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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

"Diabetes 2000" will parallel a major diabetic retinopathy public information campaign recently announced by the National Eye Institute. The NEI's National Eye Health Education Program (NEHEP), which targets both diabetic retinopathy and glaucoma, is fashioned along the lines of earlier federal initiatives against smoking and high blood pressure. By continuously updating our medical knowledge and skills related to this multisystem disorder, and by forging partnerships between physicians in the effective and efficient management of diabetic patients, we have a unique and important opportunity--we can reduce preventable blindness from diabetes by the year 2000.
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PMID:Elimination of preventable blindness from diabetes by the year 2000. 151 75

The prevalences of risk factors and angiopathy were studied in 260 diabetic patients, 100 females and 160 males, 35-54 years old, in Uppsala. The prevalence, in females and males separately, of hypertension (WHO-criteria) was 46-34%, of hypercholesterolaemia (greater than or equal to 6.7 mmol.l-1) 32-29%, and of obesity (relative BMI greater than or equal to 120%) 25-20%. Those smoking greater than 15 cigarettes/day were 11-20%. Mean HbA1 was 10.6-10.5%. The prevalence of angina pectoris was 11-6%, of possible infarction 4-6%, and of major ECG abnormalities 6-4%. Large vessel (cardiovascular) disease was independently related to HbA1 (strongly), hypertension, cholesterol, age and familial NIDDM. The prevalence of severe retinopathy (blindness, new vessels or large hemorrhage) was 0% with 7-13 years of diabetes duration, and 26% with greater than or equal to 14 years of duration. The prevalence of severe proteinuria was 4% with 7-13 years of diabetes duration, and 15% with greater than or equal to 14 years of duration. Small vessel (retinopathy and nephropathy) disease was independently related to diabetes duration (strongly), HbA1 and hypertension. The data were discussed related to data from the London, Berlin and Tokyo centres of the WHO Multinational Study of Vascular Disease in Diabetics, using the same study protocol in the present study.
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PMID:Prevalences of risk factors and angiopathy in diabetic patients in Uppsala. 152 37

The movement of calcium into neurons may be the common denominator for the triggering and propagation of seizure activity. We report results of the first double-blind, placebo-controlled, crossover trial with the dihidropyridine calcium antagonist nifedipine (NFD) as adjuvant therapy in refractory epilepsy. Twenty-two students (12 male, 10 female, age 17-22 years) attending Lingfield Hospital School received NFD retard and matched placebo for 8 weeks in 2 doses (20 and 40 mg b.i.d. each for 4 weeks) with a washout period of 8 weeks between treatment phases. In the 20 students who completed the trial, fewer partial seizures (p less than 0.05) were documented during the first 2 weeks of NFD administration. Similarly, fewer seizure days (p less than 0.05) were reported in the first month of active treatment. This response was not sustained into the second month of the trial. Blind scoring of EEGs suggested a small improvement with NFD (p less than 0.05). More patients reported headache when receiving NFD (p less than 0.02) than placebo, but heart rate and erect and supine blood pressure remained unaffected. Mean maximum NFD concentrations were 13.1 +/- 10.4 ng/ml. A weak correlation was noted between total (p less than 0.05) and partial (p = 0.025) seizure numbers and NFD concentrations following 8 weeks of treatment. This study does not support important anticonvulsant efficacy for NFD as adjuvant therapy for refractory epilepsy at doses appropriate for the treatment of angina or hypertension. Further trials are recommended using higher doses of NFD in less severely affected patients.
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PMID:Nifedipine for epilepsy? A double-blind, placebo-controlled trial. 154 65

