[Effect of anthocyanosides on the capillary fragility of the eye in diabetes and arterial hypertension].
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Plasma total ascorbate status measured by 2.4 dinitrophenyl hydrazine method showed that diabetics (N = 100) had significantly lower plasma total ascorbate compared with 45 age and sex matched non-diabetic controls; 0.34 +/- 0.16 mg/dl vs 0.68 +/- .06 mg/dl, P less than 0.001) regardless of presence or absence of retinopathy and irrespective of mode of treatment. The finding unique to this study was that plasma total ascorbate status in diabetics with retinopathy (0.19 +/- 0.07 mg/dl) was significantly lower than that of uncomplicated diabetics (0.49 +/- 0.06 mg/dl; P less than 0.001). Plasma Glucose had no correlation with plasma ascorbate levels and effect of duration of Diabetes Mellitus (DM) on ascorbate status in diabetics was ambiguous. Diabetics had abnormally fragile cutaneous capillaries detected by Hess test. The incidence of capillary fragility was more in patients with retinopathy. Hess test can be used as an easy and non-invasive test to assess plasma ascorbate status to detect microvascular involvement in DM. The experience of this study reflects that the two distinct microvascular lesions in diabetes, i.e. abnormal dermal capillary fragility and retinopathy may have a common link to ascorbic acid deficiency. An early switching on of the supplementation of ascorbic acid may retard the development of microvascular complications in diabetes.
Hypertension (210 mm Hg), hyponatremia, hypochloremia, and hypokalemia were observed in an 11-day-old infant. After electrolyte repletion, blood pressure rose to 320 mm Hg in spite of administration of antihypertensive drugs. The child died of a massive cerebral hemorrhage on the 17th day of life. At autopsy, the left renal artery was partially thrombosed and the left kidney partially infarcted. The glomeruli in the preserved cortical areas were of normal size; the juxtaglomerular apparatuses markedly enlarged. The blood vessels were inconspicuous. Enlarged glomeruli, multiple ruptures in the mesangium, ectactic glomerular capillaries, and fragile capillary walls were found in the nonconstricted right kidney. Fibrinoid necrosis with occasional fibrin thrombi in the lumina was present in the arterioles. Pronounced intimal edema with fragmented cells and monocytes embedded in the intima were observed in the interlobular and larger arteries. The histologic findings in the blood vessels of the nonconstricted kidney resembled those found in the hemolytic-uremic syndrome (Gasser's syndrome).
Medical practitioners often have difficulty in assessing the presence or severity of diabetic retinopathy. The tourniquet test is a method of assessing diabetic capillary fragility that has been felt to reliably correlate with background and proliferative diabetic retinopathy. We studied 100 consecutive diabetic patients and 50 age-matched controls in a masked fashion, using fundus photographs and fluorescein angiography to correlate the amount of capillary fragility with the presence and severity of background and proliferative diabetic retinopathy. Although the severity of diabetic capillary fragility did correlate with the presence and severity of diabetic retinopathy (p less than 0.001), this test was not as good an indicator of diabetic retinopathy as were other risk factors such as duration of diabetes (p much less than 0.001). The tourniquet test is unreliable in predicting the presence or severity of diabetic retinopathy because of its high false negative response rate.
The incidental discovery of scurvy in a patient with a symptomatic hiatal hernia has led to the identification of 9 other individuals with chemically proved vitamin C deficiency secondary to an expressed aversion to "acid" food in any form. These patients were screened with capillary fragility tests and serum ascorbic acid determinations from approximately 200 hiatal hernia and reflux patients. With resumption of a normal vitamin C intake, scattered deficiency symptoms disappeared and both capillary fragility tests and serum ascorbic acid levels returned toward normal. There were no wound healing problems.
Features of metabolism and haemostasis which are different in diabetics of both types in comparison with normal subjects were covered by the statistical method of multivariance analysis depending on the severity of diabetic retinopathy. In 29 diabetics without retinopathy, 46 patients with stage I or II, and 36 patients with stage III the following parameters could be found as optimal criteria for characterizing the extent of vascular changes: blood sugar concentration, concentration of sialic acid and HDL cholesterol in the serum, serum protein, sialic acid per protein volume, total cholesterol in the serum and capillary fragility and number of large spreading forms of platelets features of hemostasis. Thus, diabetic retinopathy is characterized by a wide spectrum of different features containing the parameters of hemostasis. Thrombocytic vascular interactions are characterized by platelet spreading and capillary fragility which are significant for the development of diabetic retinopathy.
