Biophysical characteristics of skin in diabetes: a controlled study

Background  Cutaneous complications are common in diabetes. Previous assays suggest that hyperglycemia and decreased insulin signal are involved in the impairment of skin function. The aim of this study was to evaluate the biophysical characteristics of skin in patients with diabetes mellitus and compares them with healthy non-diabetic controls.
Objective  To measure biophysical characteristic of skin including transepidermal water loss (TEWL), water content, sebum and skin elasticity in patients with diabetes mellitus and compare them with healthy non-diabetic controls.
Methods  This case-control study was conducted on 38 patients with diabetes and 40 age- and sex-matched healthy people. The biophysical properties of skin including stratum corneum (SC) hydration, sebum content, TEWL and skin elasticity were measured and compared between the two groups at three different locations of the body.
Results  The measurement of SC hydration and TEWL showed no significant difference between diabetics and controls. The skin surface lipids on the forehead but not other sites were significantly lower in the diabetics than in the controls. Acoustic wave propagation speed, a measurement related to skin elasticity, was significantly lower in forearm and forehead of diabetics.
Conclusion  Diabetes affects some functional properties of epidermis and dermis that may responsible for many cutaneous manifestations of diabetes. These results suggest that patients with diabetes mellitus tend to show a normal hydration state of the SC together with decreased sebaceous gland activity and impaired skin elasticity, without any impairment of the SC barrier function.

Conflicts of interest

None declared     

ACUTE EFFECTS OF ORAL GLIBENCLAMIDE ON BLOOD PRESSURE AND FOREARM VASCULAR RESISTANCE IN DIABETICS

1. To determine the effects of an acute oral dose of glibencla-mide on blood pressure (BP), basal forearm vascular resistance (FVR) and FVR responses to the K⁺_ATP channel activating vasodilator diazoxide, a placebo-controlled, double-blind cross-over study was performed in eight male volunteers with non-insulin-dependent diabetes mellitus. 2. Changes in vascular responses to progressively increasing concentrations of diazoxide (3.75–30 mg/kg per min) and noradrenaline (25–100 ng/kg per min) were measured by venous occlusion plethysmography. 3. Glibenclamide significantly lowered plasma glucose levels compared with placebo (P < 0.02) and attenuated the decrease in FVR (P < 0.05) and the decrease in systolic BP (P < 0.05) that followed a meal. However, vasodilator responses to diazoxide were potentiated by the administration of oral glibenclamide (P < 0.01). 4. Acute administration of oral glibenclamide attenuates the normal decrease in FVR and systolic BP that follows a meal and potentiates rather than inhibits forearm vasodilator responses to intra-arterial diazoxide, probably via indirect humoral effects. These results suggest that glibenclamide has direct or indirect vasoconstrictor effects that antagonize the normal increase in forearm blood flow that follows a meal and that the inhibition of vascular K⁺ATP channels following acute oral glibenclamide administration is clinically insignificant compared with other indirect vascular effects of the drug.     

Iopamidol and meglumine diatrizoate: comparison of effects on patient discomfort during aortofemoral arteriography

Iopamidol was compared with Renografin-60 (meglumine diatrizoate, Squibb) in a controlled, randomized double-blind study of 40 patients undergoing peripheral arteriography for arteriosclerotic occlusive disease to determine which agent caused less discomfort. Each patient was evaluated for objective signs of discomfort and subjective feelings of pain and heat. Monitoring was achieved by multiple physical examinations, chemical tests, electrocardiograms, and intra-arterial pressure recordings. It is concluded that iopamidol is safe and causes significantly less patient discomfort than Renografin-60.     

Effect of chronic ethanol ingestion on the metabolism of copper, iron, manganese, selenium, and zinc in an animal model of alcoholic cardiomyopathy

Alcoholic cardiomyopathy (AC) is one of the diseases caused by alcohol abuse, and there has been considerable debate about the possibility that nutritional factors may be important in the etiology of AC. In addition, there is evidence that ethanol may affect the metabolism of trace elements. The purpose of this investigation was to determine if chronic ethanol administration produces changes in the metabolism of the essential metals copper, iron, manganese, zinc, and selenium using an animal model of AC. Eighteen male Sprague-Dawley rats were divided into three groups: an ad libitum control group (AL), a pair-fed control group (PF), and an ethanol-dosed group (ETOH). The latter group received gradually increasing concentrations (5-25%) of ethanol in the drinking water for 15 wk. Food intake was monitored and urine and feces collected for a 4-d period during the study to determine ethanol effects on trace-element balance. Growth of both the PF and ETOH animals was inhibited. Ethanol produced substantial increases in liver manganese and decreases in liver copper and zinc. Metal concentrations in heart and concentrations in other tissues studied (spleen, testes, brain, bone, kidney, and muscle) did not differ significantly among the groups, except for testes selenium and kidney zinc. Reduced food intake and ethanol ingestion were associated with a reduced percentage of ingested selenium excreted in the urine. Deficiencies of copper, iron, manganese, selenium, and zinc in myocardial tissue are not likely to be involved in the pathogenesis of AC in the rat.     

Prostaglandins and angioplasty. An experimental study in canine arteries

To prevent platelet aggregation following percutaneous transluminal angioplasty (PTA), cyclooxygenase inhibitors such as acetylsalicylic acid (ASA) and indomethacin are recommended. However, ASA blocks both the proaggregating effects of thromboxane (TXA2) and the antiaggregating and vasodilating effects of prostacyclin (PGI2). The authors measured the contractile response of dilated canine carotid arteries in situ and in vitro using an isometric force transducer. Following PTA, contraction of the arterial wall was significantly reduced (p less than 0.01). By blocking cyclooxygenase with indomethacin (3 micrograms/ml), contraction was greatly improved (p less than 0.001). These results suggest that PTA may result in marked release of prostacyclin by the damaged arterial wall, which could account for the decreased responsiveness of the artery to exogenous norepinephrine.