Late complications of diabetes mellitus include a variety of clinical pictures, mainly related to the involvement of the arterial wall both of large vessels (macroangiopathy) and small vessels (microangiopathy), and of the peripheral nervous system (neuropathy). Their presence in almost all types of diabetes indicates that there is a common pathogenetic mechanism, which can be substantially identified in high blood glucose levels and related alterations. Hyperglycemia, in fact, leads to some metabolic abnormalities, i.e. non-enzymatic glycosylation of proteins and polyol pathway activity; moreover it can negatively affect the pattern of some hormones, especially GH and sex steroids, and normal rheological and clotting properties of blood. These abnormalities, confirmed by experimental models, play a key role in the development of late diabetic complications. However some evidence indicates that a genetic background may predispose to their development or protect from their onset. The two main forms of diabetic retinopathy, non-proliferative and proliferative, show an incidence which increases with age and duration of diabetes, reaching 100% when diabetes lasts for more than 20 years. The risk of blindness, which is very high for the proliferative form, has been dramatically reduced by laser-photocoagulation. Diabetic nephropathy affects a lesser number of diabetics but, after a silent or preclinical stage, leads to renal failure and subsequent replacement therapy. Strict metabolic control in the silent stage and later rigid anti-hypertensive treatment can prevent or retard the evolution of this complication. A close association has been observed between diabetes and hypertension, which can directly affect the onset and evolution of diabetic nephropathy, probably through a common genetic mechanism. Diabetic neuropathy has a wide variety of clinical manifestations, at somatic, autonomic and central levels and can greatly modify the quality and expectancy of life. However, the major cause of death in diabetic subjects is large vessel disease or macroangiopathy, which is similar to non-diabetic atherosclerosis regarding the main histopathological and clinical manifestations but has a much higher prevalence and severity. Finally, a specific cardiomyopathy has also been described in diabetes mellitus and can account for the high rate of heart failure observed in these patients.
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PMID:The late complications of diabetes mellitus. 174 48

Anterior ischemic optic neuropathy is an uncommon and devastating event that can result in unilateral or bilateral blindness. It has been reported as a complication of ophthalmologic or general surgical and cardiothoracic procedures as well as a spontaneous event in severe systemic disease. Aggravating intraoperative factors include anemia, hemorrhage, hypotension, preexisting small-vessel disease, and increased intraocular pressure. We present a case of anterior ischemic optic neuropathy as a complication in a 48-year-old man undergoing extensive resection of recurrent carcinoma of the head and neck. Possible contributing risk factors in our patient include preexisting hypertension, intraoperative blood loss, previous radical neck dissection with venous compromise, intraoperative head and neck edema, and the use of tightly adherent plastic bubble-type intraoperative eye protection. The possible pathogenesis of this devastating complication and recommendations for prevention and management of anterior ischemic optic neuropathy are described.
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PMID:Anterior ischemic optic neuropathy causing blindness in the head and neck surgery patient. 174 39

Causes and risk factors of deaths from subacute myelo-optico neuropathy (SMON) were studied in a prospective cohort of 4,329 SMON patients followed for 3 years and 7 months (Sept. 1985-March 1989) with the following findings: (1) Recent excess deaths of SMON patients was estimated as 4% from ratio of O/E (SMR = 104) and deaths due to SMON itself was 6.4%. (2) The ratio of O/E was significantly higher for deaths from cancer of colon/rectum in females, cancer of pancreas in males, hypertension in males, pneumonia/influenza in females, chronic obstructive pulmonary diseases in males, tuberculosis and intestinal obstructive disease in males and females. (3) The ratio of O/E was 1.8 times or greater for those SMON patients with complications of cerebrovascular disease, severe blindness, complete loss of ambulation, and who were bedridden, and who are unable to receive home care from family members or trained home helpers.
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PMID:[A cohort study on deaths from SMON in Japan]. 174 33

Vision loss in orbital hypertension secondary to sudden space-occupying lesions is usually attributed to one of three causes: central retinal artery occlusion, direct compressive optic neuropathy, or compression of optic nerve vasculature. Accepted modes of decompressive therapy include lateral canthotomy and cantholysis; drainage of localized orbital air, hematoma, or abscess; and bony wall decompression. Five cases are presented in which orbital hypertension caused severe proptosis with traction on the optic nerve and tenting of the posterior globe. Another mechanism contributing to visual loss is proposed in these cases: ischemic optic neuropathy due to stretching of nutrient vessels. In these cases, rapid posterior decompression should theoretically be favored to reduce orbital pressure and relieve traction on the optic nerve vasculature.
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PMID:Mechanisms of visual loss in severe proptosis. 176 22

