Acute bilateral cataract in a non-complicated type 1 diabetic youngster: a case report

It is rare for young type 1 diabetics to develop cataract within the first five years of their disease. The overall prevalence of cataract in young diabetics is < 1%. We describe a case of a 13-year- old type 1 diabetic female, known to be diabetic for last three years, who presented with severe diabetic ketoacidosis and decreased vision over the past three weeks. Initial examination revealed absent red reflex and bilateral cataracts, confirmed by an opthalmological assessment to be bilateral mature cortical cataracts. The vision was totally restored after successful bilateral cataract extractions and intra-ocular lens implantation. Development of cataract in early stage of diabetes is very exceptional. This raises the possibility of the presence of unusual genetic susceptibility and perhaps, some environmental elements. We emphasize the need for vigilant examination for ocular complication in type 1 diabetic patients, even in the first few years of their disease

Insulin therapy induced adiposity evaluted by computed tomography is not visceral

In individuals with type 2 diabetes, weight gain during treatment with insulin and other agents prevents the attainment of glycemic targets and probably limits the success of treatment. Studies have attempted to elucidate the mechanisms behind the apparent paradox of insulin improving glycemic control and cardiovascular risks, while causing weight gain. The aim of this study is to clarify the influence of insulin therapy on body weight and differential fat distribution [visceral or peripheral] in newly insulin treated type 2 diabetic male patients. The study was conducted on 26 type 2 diabetic male patients evaluated at baseline and 12 months after instituting insulin therapy. Body mass index [BMI], absolute waist circumference [AWC], systolic and diastolic blood pressure, HbA1c% were estimated. Abdominal Computed tomography was applied to evaluate areas of subcutaneous fat [SF] and visceral fat [VF] before and after insulin therapy. There is significant reduction in HbA1c [9.03 +/- 0.72 vs. 7.50 +/- 0.58, p<0.001] and significant increase body mass index [BMI =28.92 +/- 1.39 vs. 29.81 +/- 1.27, p=0.02] .However there was non significant changes in the AWC 103.27 +/- 3.87 Vs 105.14 +/- 3.25, P=0.065, VF 121.01 +/- 5.84 Vs 123.01 +/- 5.55, p=0.213, SF 206.54 +/- 9.93 Vs 212.12 +/- 11.62, P = 0.069and V/S ratio 0.59 +/- 0.03 vs. 0.58 +/- 0.03, P=0.365. Weight gain in the newly insulin treated type 2 diabetic patients during 12 months duration is equally distributed in both peripheral and visceral fat. So, insulin therapy does not appear to increase the visceral fat in type 2 diabetic patients which is strongly liked to atherosclerosis. Longer-term follow up and bigger sample size are necessary to address the issue of the kinetics of weight gain and to establish the possible correlation with other cardiovascular risk markers

Clinical and biochemical characteristics of early onset type 2 diabetes in young diabetics

Early onset type 2 diabetes is no longer rare. Many studies have shown a trend to an earlier age of onset of type 2 DM and pointing to a loosing of the relative protection of young age to type 2 DM, largely attributable to the fattening of modem society. A descriptive study was conducted on a series of 19 early onset type 2 diabetics. Typical insulin-resistant phenotypes were described in these youngsters. Mean Age 17.53 +/- 1.4 years. All patients are overweight [n = 6, 16%] to obese [n = 13, 84%] at diagnosis with mean BMI [31.43 +/- 2.09 Kg/ m2] and mean waist circumference is [94 +/- 1.7 cm in females and 103.43 +/- 1.24 cm in males]. Hypertension was reported in 3 cases with mean systolic blood pressure [SBP] 134.32 +/- 8.45 and mean diastolic blood pressure [DBP] 87.05 +/- 10.34. Family History of type 2 diabetes was reported in 68.4% of the patients and maternal history Of Gestational DM presents in 52.6%. Ten patients [52.6%] have acanthosis nigricans; a cutaneous marker of insulin resistance. 6 female patients [out of 12] had clinical features suggestive of PCOS in the form of irregular menses and hirsutism. HOMA as a measure of insulin resistance was found to have a strong positive correlation with BMI, waist circumference in females, TG, DBP and a negative correlation with HDL-C and Apo A-1.Similarly hsCRP showed a positive correlation with BMI, waist circumference in females and males, TG, DBP and a negative correlation with HDL-C. In conclusion, early onset type 2 DM is increasingly recognized as a part of the accelerating epidemic in the world. This phenomenon is strongly associated with obesity and in particular, central adiposity, as a determinant of insulin resistant and chronic inflammatory states which seam to appear very early in these youngsters. Type 2 DM is frequently asymptomatic and should be considered in obese adolescent from at-risk ethnic groups who have positive family histories

Lean PCOS: is it inflammatory or insulin resistant state?

