Prevalence of diabetic foot disorders and related risk factors among Egyptian subjects with diabetes.

INTRODUCTION: Multiple pathologies including diabetic neuropathy, peripheral vascular disease (PVD) and infection contribute to lower extremities amputation in diabetes. AIM: We examined the prevalence of diabetic foot problems and related risk factors in Egypt. SUBJECTS AND METHODS: Between July 2008 and December 2009, 1000 male and 1000 female consecutive adult patients with diabetes (≥ 18-year-old) attending the Alexandria University Diabetic Foot Screening Clinic were surveyed for history/presence of foot ulcers and/or amputations, skin/nail changes, joint mobility, sensory neuropathy (10 g-Semmes-Weinstein Monofilament) and peripheral vascular disease (PVD) using Ankle Brachial Index (ABI). RESULTS: The majority of patients had type 2 diabetes (96.75%) with a mean age of 57.30 ± 10.47 years and a mean disease duration of 11.76 ± 8.26 years. The mean body mass index was 32.84 ± 6.31 kg/m(2) with 29.55% being current or ex-smokers. In these subjects, 4.4% had a past history of non-traumatic amputation (male:female: 6.2% vs. 2.6%, p < 0.001); 6.1% had past history (10.3% vs. 7%, p = 0.009) and 8.7% had active foot ulceration (8.1% vs. 4.1% p < 0.001) with a male preponderance. The prevalence of sensory neuropathy was 29.3% (M:F: 30.7%: 27.9%) and peripheral vascular disease (PVD) was 11% (M:F 11.8%:10.2%). Diabetic foot complications were associated with disease duration (p < 0.001), history of coronary artery disease (p = 0.001), stroke (p = 0.009), PVD (p < 0.001), laser photocoagulation (p < 0.001), sensory neuropathy (p < 0.001) and renal replacement therapy (p < 0.001). On multivariate analysis, diabetes duration, foot fissures, Charcot's foot, limited joint mobility, PVD and sensory neuropathy remained independently associated with diabetic foot disorders. CONCLUSION: In Egypt, a mosaic of risk factors contributes to the high prevalence of diabetic foot disease in type 2 diabetes. These findings call for regular assessment of vascular, neuropathic and skin status to prevent these serious foot complications.

Similar glucose control with basal-bolus regimen of insulin detemir plus insulin aspart and thrice-daily biphasic insulin aspart 30 in insulin-naive patients with type 2 diabetes: Results of a 50-week randomized clinical trial of stepwise insulin intensification.

OBJECTIVE: This study aimed to demonstrate the non-inferiority of 50-week treatment with stepwise insulin intensification of basal-bolus insulin analogues [insulin detemir (IDet) and aspart (IAsp)] versus biphasic insulin aspart 30 (BIAsp30) in insulin-naive type 2 diabetes mellitus (T2DM) patients not controlled by oral glucose-lowering drugs (OGLDs). RESEARCH DESIGN AND METHODS: In this open-label multicentre, multinational, randomized, parallel-arm treat-to-target trial, 403 insulin-naive patients with T2DM in four African countries were randomized to either an IDet+IAsp (n = 200) or BIAsp1-2-3 (n = 203) treatment group. Stepwise insulin intensification was performed at the end of 14, 26 and 38 weeks, depending on HbA1c values. The primary endpoint was change in HbA1c after 50 weeks of treatment. Safety variables were hypoglycaemia incidence, occurrence of adverse events and weight gain. RESULTS: Non-inferiority of the IDet+IAsp versus BIAsp1-2-3 treatment regimen was demonstrated by their similar HbA1c levels at the end of trial (IDet+IAsp: baseline 8.6%, 50 weeks 7.4%; BIAsp1-2-3: baseline 8.7%, 50 weeks 7.3%; full analysis set difference: 0.1% [95% CI: -0.1, 0.3]; per protocol: 0.2% [95% CI: -0.1, 0.4]). At week 50, 40.3 and 44.9% of patients achieved HbA1c <7.0% with IDet+IAsp and BIAsp1-2-3, respectively. The rate of overall hypoglycaemia during the trial was also similar in both groups (IDet+IAsp: 9.4 events/patient-year; BIAsp1-2-3: 9.8 events/patient-year). CONCLUSION: Insulin initiation and intensification using IDet+IAsp was not inferior to BIAsp1-2-3 in insulin-naive patients with T2DM not controlled by OGLDs. Both regimens led to similar reductions in HbA1c values after 50 weeks of treatment.

Barriers to the delivery of optimal antidiabetic therapy in the Middle East and Africa.

