Abstract We investigated the association of PON1 55/192 polymorphisms with type, severity and prognosis of stroke and oxidative markers. Paraoxonase1 (PON1), Glutathione Reductase (GSH‐Rd) and Malondialdehyde (MDA) levels were measured at day 1 and at day 5 following the onset of stroke. Genotypes were determined by polymerase chain reaction and restriction digestion. The frequencies of QQ and MM genotypes of PON1 192 and PON1 55, respectively, were significantly higher in controls than in patients. However, the allele frequencies of PON1 192 R and PON1 55 L were significantly more frequent in patients compared to controls. The frequency of combined genotype of RR/LL was significantly higher in cardioembolic group than in atherothrombotic group. PON1 activities were significantly diminished in stroke patients compared to controls. In contrast, serum MDA levels were significantly greater in patients than the values in controls. GSH‐Rd activity was higher in patients with small lesion and good prognosis than those with large and poor prognosis. Low density lipoprotein (LDL) levels in patients with large lesions were higher than those with small lesions. PON1 55/192 polymorphisms influence activity of the enzyme. PON1 55/192 genotypes have been associated with MDA levels. In conclusion, PON1 genetic variations are associated with risk factors, severity, type and prognosis of stroke and oxidative stress. IUBMB Life, 58: 165 ‐ 172, 2006
Migraine is a common and debilitating episodic disorder characterized by recurrent headache attacks associated with autonomic symptoms. It affects an estimated 12% of the population. The etiology of the underlying neurodegenerative process is widely unknown; however, oxidative stress is a unifying factor in the current theories of migraine pathogenesis. After demonstrating the observation that oxidative DNA damage is detectable in migraine disease, searching the role played by DNA repair systems in migraine diseases could bring us much significant information about the pathogenesis of migraine. We prospectively investigated whether DNA repair gene polymorphisms (XRCC1 Arg399Gln, XRCC3 Thr241Met XPD Lys751Gln, XPG Asp1104His, APE1 Asp148Glu, hOGG1 Ser326Cys) account for an increased risk of migraine. The present analyses are based on 135 case subjects with migraine disease and 101 noncase subjects. Genotyping of DNA repair gene polymorphisms (XRCC1 Arg399Gln, XRCC3 Thr241Met XPD Lys751Gln, XPG Asp1104His, APE1 Asp148Glu, hOGG1 Ser326Cys) was detected by polymerase chain reaction-restriction fragment length polymorphism.We demonstrated that apurinic endonuclease (APE), X-ray repair complementing defective repair in Chinese hamster cells 3 (XRCC3), xeroderma pigmentosum D (XPD), and hOGG1 gene variants were associated with an increased risk for development of migraine disease (p<0.05). In contrast, no statistically significant differences were found in genotype distributions of X-ray repair complementing defective repair in Chinese hamster cells 1 (XRCC1) and XPG between migraine cases and controls (p>0.05).Our findings have suggested that APE1, XRCC3, XPD, and hOGG1 gene variants could facilitate the development of migraine disease.
We determined the reliability of ultrasonography (US) measurements for diagnosing carpal tunnel syndrome (CTS) and their correlation with symptom duration and electrophysiology findings. We determined whether the ratio of the median-to-ulnar cross-sectional areas (CSAs) can support CTS diagnoses.The pisiform CSA (CSA(pisiform)), swelling ratio (SR), palmar bowing, and CSA(pisiform)/ulnar CSA (CSA(ulnar)) measurements made in two subgroups of CTS patients (having sensory affection alone or having both sensory and motor affection) were compared with controls. CSA(ulnar) was measured in Guyon's canal at the level of most-protuberant portion of the pisiform bone.The values of all of the measured US parameters were higher in patients with CTS (n=50) than in controls (n=62). CSA(pisiform) could be used to diagnose CTS of mild severity. All of the parameters were positively correlated with the distal latency of the compound muscle action potential, and all of them except for SR were negatively correlated with the sensory nerve conduction velocity. A CSA(pisiform)/CSA(ulnar) ratio of ≥1.79 had a sensitivity of 70% and a specificity of 76% for diagnosing CTS.Only CSA(pisiform) measurements were reliable for diagnosing early stages of CTS, and CSA(pisiform)/CSA(ulnar) had a lower diagnostic value for diagnosing CTS.