Eclampsia is a syndrome that may be characterized by functional derangement of multiple organ systems including the central nervous system. Cerebral manifestations are rare in eclampsia but may include cerebral hemorrhage, blindness, and coma. Management of eclampsia involves the control of convulsions and hypertension as well as delivery. Cerebral manifestations such as increased intracranial pressure or coma require aggressive well-formulated intervention.
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PMID:Cerebral pathology in eclampsia. 176 88

The UK Prospective Diabetes Study (UKPDS) is a multi-centre, prospective, randomised, intervention trial of 5100 newly-diagnosed patients with Type 2 (non-insulin-dependent) diabetes mellitus which aims to determine whether improved blood glucose control will prevent complications and reduce the associated morbidity and mortality. Newly presenting Type 2 diabetic patients aged 25-65 years inclusive, median age 53 years, median body mass index 28 kg/m2 and median fasting plasma glucose 11.3 mmol/l, were recruited and treated initially by diet. Ninety five percent remained hyperglycaemic (fasting plasma glucose greater than 6 mmol/l) and were randomly allocated to different therapies. In the main randomisation, those who were asymptomatic and had fasting plasma glucose under 15 mmol/l were allocated either to diet policy, or to active policy with either insulin or sulphonylurea aiming to reduce the fasting plasma glucose to under 6 mmol/l. Over 3 years, the median fasting plasma glucose in those allocated to diet policy was 8.9 mmol/l compared with 7.0 mmol/l in those allocated to active policy. The Hypertension in Diabetes Study has been included in a factorial design to assess whether improved blood pressure control will be advantageous. Patients with blood pressure greater than or equal to 160/90 mm Hg were randomly allocated to tight control aiming for less than 150/85 mm Hg with either an angiotensin-converting enzyme inhibitor or a Beta-blocker or to less tight control aiming for less than 200/105 mm Hg. The endpoints of the studies are major clinical events which affect the life and well-being of patients, such as heart attacks, angina, strokes, amputations, blindness and renal failure. To date, 728 patients have had at least one clinical endpoint. Surrogate endpoints include indices of macrovascular and microvascular disease detected by ECG with Minnesota Coding, retinal colour photography and microalbuminuria. The studies also aim to evaluate potential risk factors for the development of diabetic complications such as smoking, obesity, central adiposity, plasma LDL- and HDL-cholesterol, triglyceride, insulin, urate and other biochemical variables. The studies are planned to terminate in 1994, with a median follow-up of 9 years (range 3-16 years) for the glucose study and 5 years (range 2-6 years) for the hypertension study.
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PMID:UK Prospective Diabetes Study (UKPDS). VIII. Study design, progress and performance. 177 53

Among 407 patients (416 eyes) with retinal vein occlusion (RVO), 196 eyes had branch RVO, 185 eyes central RVO, and 26 eyes hemi-central RVO. The ischemic type accounted for 39.7%, and the non-ischemic type 60.3%. The risk factors were vascular hypertension (59.8%), retinal arteriosclerosis (58.0%), increased blood beta-lipoprotein (49.0%) and fibrinogen (21.7%), and high blood viscosity. The mean levels of whole blood and plasma viscosity were significantly higher in the patients than in the controls. The therapeutic effective rate was 63.2% for branch RVO, 52.4% for central RVO, and 69.2% for hemicentral RVO. The resultant rate of blindness was 15.9%, and that of low vision 23.1%, due to cystoid macular edema (44.4%) and vitreous hemorrhage (15.4%). The incidence of neovascular glaucoma was 9.5% in central RVO.
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PMID:[Risk factors and visual prognosis of 407 patients with retinal vein occlusion]. 181 18


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