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PubMed2006

An update on the etiology and epidemiology of diabetes mellitus.

Diabetes mellitus is one of the most common endocrine disorders affecting almost 6% of the world's population. The number of diabetic patients will reach 300 million in 2025 (International Diabetes Federation, 2001). More than 97% of these patients will have type II diabetes. The projected increase in the number of diabetic patients will strain the capabilities of healthcare providers the world over. Thus it is of paramount importance to revisit the causes and epidemiology of diabetes mellitus. Diabetes mellitus is caused by both environmental and genetic factors. The environmental factors that may lead to the development of diabetes mellitus include physical inactivity, drugs and toxic agents, obesity, viral infection, and location. While type I diabetes is not a genetically predestined disease, an increased susceptibility can be inherited. Genetic susceptibility plays a crucial role in the etiology and manifestation of type II diabetes, with concordance in monozygotic twins approaching 100%. Genetic factors may have to be modified by environmental factors for diabetes mellitus to become overt. An individual with a susceptible gene may become diabetic if environmental factors modify the expression of these genes. Since there is an increase in the trend at which diabetes prevail, it is evident that environmental factors are playing a more increasing role in the cause of diabetes mellitus. The incidence of type I diabetes ranged from 1.9 to 7.0/100,000/yr in Africa, 0.13 to 10/100,000/yr in Asia, approximately 4.4/100,000/yr in Australasia, 3.4 to 36/100,000/yr in Europe, 2.62 to 20.18/100,000/yr in the Middle East, 7.61 to 25.7/100,000/yr in North America, and 1.27 to 18/100,000/yr in South America. The epidemiology of type II diabetes is equally bleak. The prevalence of type II diabetes ranged from 0.3 to 17.9% in Africa, 1.2 to 14.6% in Asia, 0.7 to 11.6% in Europe, 4.6 to 40% in the Middle East, 6.69 to 28.2% in North America, and 2.01 to 17.4% in South America.

Africa↗
PubMed1997

Prospective randomised study of intensive insulin treatment on long term survival after acute myocardial infarction in patients with diabetes mellitus. DIGAMI (Diabetes Mellitus, Insulin Glucose Infusion in Acute Myocardial Infarction) Study Group.

OBJECTIVES: To test the hypothesis that intensive metabolic treatment with insulin-glucose infusion followed by multidose insulin treatment in patients with diabetes mellitus and acute myocardial infarction improves the prognosis. DESIGN: Patients with diabetes mellitus and acute myocardial infarction were randomly allocated standard treatment plus insulin-glucose infusion for at least 24 hours followed by multidose insulin treatment or standard treatment (controls). SUBJECTS: 620 patients were recruited, of whom 306 received intensive insulin treatment and 314 served as controls. MAIN OUTCOME MEASURE: Long term all cause mortality. RESULTS: The mean (range) follow up was 3.4 (1.6-5.6) years. There were 102 (33%) deaths in the treatment group compared with 138 (44%) deaths in the control group (relative risk (95% confidence interval) 0.72 (0.55 to 0.92); P = 0.011). The effect was most pronounced among the predefined group that included 272 patients without previous insulin treatment and at a low cardiovascular risk (0.49 (0.30 to 0.80); P = 0.004). CONCLUSION: Insulin-glucose infusion followed by intensive subcutaneous insulin in diabetic patients with acute myocardial infarction improves long term survival, and the effect seen at one year continues for at least 3.5 years, with an absolute reduction in mortality of 11%. This means that one life was saved for nine treated patients. The effect was most apparent in patients who had not previously received insulin treatment and who were at a low cardiovascular risk.

Aged↗
PubMed1991

HLA antigens in insulin-dependent diabetes mellitus.

