The Relationship Between Diabetic Peripheral Neuropathy and (MPV) Mean Platelet Volume Values in Patients With Type 2 Diabetes Mellitus

Aim:We aimed to evaluate the relationship between diabetic peripheral neuropathy and MPV values in type 2 diabetes mellitus patients.Materials and Methods:We investigated type 2 diabetic patients’ data retrospectively. The data was divided as two groups (with and without diabetic peripheral neuropathy) according to their history, physical examination, laboratory results and electro-physiological study results. The patients with cardiovascular, hematological, oncological, hepatic, renal, infectious disease or a recent history of trauma and surgery were excluded. Statistical analysis was studied by SPSS 21 soft-ware statistics programme.Results:We included 83 diabetic patients (ages between 31 and 76) that 39 of them were patients with diabetic peripheral neuropathy (25 women, 14 men) and 44(27 women, 17 men) were without neuropathy. While the means of non-neuropathic group for the age was 57,89±8,8(31-75), A1c 7,3%(5,5-12,7), platelet counts 260.800±68,900/mm3, MPV value 8,96±0,67 fl(7,6-10,4); the means of neuropathic group were 56,54±8,4(37-76) years, 8,3 (5,6-14,4)%, 269.050±74.195/mm3 and 9,03 ± 0,75(7,4-10,5) fl respectively. There were no statistically significant differences in terms of age(p=0,482), platelet count(p=0,601), body mass index(p=0,299), MPV(p=0,596) and A1c(p=0,076). But statistically significant differences were found in terms of diabetes age(p=0,002) and fasting plasma glucose(p=0,04). A statistically significant correlation was not found between MPV and neuropathy existence by Spearman correlation analysis(p=0,599).Conclusion:We didn't find any correlation between MPV value and neuropathy development in our study. We suggest that to clarify this relationship certainly, we need a prospective, multi-centered study with a bigger cohort

The Relationship Between Diabetic Peripheral Neuropathy and (Mpv) Mean Platelet Volume Values in Patients with Type 2 Diabetes Mellitus