The syndrome of polycystic ovary [PCOS] is one of the most frequent disorder in women [obese and lean]. PCOS is a complex and heterogenous disorder and there is still a debate for its endocrine, metabolic and inflammatory pathogenesis our aim to evaluate the insulin resistance and the inflammatory marker in lean PCOS women. A total of 28 lean women fulfilling the diagnostic criteria of PCOS compared with a 20 age and BMI matched healthy control women were enrolled in the study. C reactive protein, insulin resistance index [HOMA-IR], Adiponectin and endocrin parameters [LH, FSH, Testosterone, SHBG, 17 OH progesterone, TSH and prolactin] were measured. HOMA-IR was significantly higher in lean PCOS as compared with control group [p < 0.05], however CRP and serum adiponectin were not statistically different between the two groups. Lean PCOS is associated with insulin resistance which is independent of adiposity. Adiponectin does not seem to be actively involved in the pathogenesis of PCOS and lean PCOS is not associated with low grade inflammation

Elevated serum resistin levels in women with prior gestational diabetes

Resistin was not studied before as a potential biochemical mediator of insulin resistance in patients with prior GDM. Gestational diabetes mellitus [GDM] is a risk factor for both type 2 diabetes [DM2] and insulin resistance syndrome. Early reports suggested that resistin is associated with insulin resistance and type 2 DM. However subsequent studies have not supporting these findings. The aim of this study is to evaluate the role of resistin as a biomarker of insulin resistance in women with prior GDM. This study was conducted on 20 women with a history of GDM and 16 women with a history of normal pregnancy [control group]. The two groups were matched regarding the age, BMI, postpartum duration and the parity numbers. For all subjects, Serum resistin and HOMA IR were measured. As compared with control group, HOMA IR and serum resistin were significantly higher in women with history of previous GDM [3.97 +/- 0.71 Vs 3.51 +/- 0.5, P = 0.034], [4.9 +/- 0.89 Vs 3.5 +/- 1.06, P = 0.011] respectively. Furthermore serum resistin levels was significantly positively correlated with both BMI and HOMA IR in women with prior GDM [r 0.500, P = 0.025; r 0.527, P = 0.017] respectively. To the best of our knowledge, this is the first study addressing resistin in women with prior GDM which might explain the underlying pathogenetic mechanisms for future development of type 2 DM

Insulin-like growth factor-1 [IGF-1]: its role in diabetic kidney disease

Insulin like growth factor-1 has incriminated as a key role in the pathogenesis of immediate and late diabetic complications. IGF-1 concentration changes either in blood or renal tissues may contribute to the pathogenesis of diabetic nephropathy. The objective of this study is to compare the level of urinary and serum IGF-1 in diabetics and non-diabetic subjects and to predict the relation between IGF-1 and development of diabetic nephropathy. It is released from various organs with the liver being the most important source. The present study assessed urinary and serum 1GF-1 in 24 patients, twelve of them are diabetics with microalbuminuria and twelve of them are diabetic with overt nephropathy and also in twelve control non-diabetic subjects of matched age and sex. Every group contain six males and six females, the differentiation between diabetic groups was based on Cambur-lll and Micral-l tests. The immunoassay of IGF-1 is a "sandwich type assay" by using mouse monoclonal antibodies directed against two different epitopes of IGF-1 which are employed in the kit. Serum IGF-1 showed statistically non-significant difference between the three test groups. Urinary IGF-1 showed marked significant difference between the three test groups. The highest value was in overt nephropa thy group [group III] [0.800:0.100 pg/ ml], then microalbuminuria diabetic group [group II] [0.408:0.007 pg/ml]. The lowest value was found in control group [group I] [0.189+0.0028 pg/ml], p value <0.01 when comparing group III with group I. Also urinary IGF-1 showed a positive correlation with the diabetic duration, mean blood pressure and serum creatinine level [P<0.001]. These results indicate that urinary 1GF-1 may reflect the important role of tissue IGF-1 in the pathogenesis and development of diabetic kidney disease