bladder are important cancers associated with chronic arsenic toxicity. Stoppage of drinking of arsenic contaminated water is the main stay in the management of arsenicosis as specific chelation therapy has limited value. Early skin cancer, detectable by regular active surveillance, is curable. In addition to dermatological features, CAT produces protean clinical manifestations. Treatment of arsenicosis is unsatisfactory and is mostly symtomatic.
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PMID:Chronic arsenic toxicity & human health. 1910 39

Both the central nervous system (CNS) and the peripheral nervous system (PNS) are major target organs in primary vasculitides. They may either be affected in the setting of systemic vasculitis, potentially involving any other organ, or they may be the sole site of the inflammatory process. In both cases, the clinical pattern of PNS involvement is essentially uniform, presenting as sensory axonal polyneuropathy or mononeuritis multiplex. The damage is related to the ischemic occlusion of the vasanervorum due to small-vessel vasculitis. On the contrary, the range of manifestations of CNS vasculitis is much wider and several pathogenetic mechanisms are implicated, including angiitis of the hemispheres and spinal cord, thrombosis of dural sinuses, stenosis and aneurysms of medium and large arteries, granulomatous meningeal involvement and direct cytokine damage presenting with encephalopathy. Besides, even extracranial noninflammatory vascular disease may induce CNS symptoms, as is the case of carotid stenosis, vena cava syndrome and renovascular hypertension. In this paper we will review the broad spectrum of clinical manifestations of CNS and PNS neuropathy as they occur in primary systemic and non systemic vasculitides.
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PMID:The clinical spectrum of the neurological involvement in vasculitides. 1949 86


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