Amaç: Bu çalışmada multipl skleroz (MS) hastalarında tiroid otoantikorlarının prevalansını saptamak ve genel populasyonla karşılaştırmak amaçlanmıştır. Gereç ve Yöntemler: Çalışmaya tiroid hastalığı olmayan ve tiroid ilacı kullanmayan 200 (140 kadın, %70; 60 erkek, %30) MS hastası ve kontrol grubu olarak da 200 (145 kadın, %72,5; 55 erkek, %27,5) sağlıklı birey dâhil edilmiştir. Hasta grubunda immünmodülatuar tedavi öncesi ve tedaviye başlandıktan sonra tiroid hormonları [serbest T3, serbest T4 ve tiroid stimüle edici hormon (TSH)] ve antitiroid peroksidaz antikor (anti-TPO) düzeyleri çalışılmıştır. Aynı tetkikler kontrol grubunda da bakılmıştır. Bulgular: Hasta grubunda tedavi öncesi 36 (%18) olguda anti-TPO pozitif bulunmuştur. Kontrol grubunda ise 10 (%5) kişide anti-TPOpozitifliği saptanmıştır. İmmünmodülatuar tedavi sonrası anti-TPO'nun pozitif hâle gelmesi sadece 2 (%1) hastada gözlenmiştir. Serbest T3, serbest T4 ve TSH değerlerinde hasta ve kontrol grubu arasında anlamlı fark görülmemiştir. Sonuç: Çalışmamızın sonuçları, otoimmün tiroid hastalığının MS hastalarında sağlıklı bireylere göre çok daha fazla görüldüğünü göstermektedir. Bu sebeple tiroid testleri ve tiroid otoantikorları MS hastalarında tedavi öncesinde bakılmalı, özellikle tiroid otoimmünitesi eşlik edenlerde tedavi süresince de tiroid fonksiyon testleri periyodik aralıklarla takip edilmelidir.
Acute movement disorders associated with bilateral basal ganglia lesions are becoming more common in patients with diabetes and uremia. Pathophysiology is not fully known, although it is believed to be complex, with ischemic/microvascular as well as metabolic/toxic variables influencing lesions and symptoms. We have reported here a uremic diabetic patient who has sudden developed severe akathisia, in magnetic resonance imaging (MRI) showed bilateral symmetric basal ganglia lesions with regression at follow-up. A condition linked with acute bilateral basal ganglia lesions in diabetic uremic individuals is uncommon, with clinical and imaging data demonstrating reversible alterations. Akathisia secondary to uremia is rarely seen in the literature. Our goal is to improve awareness of this condition among doctors and radiologists in order to identify more cases.
Today, diabetes, due to its frequency and the problems it causes, has become a health problem which is increasingly becoming more important around the world.Along with the changes in lifestyle in all of the developed and developing countries, prevalence of especially type 2 diabetes increases at a fast pace.According to the data of 2013, while the number of diabetic patients was 382 million in the world, this number is predicted to reach 592 million by increasing at a rate of 55% by 2035 (1).The diabetes or prediabetes is diagnosed with fasting plasma glucose, 2-hour oral glucose tolerance test and glycated hemoglobin A1 c (HbA1c) measurements.It is reported that the increase in HbA1c level increases the diabetes development risk.Therefore, determination of HbA1c as a strong indication for future diabetes development has caused HbA1c levels that are above normal but not within diabetic limits to be accepted as prediabetes (2).The changes brought by diabetic neuropathy known to be associated with DM (diabetes mellitus) and correlated with glycemic control in nerve conduction examinations have been stated in numerous studies.However, whether the elevations of HbA1c that can be named as prediabetes lead to neuropathy is a field that needs more investigation.For this reason, in this study, it is aimed to investigate the relationship between the elevation of HbA1c in asymptomatic and still prediabetic patients and peripheral nerve activation with electroneuromyography (ENMG).