Diabetes mellitus is largely determined by genetic factors but environmental factors are necessary to convert genetic susceptibility into overt disease. Studies of twins show that the genetic impact in non-insulin-dependent diabetes mellitus is stronger than in insulin-dependent diabetes mellitus. The genetic factors involved in non-insulin-dependent diabetes mellitus are not known and the outcome of molecular genetic research has so far been disappointing. The major genetic susceptibility to insulin-dependent diabetes mellitus is conferred by genes in the HLA region on chromosome 6. Despite many advances in molecular genetics in insulin-dependent diabetes mellitus the serologically detectable HLA antigens and haplotypes are still the best available markers. This review describes the important developments in immunogenetics in insulin-dependent diabetes mellitus and summarises the main findings from earlier studies. Genetically the potential for primary prevention of insulin-dependent diabetes mellitus already exists and will become a reality as soon as the environmental determinants are identified. A wide application of immunogenetic methods will be needed in the prevention of insulin-dependent diabetes mellitus.

Chromosomes, Human, Pair 6↗
PubMedDate not supplied

[Rehabilitation after stroke in patients with diabetes mellitus].

Diabetes mellitus is not only one of the fundamental risk factors for stroke, but it may also constitute a significant impediment and limitation of rehabilitation process in diabetic patients after stroke. Insufficiently controlled diabetes or insufficient insulin therapy inadequately carried out, especially during the period of acute cerebrovascular complications, may increase the risk of repeated stroke or increase the size of ischaemic area. In patients suffering from diabetes the course of stroke is more severe, cerebral oedema appears more often and mortality is higher. In the present paper methods of rehabilitation and results achieved in a group of patients with stroke and a group of patients with stroke and diabetes mellitus are described, as well as effects of rehabilitation in both those groups. Fifty one (20%), out of 251 patients with cerebral stroke in the past who were rehabilitated in a Rehabilitation Department in 1997, had diabetes mellitus lasting, on average, 21 years. Individual rehabilitation programme for each patient was arranged collectively, taking into consideration restrictions necessary in the course of diabetes, including education of patients. Multidirectional assessment of initial condition and condition after termination of the rehabilitation was carried out taking into consideration the scale of lesions (the Brunnstrom stages), functional scales and the quality of life index (the Barthel index). More objective parameters, i.e. the index of symmetry of loading of lower extremities and walking speed, were also applied. All the patients with both stroke and diabetes mellitus completed the planned rehabilitation programme, although the initial condition of patients with concomitant diabetes was worse than that of patients with stroke only, as far as most of the applied parameters of assessment were concerned. Also improvement achieved in diabetic patients was not observed in each of the parameters examined and differed from that achieved in the group of patients with stroke alone. We found, that in-hospital rehabilitation of patients with stroke and concomitant diabetes mellitus (even long lasting) resulted in a measurable and significant improvement of their condition evaluated multidirectionally, and that diabetes mellitus coexisting with stroke is not a contraindication to in-hospital rehabilitation. In patients with concomitant diabetes mellitus significant disturbances of during the rehabilitation were not found course diabetes mellitus. However they all required meticulous care and monitoring of carbohydrate metabolism, and the average time of their hospitalisation was longer by about 3 days.

Adult↗
PubMed2005

Depressed cardiac myofilament function in human diabetes mellitus.

Diabetes mellitus is associated with a distinct cardiomyopathy. Whether cardiac myofilament function is altered in human diabetes mellitus is unknown. Myocardial biopsies were obtained from seven diabetic patients and five control, nondiabetic patients undergoing coronary artery bypass surgery. Myofilament function was assessed by determination of the developed force-Ca2+ concentration relation in skinned cardiac cells from flash-frozen human biopsies. Separate control experiments revealed that flash freezing of biopsy specimens did not affect myofilament function. All patients in the diabetes mellitus cohort were classified as Type 2 diabetes mellitus patients, and most showed signs of diastolic dysfunction. Diabetes mellitus was associated with depressed myofilament function, that is, decreased Ca2+ sensitivity (29%, P < 0.05 vs. control) and a trend toward reduction of maximum Ca2+-saturated force (29%, P = 0.08 vs. control). The slope of the force-Ca2+ concentration relation (Hill coefficient) was not affected by diabetes, however. We conclude that human diabetes mellitus is associated with decreased cardiac myofilament function. Depressed cardiac myofilament Ca2+ responsiveness may underlie the decreased ventricular function characteristic of human diabetic cardiomyopathy.

Actin Cytoskeleton↗
PubMed2000

Stress and coping behavior in patients with diabetes mellitus.

