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)

A woman with hypertension had been treated with hydralazine and propranolol for the past 6 years. Leg ulcers and mild joint involvement had been observed for 3 years. When oral zinc therapy was started, multisystemic manifestations of a lupus erythematosus-like syndrome developed within one week. The possible implication of zinc in drug-induced lupus is discussed.
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PMID:Drug-induced lupus erythematosus aggravated by oral zinc therapy. 9 57

The most common causes of leg ulcers in elderly patients are arteriosclerosis obliterans, venous insufficiency, hypertension, and prolonged pressure over relatively small body areas. The goal of treatment is to clear infection and stimulate good granulation tissue that can accept either a skin graft or epithelial regrowth from the borders of the ulcer.
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PMID:Leg ulcers in the elderly. 37 6

The presence of pericapillary fibrin and complement C3c in the ulcers of 19 patients with venous hypertension and 14 patients with ischaemic leg ulcers was investigated using histochemical and immunohistochemical techniques. There was deposition of fibrin around the capillaries in the central part of the ischaemic ulcers, and the venous hypertension ulcers, and in the non-ulcerated skin around one of the venous hypertension ulcers and two of the ischaemic leg ulcers. The deposition of fibrin is a secondary phenomenon that occurs in the area of ulcerated skin and does not play a major causal role in the formation of chronic leg ulcers.
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PMID:The occurrence of pericapillary fibrin in venous hypertension and ischaemic leg ulcers: a histopathological study. 161 Jul 9

The aim of this study was to understand the possible mechanisms by which deep venous insufficiency and venous hypertension are associated with trophic skin changes and ulceration and to explain the therapeutic effect of Pentoxifylline in patients with leg ulcers due to deep venous incompetence. Twenty patients were included in this pilot study. They were graded into two groups: group 1, included 10 patients (5 F and 5 M) with deep venous incompetence and normal arteries; group 2, included 10 patients (1 F and 9 M) with deep venous incompetence and moderate arterial disease. Skin and muscle biopsies were carried out before and after the oral administration of 1,200 mg of Pentoxifylline daily (400 mg t.d.s). The following parameters were investigated by means of light microscopy and immunofluorescence tests: engorgement of venous stroma; decrease of intimal elastica; hyaline degeneration; floccular degeneration; pericapillary fibrin deposits and fibrin degradation products; inflammation and fat necrosis; myofibril degeneration; fibrous scar; regeneration and reconstitution of muscle fibres. The results indicated that local inflammation at the ulcer's area cause accumulation of white blood cells in the capillaries and the interstitial fluid, where there is also accumulation of fibrinogen. These changes may lead to chronic tissue ischaemia and ulceration. The known favourable effect of Pentoxifylline on red cells and leucocyte function as well as its lowering effect on plasma fibrinogen level, may be responsible for the observed therapeutic effect of Pentoxifylline on venous leg ulcers.
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PMID:Comparison of skin and muscle biopsies before and after pentoxifylline treatment in patients with leg ulcers due to deep venous incompetence. 186 Oct 90

Much of the morbidity and mortality in sickle cell disease (SCD) is caused by tissue ischemia and infarction resulting from vascular occlusion. Research in this area has been dominated by the hypothesis that vascular occlusion in SCD is due primarily to microvascular obstruction by sickle erythrocytes (SS RBC), yet there is no direct evidence that microvascular occlusion is responsible for any of the vasocclusive complications of SCD. In this paper an alternate hypothesis is proposed: that thrombotic occlusion of larger arteries and veins is an important factor in many of the vasocclusive complications of SCD. Large-vessel cerebral arterial disease (intimal hyperplasia with superimposed thrombosis) has clearly been established as the most important cause of stroke in SCD, and considerable evidence suggests that pulmonary arterial thrombosis/embolism is a major cause of pulmonary infarction and hypertension. The involvement of large-vessel thrombosis in painful crisis, aseptic necrosis of bone, priapism, leg ulcers, retinopathy, and miscarriage has not been adequately investigated. Large-vessel occlusion in SCD is probably a consequence of the abnormal adhesive and procoagulant properties of SS RBC, which produce endothelial damage, secondary intimal proliferation, and thrombosis. Techniques currently used to treat large-vessel occlusion in other disorders (antiplatelet and anticoagulant agents, thrombolytic therapy, angioplasty, endarterectomy, and vascular bypass surgery) should be considered in sickle cell subjects with large-vessel occlusion, especially in the cerebral vasculature.
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PMID:Large-vessel occlusion in sickle cell disease: pathogenesis, clinical consequences, and therapeutic implications. 189 Sep 82