BACKGROUND: The prevalence of type 2 diabetes is increasing worldwide, but developing nations will bear a disproportionate share of this burden. Countries in the Middle East and Africa are in a state of transition, where marked disparities of income and access to education and healthcare exist, and where the relatively young populations are being exposed increasingly to processes of urbanisation and adverse changes in diet that are fuelling the diabetes epidemic. Optimising diabetes care in these nations is crucial, to minimise the future burden of complications of diabetes. METHODS: We have reviewed the barriers to effective diabetes care with special relevance to countries in this region. RESULTS: The effects of antidiabetic treatments themselves are unlikely to differ importantly in the region compared with elsewhere, but economic inequalities within countries restrict access to newer treatments, in particular. Values relating to family life and religion are important modifiers of the physician-patient interaction. Also, a lack of understanding of diabetes and its treatments by both physicians and patients requires more and better diabetes education, delivered by suitably qualified health educators. Finally, sub-optimal processes for delivery of care have contributed to a lack of proper provision of testing and follow-up of patients in many countries. CONCLUSION: Important barriers to the delivery of optimal diabetes care exist in the Middle East and Africa.

Barriers to the delivery of diabetes care in the Middle East and South Africa: a survey of 1,082 practising physicians in five countries.

AIMS: Developing countries face a high and growing burden of type 2 diabetes. We surveyed physicians in a diverse range of countries in the Middle East and Africa (Egypt, Kingdom of Saudi Arabia, United Arab Emirates, South Africa and Lebanon) with regard to their perceptions of barriers to type 2 diabetes care identified as potentially important in the literature and by the authors. METHODS: One thousand and eighty-two physicians completed a questionnaire developed by the authors. RESULTS: Most physicians enrolled in the study employed guideline-driven care; 80-100% of physicians prescribed metformin (with lifestyle intervention, where there are no contraindications) for newly diagnosed type 2 diabetes, with lifestyle intervention alone used where metformin was not prescribed. Sulfonylureas were prescribed widely, consistent with the poor economic status of many patients. About one quarter of physicians were not undertaking any form of continuing medical education, and relatively low proportions of practices had their own diabetes educators, dieticians or diabetic foot specialists. Physicians identified the deficiencies of their patients (unhealthy lifestyles, lack of education and poor diet) as the most important barriers to optimal diabetes care. Low-treatment compliance was not ranked highly. Access to physicians did not appear to be a problem, as most patients were seen multiple times per year. CONCLUSIONS: Physicians in the Middle East and South Africa identified limitations relating to their patients as the main barrier to delivering care for diabetes, without giving high priority to issues relating to processes of care delivery. Further study would be needed to ascertain whether these findings reflect an unduly physician-centred view of their practice. More effective provision of services relating to the prevention of complications and improved lifestyles may be needed.

Some genetic, clinical and immunologic interrelations in schistosomiasis mansoni.

The aim of the present work was to study the possible association of some class I, II MHC gene products with variations in the clinico-pathological outcome of human schistosomiasis mansoni as well as with the variability in immune responsiveness. The study was carried out on 47 patients with schistosomiasis mansoni and 20 healthy volunteers served as control group for the immunological parameters and 200 subjects for the genetic studies. The following were determined: class I, II HLA typing, serum IgG, IgM, C3c, immediate intradermal test and passive haemagglutination using S mansoni worm antigen, T lymphocyte subsets, delayed intradermal test and leukocyte migration inhibition using phytohaemagglutinin (PHA) and soluble egg antigen (SEA) of S mansoni. A statistically significant association was found between HLA-B5 and DR3 and with the occurrence of hepatosplenic disease; this phenotype also correlated with changes in T lymphocyte subsets and high immune reactivity, both humoral and cell mediated. HLA-DQI was also associated with failure to develop hepatosplenic disease. The present study consolidates also the view of the important role of host immune reactivity in the clinical outcome of schistosomiasis mansoni and demonstrates the contribution of the genetic impact on both clinical and immunological heterogeneity of the disease.

Immuno-metabolic factors in schistosomal hepatic fibrosis modulating atherogenesis.

Clinical expression of atherosclerosis is infrequent among patients with schistosomal hepatic fibrosis (SHF), besides, the latter disease is a disease with many immunological expressions. The aim of the present work was to search for a possible immunological and metabolic interaction which would modulate atherogenic mechanisms. The study was carried out on 31 patients with SHF and 20 non-schistosomal subjects (10 with evident clinical atherosclerosis and 10 without). All investigated subjects were males aged above 40 years, and were subjected to the following: serum lipoprotein pattern, total cholesterol, phospholipids, triglycerides, ApoA, ApoB, IgG, IgM, IgA, C3 + circulating immune complexes (CICs) and passive haemagglutination using S mansoni adult worm antigens. The results showed low levels of blood lipids in patients with SHF especially in those with porto-systemic collaterals; serum levels of IgG and IgM were significantly increased in all patients with SHF, while IgA was only increased in patients with collaterals who in turn showed the least incidence of clinically evident atherosclerosis; serum C3 was increased in patients with clinical atherosclerosis, both schistosomal and non-schistosomal. CICs have been higher in patients with SHF without atherosclerosis while decreased in atherosclerosis patients, both schistosomal and non-schistosomal. Our results may consolidate the view of a protective role of liver affection against atherogenesis as well as the important contribution of the immune mechanisms in this context.