Diabetes mellitus is a disease which must be controlled over the lifetime of a patient. We investigated the issues of stress and coping for diabetes mellitus which may influence self-management. In addition, we examined the association of these factors with blood glucose control, in order to review self-management instructions for diabetes mellitus. The study included 153 patients with diabetes mellitus. The patients were divided into two subgroups: good-control group, comprising patients with glycohemoglobin (HbA1c) values less than 7.0%; and poor-control group, comprising those with HbA1c values of 7.0% or more. All patients responded to a questionnaire regarding stress tolerance, Jalowiec and Power's coping scale and awareness of diabetes mellitus. Stress tolerance was not significantly different between the good-control and poor-control groups. No significant gender differences in coping score were evident for the good-control group. However, in the poor-control group, the coping score in men was significant higher than that in women. The problem-oriented coping score for men in the poor-control group was significantly higher than that for the good-control group (p < 0.01). In a comparison of awareness of diabetes mellitus, the proportion of patients who replied that they were rigidly following diabetes treatment was higher in the poor-control group than the good-control group. Patients with diabetes mellitus may have a knowledge of the disease and a strong will to resolve problems. This is especially true for male patients in that their will appeared to be stronger, but they may not have the resolve to establish appropriate behavior patterns. In the future, methods for evaluating self-management should be included in diabetes education.

Adaptation, Psychological↗
PubMed2000

Periodontal management of the patient with diabetes mellitus.

Diabetes mellitus is a common medical disorder that will be encountered by every practicing dentist. Knowledge by the dentist of the general and oral signs and symptoms of undiagnosed or poorly controlled diabetes mellitus are essential, and patients displaying these signs or symptoms should receive medical referral. Patients suspected, or known to suffer from undiagnosed or uncontrolled diabetes mellitus should receive only emergency care until their health status has been properly evaluated. In the event the degree of control of a known diabetic is unknown or the patient is poorly controlled, antibiotic therapy should be administered in conjunction with any necessary surgical procedure or in the presence of oral infection. The practitioner must be prepared to manage diabetic emergencies should they occur in the dental office, and hypoglycemic incidents are most likely. The developing therapies now available for medical management of diabetes mellitus suggest that this condition will be more effectively controlled in the future, but medical consultation is important to proper periodontal patient management. New evidence suggests that advanced periodontal disease may interfere with diabetes mellitus control and the physician should be made aware of the patient's periodontal status. Under most circumstances, the well-controlled diabetes mellitus patient can receive safe and effective periodontal therapy with some modification of office protocol, and there is little reason to anticipate that the controlled diabetes mellitus patient cannot look forward to a lifetime of periodontal health if proper and timely periodontal therapy is rendered and the patient maintains effective oral hygiene measures accompanied by appropriate supportive periodontal recall therapy.

Dental Care for Chronically Ill↗
PubMed2006

Role of islet amyloid in type 2 diabetes mellitus.

Diabetes mellitus is one of the most common metabolic diseases worldwide and its prevalence is rapidly increasing. Due to its chronic nature (diabetes mellitus can be treated but as yet not cured) and its serious complications, it is one of the most expensive diseases with regard to total health care costs per patient. The elevated blood glucose levels in diabetes mellitus are caused by a defect in production and/or secretion of the polypeptide hormone insulin, which normally promotes glucose-uptake in cells. Insulin is produced by the pancreatic 'beta-cells' in the 'islets of Langerhans', which lie distributed within the exocrine pancreatic tissue. In type 2 diabetes mellitus, the initial defect in the pathogenesis of the disease in most of the patients is believed to be 'insulin resistance'. Hyperglycemia (clinically overt diabetes mellitus) will not develop as long as the body is able to produce enough insulin to compensate for the reduced insulin action. When this compensation fails ('beta-cell failure') blood glucose levels will become too high. In this review, we discuss one of the mechanisms that have been implicated in the development of beta-cell failure, i.e. amyloid formation in the pancreatic islets. This islet amyloid is a characteristic histopathological feature of type 2 diabetes mellitus and both in vitro and in vivo studies have revealed that its formation causes death of islet beta-cells. Being a common pathogenic factor in an otherwise heterogeneous disease, islet amyloidosis is an attractive novel target for therapeutic intervention in type 2 diabetes mellitus.