In 38 diabetic patients, admitted on a long-term basis to a nursing home, the clinical situation and presence of secondary diabetic complications were assessed, and their macrovascular complications and degree of glycemic control compared with those in ambulatory diabetic patients, matched for age, sex, known duration of diabetes and specific antidiabetic therapy. No differences in blood glucose control, plasma triglycerides, blood pressure and serum creatinine were observed between both groups of patients. Plasma cholesterol levels were higher in the ambulatory patients (6.4 +/- 1.0 vs 5.6 +/- 1.1 mmol/l, P = 0.008). Twenty-two nursing home patients had suffered from stroke, against 4 ambulatory patients. Hypertension was found in almost 50% of all patients, whereas its prevalence was highest in the stroke patients (69 vs 36%, P less than 0.01). In the nursing home patients, peripheral vascular abnormalities, skin necrosis or leg ulcers and recurrent urinary tract infections were frequently encountered, whereas in the ambulatory patients cardiac complaints were more prevalent. Use of medication, especially diuretics and anticoagulant agents, was higher in the nursing home patients. Diabetes and the sequelae of its macrovascular complications may greatly impair the quality of life of the diabetic patient, and place a large financial and personal burden on the health care in general. Better identification of diabetic patients with a high risk of stroke is necessary.
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PMID:Clinical characteristics and management of diabetic patients residing in a nursing home. 195 83

Lipodermatosclerosis of the lower extremity, with or without ulceration, is a common manifestation of severe venous disease and the result of sustained venous hypertension. The latter is generally a sequela of deep vein thrombosis. Factors that enhance clot formation or impair fibrinolysis contribute to the pathogenesis of venous disease. It is already established that faulty fibrinolysis may play a pathogenic role in patients with venous disease. We examined the possibility that patients with venous disease have abnormally low plasma levels of proteins C and S, two proteins whose deficiencies have been reported to cause an increased frequency of thromboembolic disease. Using immunologic and functional assays for plasma proteins C and S, we found that 4 (21%) of 19 patients with lipodermatosclerosis and leg ulcers had abnormally low levels of protein C or protein S. One of 7 patients with lipodermatosclerosis without ulceration had a profoundly depressed level of protein C and a history of cerebral stroke at a young age. Plasma levels of protein C were normal in five patients with arterial insufficiency severe enough to cause leg ulceration. We conclude that abnormally low plasma levels of proteins C and S may be found in patients with lipodermatosclerosis and venous ulceration. As with the abnormally low fibrinolytic activity in these patients, our findings indicate a possible propensity for increased thrombotic disease.
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PMID:Protein C and protein S plasma levels in patients with lipodermatosclerosis and venous ulceration. 203 43

The incidence of pericapillary fibrin cuffs was investigated in 49 biopsies of venous leg ulcers and 67 biopsies of leg ulcers of non-venous etiology. Pericapillary fibrin cuffs were seen in 28 biopsies (57.1%) of venous leg ulcers, but only in 11 biopsies (16.4%) of non-venous leg ulcers. In the venous leg ulcers pericapillary fibrin cuffs occurred predominantly near the ulcer surface and around dilated capillaries. Dilation of the capillaries and inflammation probably contribute more to the pathogenesis of pericapillary fibrin cuffs than venous hypertension.
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PMID:Pericapillary fibrin cuff: a histological sign of venous leg ulceration. 225 74

Four patients with systemic scleroderma and 1 patient with localized scleroderma were treated with ciclosporin (CS), given in daily doses between 2.2 and 5.6 mg/kg body weight for 3-26 months. Under this medication clinical improvement was observed in 4 patients with partial regression of cutaneous sclerosis and inflammation, healing of fingertip ulcerations or leg ulcers and improvement of articular mobility. However, in 1 patient with rapidly advancing systemic scleroderma a short-term therapy with CS in low doses (2-3 mg/kg body weight) resulted in arterial hypertension and renal dysfunction. Therefore careful selection of patients and close-meshed controls are indicated when CS is considered as anti-inflammatory treatment in scleroderma.
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PMID:Cyclosporin in localized and systemic scleroderma--a clinical study. 226 81

We studied the therapeutic action of CO2 Laser on leg ulcers due to chronic venous hypertension in 30 subjects. Our findings show good results in reducing pain and leg oedema and wound healing.
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PMID:[Defocused CO2 laser in the treatment of leg ulcers. Preliminary results]. 251 23


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