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Maintenance hemodialysis and renal transplantation are increasingly used for treating diabetic patients with end-stage renal failure. The use of the artificial pancreas is able to prevent large blood glucose fluctuations in these patients with atherosclerosis, advanced retinopathy or neuropathy in which hyper- and hypoglycemia are potentially deleterious. For this purpose, we have developed and are utilizing an artificial pancreas easily utilizable without special training by the staff of a dialysis unit. This artificial pancreas uses a polarographic glucose electrode with a fast response time (45 to 90 seconds), a terminal display for operator communication, and a continuous digital and analogyl display for control of the running operation. There is also a printer to display in tabular and graphical form the values at any time during the operation. In this preliminary study, 7 patients have been studied: five under repetitive hemodialysis for four hours, 3 times a week; one treated by peritoneal dialysis for 12 hours, twice a week and one controlled during, and 48 hours after, renal transplantation. The macroscopic pancreas normalizes blood glucose under these circumstances, helps in a better understanding of blood glucose homeostasis in uremic patients under dialysis, leads to a more precise evaluation of insulin needs, may help to improve the nutritional status of the patients, and has an educational value for the patient and the medical staff.
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PMID:The use of the artificial pancreas in uremic diabetic patients. 39 76

Energy-calorie malnutrition (ECM) is the commonest nutritional problem in developing countries in Africa: 0.5-5% of the population under 6 years of age suffer from the severe forms and 4-40% from the moderate forms. It is possible that as many as two-thirds of the preschool children in developing countries in Africa suffer from some EPM (protein-calorie malnutrition). The recent Sahelian drought and civil wars in some countries in Africa have increased the size of the problem and the severity and prevalence of EPM in several parts of Africa. The aetiological factors of EPM in Africa include shortage of calories and protein, as well as increasing and recent tendency to abandon too early breast feeding, sensory deprivation, psychological and emotional trauma, ignorance, superstition and cultural taboos. The evidence available at the moment does not clearly indicate that effects of EPM on learning and behaviour are permanent, although the functions of the brain in the acutely malnourished child are defective. Malnutrition impairs immunological capability and surveillance, and hence augments the mortality and morbidity of infections such as measles especially by impairing cell-mediated immunity and, to a lesser extent, synthesis of immunoglobulins. Endemic goitre (prevalence varies from 2 to 90% in various age groups) in several parts of Africa is due to either iodine deficiency (Ethiopia) or to the goitrogenic effect of cassava diet (Zaire and Nigeria). Deficiencies of vitamins A, B complex and D have been reported in several parts of Africa, albeit sporadically. Dietary intoxications include: a) aflatoxins which may be important in the pathogenesis of hepatic carcinoma, one of the commonest neoplasms in developing countries in Africa; b) chronic cyanide intoxication from cassava (manihot) food derivatives, which on circumstancial evidence seems to be an important aetiological factor of a crippling neurological disease, the tropical ataxic neuropathy in Nigeria and Tanzania; c) organophosphate insecticides. The rarity of certain diseases in the Africans may be related specifically to the African diet, especially the high fibre and low animal fat content of many of the African diets. Examples of such diseases are atherosclerosis in the non-hypertensive non-diabetic population, cancer of the large bowel, varicose veins and perhaps multiple sclerosis.
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PMID:Nutritional problems in the African region. 82 71

Considerable evidence points to a metabolic cause for the long-term complications of diabetes--neuropathy, retinopathy, nephropathy and atherosclerosis. Recent studies suggest potential benefits from controlling hyperglycemia as well as possible. However, the individual physician must analyze the evidence for himself and then decide on which principles to base the treatment of his patients.
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PMID:Diabetic control and the late complications of diabetes. 88 56

We report the clinical and pathologic features of a patient with peripheral neuropathy that was the first clinical expression of cholesterol emboli syndrome (CES). Biopsy of skeletal muscle and peripheral nerve revealed cholesterol clefts in lumens of small arteries, necrotizing arteritis, and severe degeneration of peripheral and intramuscular nerves. At autopsy, the peripheral nervous system was extensively affected by similar changes. We conclude that (1) peripheral neuropathy may be the initial manifestation of CES. Presumably, deposition of cholesterol leads to arteritis. (2) The underlying pathology of CES neuropathy is chronic axonal degeneration, possibly due to chronic ischemia of epineurial arteries. (3) Muscle biopsy is important in the antemortem diagnosis of CES. Nerve biopsy may show involvement of epineurial vessels. (4) CES may resemble polyarteritis nodosa clinically and pathologically. (5) CES may be under-recognized and should be included in the differential diagnosis of any neuropathy of uncertain cause, particularly when there is a history of vascular catheterization, or severe aortic atherosclerosis.
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PMID:Cholesterol emboli neuropathy. 131 May 30

Recent progress in structure elucidation of products of the advanced Maillard reaction now allows probing specifically for the role of this reaction in the pathogenesis of age- and diabetes-related complications. Pyrraline is a glucose-derived advanced glycation end product against which polyclonal and monoclonal antibodies have been raised. Immunohistochemical localization studies revealed that pyrraline is found predominantly in the sclerosed extracellular matrix of glomerular and arteriolar renal tissues from both diabetic and aged nondiabetic individuals. Pentosidine and carboxymethyllysine are Maillard end products derived from both glucose and ascorbate. In addition, pentosidine can be formed from several other sugars under oxidative conditions, and in vitro studies suggest that a common intermediate involving a pentose is a necessary precursor molecule. The highest levels of these advanced Maillard products are generally found in the extracellular matrix, but these products are also present in lens proteins and in proteins with a fast turnover such as plasma proteins. Diabetes, and especially uremia, greatly catalyzes pentosidine formation. Both conditions are characterized by accelerated cataractogenesis, atherosclerosis, and neuropathy, suggesting that molecular damage by advanced Maillard reaction products may be a common mechanism in their development.
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PMID:Maillard reaction-mediated molecular damage to extracellular matrix and other tissue proteins in diabetes, aging, and uremia. 152 33