Amyloid↗
PubMedDate not supplied

Cerebral circulation during diabetes mellitus.

Diabetes mellitus is characterized by hyperglycemia, a decrease in circulating insulin and the development of macro- and microvascular pathology. Hyperglycemia appears to be a primary determinant for the structural, biochemical and functional changes that occur in large and small blood vessels during diabetes mellitus. While much research has focused on the effects of diabetes mellitus on the peripheral circulation, it is clear that diabetes mellitus also has profound effects on the cerebral circulation. Thus, the focus of this review is to discuss morphological and functional alterations in the cerebral circulation during diabetes mellitus.

Animals↗
PubMed2004

[Skin changes in diabetes mellitus].

Diabetes mellitus is the most frequent metabolic disorder. Just under 5 million people suffer from this disease in Germany. Four types of diabetes mellitus are distinguished: type 1 diabetes, type 2 diabetes, other specific diabetes forms, and gestational diabetes. Many characteristics of diabetes mellitus including skin changes are already manifest in the "prediabetic" stage when glucose tolerance is limited so that every elevation of blood sugar levels must be considered pathological. Changes in skin due to diabetes mellitus can be categorized into four disease groups: skin infections, skin diseases found overly frequently in association with diabetes mellitus, skin alterations due to diabetic complications, and reactions to antidiabetic treatment.

Diabetes Complications↗
PubMed1997

Renoprotection and renin-angiotensin system blockade in diabetes mellitus.

Diabetic nephropathy is the most common cause of end-stage renal disease (ESRD) in the United States, and accounts for 35% of all the patients with ESRD entering a dialysis program; 63% of patients with diabetic nephropathy have type II diabetes mellitus. Hypertension is a major risk factor for renal disease and is common in people with diabetes mellitus. Strategies for preventing the progression of renal failure in patients with diabetes mellitus include glycemic control, and control of blood pressure. Blocking the renin-angiotensin system (RAS) slows the progression of established diabetic nephropathy in type I diabetes mellitus, and inhibiting angiotensin II formation retards or impedes the progression from microalbuminuria to established diabetic nephropathy (macroproteinuria) in people with type I diabetes mellitus. The situation could be the same for people with type II diabetes mellitus. The ability of RAS blockade using irbesartan, an AT1 angiotensin II receptor antagonist, to slow the progression in renal failure has been compared with that of the calcium channel blocker amlodipine and placebo in a pilot study. The results suggest that blockade of the RAS, in this case with irbesartan, is at least equivalent to calcium channel blockers with respect to antihypertensive efficacy, but provides better renoprotective benefits.

Amlodipine↗
PubMed2004

Other glomerular pathologies in three patients with diabetes mellitus.

Diabetic nephropathy is the common cause of end stage renal disease in diabetes mellitus. But other glomerular pathologies have been also described in diabetic patients. We described 3 cases with diabetes mellitus and other glomerular diseases. Case I: A 59-year-old male patient with type 2 diabetes mellitus for 4 years was evaluated for generalized edema. Physical examination showed pretibial edema and no diabetic retinopathy. The cause of nephrotic syndrome was membranoproliferative glomerulonephritis. Conservative therapy could not control the severe proteinuria and renal dysfunction. With corticosteroid and cyclophosphamide therapy partial remission was obtained. Case II: A 46-year-old diabetic woman was evaluated for severe proteinuria. Diabetic retinopathy was not found on her funduscopic examination. Mesangioproliferative glomerulonephritis was found on renal biopsy. Proteinuria did not regress with conservative therapy and corticosteroid and cyclophosphamide. Case III: A 48-year-old male patient with diabetes mellitus type 2 for 2 years was admitted to the hospital because of nephrotic syndrome and weakness. At another hospital his diagnosis with biopsy showed minimal change disease. He was treated with corticosteroid since 3 months. His renal biopsy was reevaluated and found amyloid deposition but not diabetic nephropathy or minimal change disease. In diabetic patients, nondiabetic nephropathy is not uncommon and it was reported as common as about 30%. In addition to therapy for diabetes mellitus these patients can need specific therapy.

Amyloidosis↗