Amaç: Çalışmamızda Tip 2 diyabetli hastalarda, MPV değeriyle, diyabetin mikrovasküler bir komplikasyonu olan nöropati arasındaki ilişkiyi araştırmayı hedefledik.Materyal ve Metot: Retrospektif çalışmamıza, iç hastalıkları polikliniklerimize başvuran tip 2 diyabetik hasta dosyaları değerlendirilerek, fizik muayene, elektrofizyolojik çalışma verileri, anamnez ve tetkik kayıtları incelenerek, diyabetik nöropatisi olan ve olmayan iki grup diyabetik hasta belirlendi. Bilinen kardiyovasküler, hematolojik, onkolojik hastalık, karaciğer ve böbrek hastalığı, akut veya kronik infeksiyon hastalığı, yakında geçirilmiş travma, cerrahiöyküsü olan vakalar çalışmaya dahil edilmedi. Vakaların istatistiksel değerlendirmesi SPSS 21 yazılım programı ile yapıldı.Bulgular: Yaşları 31-76 arasında değişen 39'u (25 kadın, 14 erkek) diyabetik periferik nöropatili, 44’ü (27 kadın, 17 erkek) ise nöropatisiz toplam 83 diyabetik vaka çalışmaya alındı. Nöropatisi olmayan vakaların ortalama yaşları 57,89±8,8 (31-75), A1c % 7,3 (5,5-12,7), açlık kan şekeri 144 mg/dl (80-326), trombosit sayısı 260.800±68,900/mm3, MPV değeri 8,96±0,67 fl (7,6-10,4) idi. Nöropatik vakaların ortalama yaşları 56,54±8,4 (37-76), A1c % 8,3 (5,6-14,4), açlık kan şekeri 184 (100-432) mg/dl, trombosit sayısı 269.050±74.195/mm3, MPV değeri 9,03 ± 0,75 (7,4-10,5) idi. Gruplar arasında yaş (p=0,482), trombosit sayısı (P=0,601), BKİ (p=0,299), MPV (p=0,596) ve A1c (p=0,076) değerleri açısından anlamlı fark yokken, diyabet yaşı (p=0,002) ve açlık kan şekeri (p=0,04) açısından istatistiksel anlamlı fark mevcuttu. Spearman korelasyon analizinde MPV düzeyi ile nöropati gelişimi arasında istatistiki anlamlılığa ulaşan bir ilişki bulunamadı (p=0,599).Sonuç: Tip 2 diyabetli 83 hasta ile yaptığımız çalışmamızda, MPV ile nöropati gelişimi arasında herhangi bir ilişki saptayamadık. Bu ilişkiyi daha iyi aydınlatabilmek için daha fazla vaka ile çok merkezli ve prospektif çalışmalara ihtiyaç vardır.Aim: We aimed to evaluate the relationship between diabetic peripheral neuropathy and MPV values in type 2 diabetes mellitus patients. Materials and Methods: We investigated type 2 diabetic patients’ data retrospectively. The data was divided as two groups (with and without diabetic peripheral neuropathy) according to their history, physical examination, laboratory results and electro-physiological study results. The patients with cardiovascular, hematological, oncological, hepatic, renal, infectious disease or a recent history of trauma and surgery were excluded. Statistical analysis was studied by SPSS 21 soft-ware statistics programme. Results: We included 83 diabetic patients (ages between 31 and 76) that 39 of them were patients with diabetic peripheral neuropathy (25 women, 14 men) and 44(27 women, 17 men) were without neuropathy. While the means of non-neuropathic group for the age was 57,89±8,8(31-75), A1c 7,3%(5,5-12,7), platelet counts 260.800±68,900/mm3, MPV value 8,96±0,67 fl(7,6-10,4); the means of neuropathic group were 56,54±8,4(37-76) years, 8,3 (5,6- 14,4)%, 269.050±74.195/mm3 and 9,03 ± 0,75(7,4-10,5) fl respectively. There were no statistically significant differences in terms of age(p=0,482), platelet count(p=0,601), body mass index(p=0,299), MPV(p=0,596) and A1c(p=0,076). But statistically significant differences were found in terms of diabetes age(p=0,002) and fasting plasma glucose(p=0,04). A statistically significant correlation was not found between MPV and neuropathy existence by Spearman correlation analysis(p=0,599). Conclusion: We didn't find any correlation between MPV value and neuropathy development in our study. We suggest that to clarify this relationship certainly, we need a prospective, multi-centered study with a bigger cohort

Diyabetik Bir Olguda Orbital Sellülitin Nadir Bir Komplikasyonu: Kavernöz Sinüs Trombozu

Diyabetin çeşitli enfeksiyonlara ve tromboza eğilimi artırdığı iyi bilinmektedir. Diyabette doğal, hücresel ve humoral bağışıklık mekanizmalarının çeşitli basamaklarında bozukluklar beklenir. Trombosit fonksiyonlarındaki, koagülasyon faktörlerindeki ve damar yapısındaki bozukluklar da tromboza eğilimi artırır. Hem enfeksiyonların hem de trombotik olayların diyabetteki seyri diyabetik olmayan olgulara göre daha ciddidir. Bu yazıda orbital sellülit gelişip kavernöz sinüs trombozu ile komplike olan 94 yaşında diyabetik erkek olgu sunuldu. Olgu orbital sellülit, idrar yolu enfeksiyonu, hiperozmolar non ketotik durum, akut böbrek yetersizliği ve üremiye sekonder kompanse metabolik asidoz tanıları ile endokrinoloji servisine yatırıldı. Antibiyoterapisine ve hidrasyonuna vakit kaybetmeksizin başlanıp gerekli tedavisi yapılan olgu, mortalitesi yüksek kavernöz sinüs trombozu sonrası tedaviye cevap vermeyerek kaybedildi. Özellikle diyabetik olgularda orbital enfeksiyonların komşuluk yoluyla kavernöz sinüse yayılıp septik tromboza yol açarak ölümcül seyredebileceği göz önüne alınarak erken tanı ve tedavisi yapılmalıdırIt is that diabetes mellitus increases tendency to develop infections and thrombosis. Impairment of various mechanisms and agents of humoral and cellular immune systems can be expected. Disturbances of platelet function, coagulation factors, and vascular structure predispose diabetics to thrombotic events. The course of both infections and thrombotic events is often worse than in non-diabetic patients. Presently described is 94-year-old male patient with diabetes who had orbital cellulitis that became complicated with cavernous sinus thrombosis (CST). He was admitted to endocrinology clinic with diagnoses of orbital cellulitis, urinary tract infection, hyperosmolar non-ketotic state, acute renal failure, and compensated metabolic acidosis secondary to uremia. Despite immediate antibiotherapy, hydration, and additional required treatment, patient did not respond and died as a result of CST. There must be awareness, especially for diabetic patients, that orbital infections may spread to nearby cavernous sinuses and cause potentially lethal septic CST. Early diagnosis and immediate treatment are essentia