Risk factors of tissue hypoxia was investigated in 26 patients with diabetic retinopathy (DMR), who compared with 62 patients without DMR. significant higher incidence of DMR was found in patients with poor diabetic control (HbA 1 greater than or equal to 10%), with orthostatic hypotension (OH), with peripheral neuropathy and with atherosclerosis respectively. Erythrocyte 2,3-diphosphoglycerate (2,3-DPG) was lower (P less than 0.05) and venous oxygen tension in pedal dorsum (PvO2) higher (P less than 0.05) in DMR patients than those in uncomplicated DMR patients and normal subjects. There was a rank correlation between DMR severity and PvO2 (r = 0.429, P less than 0.05), which imply that decreased blood oxygen utilization may be related to diabetic microangiopathy. These data suggested that abnormal changes of HbA 1 and 2,3-DPG, decrease of peripheral blood oxygen utilization, atherosclerosis, OH and neuropathy might be risk factors of tissue hypoxia in DMR patients.
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PMID:[Study on risk factors of tissue hypoxia in patients with diabetic retinopathy]. 158 45

Diabetes mellitus is associated with significant morbidity and mortality caused by the micro- and macro-vascular complications that all too frequently develop during the lifetime of the diabetic patient. In attempts to treat the complications of diabetes, several different treatment strategies have been investigated. The role of tight blood glucose control in the treatment of diabetic vascular complications has recently been challenged, as the existing data in support of this mode of therapy are currently inconclusive. Perhaps more effective in preventing many of the vascular complications is the rigorous treatment of hypertension that frequently accompanies diabetes mellitus. Epidemiological studies have demonstrated that the presence of hypertension significantly contributes to the development and progression of diabetic nephropathy, retinopathy, cardiovascular disease, and possibly neuropathy. Preliminary clinical studies demonstrate that the progression of diabetic renal disease can be slowed by vigorous antihypertensive therapy. Among the various antihypertensive agents used to treat the hypertension associated with diabetes mellitus, calcium channel blockers are emerging as one of the agents of first choice. This is because of their very low side effect profile and their absence of detrimental effects on serum lipid levels and glucose tolerance. Calcium channel blockers may be of additional potential benefit to the diabetic patient by slowing the progression of atherosclerosis, reversing the intracellular calcium defects that may contribute to the pathogenesis of diabetic cardiomyopathy, and protecting against the progression of chronic renal disease.
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PMID:The future of calcium channel blocker therapy in diabetes mellitus. 172 50

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

Estimates of the cost of diabetes should take into account the development of complications. Patient records identified from the 1987 National Hospital Discharge Survey were used to evaluate the risk of hospitalization due to late complications. Hospitalization for diabetic nephropathy reached a peak of 6.74/1000 between the ages of 45 and 54 years, compared to 0.14 to 1.80/1000 in controls. Diabetic patients less than or equal to 45 years of age were 46 times more likely to be hospitalized due to neuropathy. The risk of cardiovascular complications is high, with a greater incidence of arterial than venous disorders. Diabetic patients were 22 times more likely to be admitted for skin ulcers/gangrene, 15 times more likely due to peripheral vascular disease, and 10 times due to atherosclerosis. The risk of cerebrovascular accident and heart disease was 6 to 10 times greater in diabetic patients. Seventy-five per cent of diabetic cardiovascular disorders are myocardial infarction or chronic ischaemia. Hospitalization from renal complications occurs at younger ages than in the general population. Ophthalmic complications increase with age. Diabetic complications account for 2% of the total hospital admissions in the US in 1987. The total cost of the treatment of late diabetic complications was estimated at +5091 million (cardiovascular 74%; renal diseases 10%; nephropathy 3.6%; ophthalmic disorders 1.5%; other unspecified diseases 10%).
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PMID:The cost of hospitalization for the late complications of diabetes in the United States. 182 50

The effects of first generation sulphonylurea compounds carbutamide, gliclazide and tolbutamide as well as second generation compounds glibenclamide and glipizide on the cardiovascular system were investigated in dogs. Six dogs received each compound intravenously at cumulative dose levels of 74, 296, 1184 mumol/kg of carbutamide and tolbutamide, 0.4, 2.0, 10.0 mumol/kg of glibenclamide and glipizide, and 16, 48 and 144 mumol/kg of gliclazide. Mean arterial blood pressure, myocardial contractile force, cardiac output and heart rate were measured. The rate of change of myocardial contractile force development (positive dF/dt), as well as of myocardial relaxation (negative dF/dt) were measured. The first generation sulphonylureas were found, in dogs, to exert a positive inotropic effect in contrast to second generation compounds. The clinical importance of our findings may be in the potential for the malfunction of the cardiovascular system (based on cardiopathy, neuropathy, atherosclerosis, and obesity), developing in diabetes, to be further impaired by the first generation sulphonylureas. Therefore, second generation sulphonylureas should be preferred in the therapy of type 2 diabetics, if satisfactory metabolic control cannot be achieved by dietary management alone and sulphonylurea treatment becomes necessary.
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PMID:Direct effect of hypoglycemic sulphonylureas on the cardiovascular system of dogs. 201 35


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