In a short-time study, 8 patients with thrombocytopenia and clinical signs of bleeding were experimentally treated with prednisolone as the only therapeutic measure to control the bleeding tendency. 2 patients had idiopathic thrombocytopenic purpura and 6 acute non-lymphocytic leukaemia. 1 of the leukaemic patients was thrombocytopenic on admission. 5 had thrombocytopenia due to antileukaemic chemotherapy. The capillary fragility test, evaluated blindly, and bleeding time determination were performed just before treatment and repeated once after 2-4 d of treatment. Platelet counts were carried out simultaneously. Capillary resistance, determined by the capillary fragility test, improved greatly during the administration of prednisolone, irrespective of the platelet count, and no serious bleeding occurred. The bleeding time remained prolonged.
The mechanisms responsible for progestogen-induced breakthrough bleeding remain unexplained. The aim of the present study was to examine the expression of three basement membrane components, collagen IV (CIV), laminin and heparan sulphate proteoglycan (HSPG), by immunohistochemistry in sections of endometrium from women receiving the subdermal levonorgestrel implant (Norplant) and normally cycling women. Control biopsies were obtained from 20 normal subjects from Melbourne, Australia, and pre- and post-Norplant-insertion biopsies were obtained from 11 women from Sydney, Australia, with between 3 and 6 months Norplant exposure. It was postulated that in Norplant users a decrease in the amount of basement membrane material present around endometrial vessels may be responsible for increased capillary fragility. The results, however, showed that for all three components, Norplant biopsies exhibited vascular basement membrane immunostaining at least as intense as that found in the mid-late secretory phase of the normal cycle. During the normal cycle, HSPG was only detected in approximately 40% of vessels with CIV and laminin immunoreactivity, and menstrual biopsies demonstrated reduced staining for all three components. Several biopsies exhibited a degree of regional variability in staining intensity, and Norplant biopsies exhibited areas of discrete, decidual-like stromal immunostaining for CIV and laminin. Although no differences were found in microvascular basement membranes in Norplant users that might explain capillary fragility, it is possible that other techniques could yield information on changes in the integrity of basement membrane components that might influence basement membrane strength.
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The author's theory of the endoendothelial fibrin lining (EEFL), first advanced in 1953 and developed by him ever since, localizes the homeostasis between steady fibrin formation and deposition, or 'fibrination', and continuous fibrinolysis in the more or less immobile portion of the plasmatic zone next to the vessel wall. In 1971, the author advanced, in relation to the EEFL, the theory of fibrinogen gel clotting without thrombin action or 'fibrinogenin' formation in vivo. Considerable direct and indirect experimental evidence, secured by the author and by several other investigators, advanced markedly the knowledge of the normal physiology and the pathophysiology of various disease processes involving the vessel wall and blood circulation. The information presented is an extension to that given in the author's recent overview (Clin. Hemorheology 1, 9-72, 1981). It deals both with new data by several investigators including those by the author, as well as with older data from the literature. The author maintained already in 1960 that the blood together with the blood vessels, in which it circulates, constitute 'an entity'. In 1981 he postulated this entity to be a very special organ, named conveniently 'vessel-blood organ', which is ubiquitous and penetrates all other organs and adjacent tissues. The EEFL of the vessel-blood organ is considered by the author as the crucial critical interface between the blood and the vessel wall. It is the primary barrier, followed by the endothelium (comprising the endothelial cells and the interendothelial cement substance which contains or is identical with 'cement fibrin') and the basement membrane for the exchanges between the blood, the vessel wall and its surrounding tissues and spaces. The EEFL acts as anticoagulant, is antithrombogenic, maintains vascular patency and aids cardiac action by decreasing significantly the apparent viscosity of blood, referred to in the literature as the 'Copley-Scott Blair phenomenon'. A new concept of leukocyte emigration traversing the capillary wall is presented, affecting focal fibrinolysis of the EEFL and of fibrin contained in the interendothelial cement substance and in the basement membrane. The physical property of capillary (or vascular) permeability is related to the existence of the EEFL, since, as found by Copley et al, both fibrinopeptides, liberated in the transition of fibrinogen to fibrin, and plasminopeptides, freed in the conversion of plasminogen to plasmin, enhance capillary permeability. Capillary fragility, which is antagonistic to capillary permeability, is in great part due to fibrinolytic action on fibrin as a constituent of the basement membrane.(ABSTRACT TRUNCATED AT 400 WORDS)
Our observation concerns a patient aged 29 who has presented for the last two years a smooth lesion, non-infiltrated, golden yellow, and situated on the interior surface of the left knee. This lesion recalls the lichen aureus confirmed by standard histology nad Perls' coloration. There is capillary fragility without plaque anomaly. There is, however, no sign of subjacent venous incompetence.
The findings of subdural hematoma and retinal hemorrhages in infants, without any documented history of major trauma, do not always indicate child abuse. A combination of ascorbate depletion and the injection of foreign proteins can cause a very high blood histamine level, leading to capillary fragility and venular bleeding. This can be prevented by the administration of vitamin C.