Wpływ dystrybucji tkanki tłuszczowej oraz wybranych adipokin na insulinooporność w stanie przedcukrzycowym

  Introduction: The risk of developing insulin resistance and metabolic syndrome is particularly high in central obesity. In this study we evaluated the effects of fat distribution and some adipokines on insulin resistance in prediabetic patients. Material and methods: Eighty-seven age- and sex-matched patients were divided into three groups according to their 75-gram oral glucose tolerance test results as follows: impaired fasting glucose group, impaired glucose tolerance group, and normal glucose tolerance group. Fasting insulin levels were measured. Homeostatic model assessment of insulin resistance was calculated. Body fat mass measurements were assessed by bioelectric impedance analyser and abdominal fat thicknesses (subcutaneous, visceral, and preperitoneal) by ultrasonography. The fasting serum levels of several adipokines [adiponectin, leptin, resistin, vaspin, visfatin, retinol-binding protein-4 (RBP-4), tumour necrosis factor-alpha (TNF-alpha)] were measured by ELISA method. Results: The mean body mass index, fat mass measurements, and abdominal fat thicknesses of the groups were similar. There were no differences between groups in terms of the mean fasting insulin, vaspin, RBP-4, leptin, resistin, and TNF-alpha. In comparison of the prediabetic and normal groups, the levels of adiponectin (p < 0.001) and visfatin (p < 0.001) were lower in the prediabetic group. Furthermore, we found that high body mass index (p < 0.01) and fat mass (p < 0.01) and low adiponectin (p < 0.05) levels have roles in the development of insulin resistance in the prediabetic group. Conclusions: We suggested that in the prediabetic period not only obesity but also decreased adiponectin levels play some role in the pathogenesis of insulin resistance. (Endokrynol Pol 2016; 67 (3): 277–282)    Wstęp: Ryzyko rozwoju insulinooporności i zespołu metabolicznego zwiększa się zwłaszcza u osób z otyłością centralną. W niniejszym badaniu oceniono wpływ dystrybucji tkanki tłuszczowej i wybranych adipokin na insulinooporność u osób ze stanem przedcukrzycowym. Materiał i metody: Osiemdziesięciu siedmiu chorych dobranych pod względem wieku I płci podzielono na 3 grupy w zależności od wyniku testu doustnego obciążenia 75 g glukozy: osoby z nieprawidłową glikemią na czczo, osoby z nieprawidłową tolerancją glukozy i osoby z prawidłową tolerancją glukozy. Zmierzono stężenie insulin na czczo. Do oszacowania insulinooporności zastosowano model homeostazy. Masę tkanki tłuszczowej oceniono za pomocą analizatora bioimpedancji elektrycznej, a grubość brzusznej tkanki tłuszczowej (podskórnej, trzewnej i przedotrzewnowej) zmierzono metodą ultrasonograficzną. Stężenie na czczo w surowicy kilku adipokin (adiponektyna, leptyna, rezystyna, waspina, wisfatyna, białko wiążące retinol-4 [RBP-4], czynnik martwicy nowotworów alfa [TNF-alfa]) zmierzono, stosując metodę ELISA. Wyniki: Średni wskaźnik masy ciała, masa tkanki tłuszczowej I grubość brzusznej tkanki tłuszczowej były podobne we wszystkich grupach. Nie stwierdzono różnic między grupami pod względem średniego stężenia insuliny na czczo ani stężeń waspiny, RBP-4, leptyny, rezystyny i TNF-alfa. W porównaniu grup ze stanem cukrzycowym i grupy z prawidłową tolerancją glukozy wykazano, że stężenia adiponektyny (p < 0,001) i wisfatyny (p < 0,001) były niższe u osób ze stanem przedcukrzycowym. Ponadto stwierdzono, że wysoki wskaźnik masy ciała (p < 0,01) i duża masa tkanki tłuszczowej (p < 0,01) oraz niskie stężenie adiponektyny (p < 0,05) przyczyniają się do rozwoju insulinooporności u osób ze stanem przedcukrzycowym. Wnioski: Autorzy sugerują, że nie tylko otyłość, ale również obniżenie stężenia adiponektyny odgrywają pewną rolę w patogenezie insulinooporności w okresie przedcukrzycowym. (Endokrynol Pol 2016; 67 (3): 277–282)

An Acute Renal Failure Case Due To Overdose Use Of Perindopril/Amlodipin

Fixed -dose combination therapies are important alternative of hypertension treatment. The management of suicidal intoxication with these conbination preparations which might have different and sometimes interactive mechanisms is still unclear. In this case-report a 51 -yearold male patient who had taken 26 pills of perindopril 5 mg and amlodipine 10 mg combination drug. He admitted to the emergency department with the complications of dizziness and fatigue. He was followed in intensive care unit after his first medical care unitafter his first medical emergency intervensions. After development of hypotensionand acute renal failure, he improved with fluid resussitation and symtomatic treatment and he was discharged

The effect of fat distribution and some adipokines on insulin resistance in prediabetic patients

Tıpta Uzmanlık TeziPrediyabetik vakalarda vücut yağ dağılımının ve çeşitli adipokinlerin insülin direncine katkısını ortaya koymayı hedeflediğimiz bu çalışmaya 87 kişi [ Bozulmuş açlık glukozlu 27 (14 kadın, 13 erkek), bozulmuş glukoz toleranslı 36 (26 kadın, 10 erkek) vaka ile normal glukoz metabolizması saptanan 24 (16 kadın, 8 erkek) sağlıklı gönüllü kontrol vakası] dahil edildi. Tüm olguların antropometrik ölçümleri, insülin direnci göstergesi olan homeostatik model değerlendirme sonuçları, oral glukoz tolerans testleri, lipidleri, TANITA ile yağ kütlesi ölçümleri, ultrason ile abdominal bölge yağ dağılımları kaydedildi. Üç grubun karşılaştırılmasında açlık insülini, total kolesterol, yüksek dansiteli lipoprotein, düşük dansiteli lipoprotein, trigliserid, vaspin, retinol-bağlayıcı protein 4, leptin, resistin, tümör nekroz faktörü-? düzeyleri, abdominal bölge yağ dağılımları, yağ kütlesi ölçümleri arasında fark bulunmazken (p>0,05), oral glukoz tolerans testinin 0. ve 2. saatindeki glukoz düzeyleri, homeostatik model değerlendirme (HOMA-IR) sonuçları, adiponektin ve visfatin açısından fark vardı (p0,05). Vücut kitle indeksi, bel çevresi, oral glukoz tolerans testinin 2. saat glukoz değeri, total yağ yüzdesi, total yağ kütlesi, viseral yağ kalınlığı, adiponektin ve resistin düzeyinin homeostatik model değerlendirme sonuçları ile istatistiki olarak anlamlı düzeyde korele olduğu saptandı. Regresyon analizinde sadece viseral yağ kalınlığının, insülin direnci gelişiminde bağımsız bir risk faktörü olduğu sonucuna varıldı. Anahtar kelimeler: İnsülin direnci, adipokinler, yağ dağılımıÖzetIn this study, we aimed to evaluate the effect of fat distribution and some adipokines on insulin resistance in prediabetic patients. Totally 87 cases [ 27 impaired fasting glucose (14 female, 13 male), 36 impaired glucose tolerance (26 female, 10 male) and 24 healthy control subjects (16 female, 8 male)] were enrolled. Anthropometric measurements, homeostatic model assessment of insulin resistance values indicating insulin resistance, oral glucose tolerance test glucose levels, serum lipids, body fat mass measurements by TANITA and abdominal region ultrasonography for fat distribution of all cases were registered. In comparison of 3 glucose metabolism groups, there are no difference between groups in terms of fasting insulin, total cholesterol, high density lipoprotein-cholesterol, high density lipoprotein-cholesterol, triglyceride, vaspin, retinol-binding protein 4, leptin, resistin, tumor necrosis factor- values, abdominal fat distribution, fat mass measurements. But statistically significant differences were found between groups in terms of oral glucose tolerance test 0 and 2-hour glucose levels, homeostatic model assessment of insulin resistance values, adiponectin and visfatin. Insulin resistance increased while adiponectin and visfatin levels decreased. There are statistically significant correlation between homeostatic model assessment of insulin resistance values and body mass index, waist circumference, oral glucose tolerance test 2nd hour-glucose, total fat percentage, total fat mass, visceral fat thickness, adiponectin ve resistin levels. In regression analysis, only visceral fat thickness was found to be an independent risk factor for development of insulin resistance. Key words: Insulin resistance, adipokines, fat distributio

Evaluation of endocan and endoglin levels in chronic kidney disease due to diabetes mellitus

Introduction: Endocan and endoglin have been shown to play a role in angiogenesis. Aberrant excessive angiogenesis is a main factor in the development of diabetic nephropathy. In this study we evaluated endocan and endoglin levels in diabetes patients with and without albuminuria and compared them with healthy subjects. Therefore we aimed at gaining a better understanding of the role of angiogenesis in diabetic nephropathy and to assess the predictive role of endocan and endoglin as markers of diabetic nephropathy progression. Material and methods: Ninety-six type 2 diabetes patients were classified according to their 24-hour urinary albumin excretion rate. Forty type 2 diabetes patients with normoalbuminuria (urinary albumin excretion = 30 mg/day) and 35 healthy non-diabetic control subjects were included. Their anthropometric features, arterial blood pressures, fasting glucose, glycated hemoglobin, urea, creatinine, lipids, endocan and endoglin levels were measured and compared to each other. Results: Endocan and endoglin levels of diabetics patients were higher than those of the controls. In comparison of endocan and endoglin levels of diabetic nephropathy patients with controls, p-values were < 0.001 and 0.002 respectively. In comparison of normoalbuminuric diabetic patients with controls, p-values were 0.001 and 0.017 respectively. Endocan levels of diabetic nephropathy cases were higher than those of normoalbuminuric patients (p = 0.011) but there was no statistically significant difference in endoglin levels between them (p = 0.822). Conclusions: Endocan might be a more reliable marker of diabetic nephropathy development than endoglin

Ezetimib monoterapisinin lipoprotein (a) ve diğer lipid parametreleri üzerine etkisi]

The effect of ezetimibe monothrepy on decreasing lipid molecules has been widely studied in the literature so far, but scarce number of clinical studies have evaluated the effect of this pharmacological agent on lipoprotein-(a). In our study, we aimed to evaluate the effect of ezetimibe monotherapy on lipoprotein-(a) and other lipid parameters with clinical aspects. Ezetimibe monotherapy for three months was used for the hyperlipidemic patients admitted to our internal medicine outpatient clinic. Lipoprotein-(a) total cholesterol, low-density lipoprotein, very-low-density lipoprotein, high-density lipoprotein, and triglyceride levels before and after ezetimibe therapy were subjected to biochemical analysis. In addition to descriptive statistics of data, paired-t-test and Pearson Correlation analysis were used. All results were evaluated within 95% confidence interval and considered as statistically siginificant if p values were lower than 0.05. After treatment lipoprotein-(a), total cholesterol, and LDL-cholesterol levels decreased but the changes in very low-density lipoprotein, high-density lipoprotein, and triglyceride levels were not statistically siginificant (p>0.05). In the treatment of hyperlipidemia, ezetimibe can be an adjunct to other antihyperlipidemic drugs or an alternative monotherapy. © 2015, Logos Medical Publishing. All rights reserved