The place of D-dimer and L-lactate levels in the early diagnosis of acute mesenteric ischemia

INTRODUCTION: Acute mesenteric ischemia (AMI) is an abdominal-vascular emergency which is rare and has high mortality rates (60-80 %) due to late diagnosis (1-3). Although it is known that extravascular reasons like intestinal intussusception, volvulus, strangulated hernias and obstructions can cause intestinal gangrene, these are rarely the cause of AMI (1). MATERIALS AND METHODS: In this study, we used male Wistar-Albino rats weighing 250-300 grams obtained from Pamukkale University Experimental Research Laboratory. Animals were exposed to light-dark cycles for 12 hours and had free access to food and water. They were kept in cages for 7 days to stabilise their intestinal flora. In animals of group I, nothing was made other than taking 0.5 ml blood intracardially. In other animals, abdomen was reached with midline laparotomy and superior mesenteric artery (SMA) was located. In group II (operative control group), SMA was isolated and manipulated but was not ligated. In Group III (intestinal ischemia group), SMAwas isolated and ligated with 3/0 silk tie distally to the aorta. After this process, intestinal ischemia was achieved which was confirmed by paleness and pulselessness of intestines, caecum and right colon. Later on, abdomen was closed with double 3/0 polyglactin sutures. At postoperative 1st, 4th and 6th hours 0.5 ml blood was taken intracardially from the animals in groups II and III in order to quantify D-dimer and L-lactate levels. LABORATORY TESTS: D-dimer: Blood samples which were put into tubes containing sodium citrate, were seperated from plasma with centrifugation at 4000 rpm for 7 minutes. L-lactate: Blood L-lactate levels were determined from blood taken into capillary tubes with the help of immobilised enzyme electrode technology using YSI 1500 Sport portative lactate analyzer (Yellow Springs Instruments Inc., Ohio-USA). HISTOPATHOLOGIC VERIFICATION: Two cm long intestinal samples were taken from animals in which SMA was ligated in order to achieve mesenteric ischemia and these samples were fixed in 10 % formol. DISCUSSION: As a result, in rats with SMA occlusion serum D-dimer levels were not increased significantly when compared either in the group or with the basal values of the control group and values in operative control group. Therefore, it is concluded that D-dimer is not a useful marker for early diagnosis of AMI. On the other hand, it is revealed that blood L-lactate levels began to increase significantly following 4th hour of mesenteric ischemia and it is shown that this increase continued at the 6th hour. In addition, considering the utmost importance of the early diagnosis in patients with the clinical suspicion of AMI, L-lactate seems to be a suitable marker to use in emergency departments because it is achieved with a portable device that gives fast and accurate results. Nevertheless, our results are need to be supported by clinical studies with larger patient series (Tab. 2, Fig. 11, Ref. 39). Text in PDF www.elis.sk

Obesity is associated with increased serum TSH level, independent of thyroid function

Objective: To reinvestigate the relationship between circulating TSH levels and adiposity in a cohort of obese people, who have normal thyroid function. Methods: Retrospective cross-sectional analysis was carried out on 226 euthyroid obese or overweight female patients. Thirty-nine female lean and euthyroid subjects (BMI <25 kg/m2) were included in the study group. TSH, free thyroxine (FT4), free triiodothyronine (FT3), fasting plasma levels of insulin and glucose, homeostasis model assessment (HOMA) for insulin resistance (HOMA-IR) and insulin secretion (HOMA-β cell), body weight, height, body mass index (BMI) and waist circumference were assessed. Results: Serum TSH levels were higher in the obese than in the lean subjects. In the study group (lean and obese subjects), there was a significant positive correlation between serum TSH and body weight (r = 0.231, p <0.001), BMI (r = 0.270, p <0.001), waist circumference (r = 0.219, p = 0.001), fasting insulin (r = 0.201, p = 0.002) and HOMA-IR (r = 0.201, p = 0.002); there was no correlation between serum FT4 and any of the parameters. A multivariate linear regression analysis revealed that only BMI (p = 0.012, 95% CI = 0.01-0.08) contributed significantly to the variance of TSH. Conclusions: This study strongly supports existing, but contradictory evidence that serum TSH levels are positively correlated with the degree of obesity and some of its metabolic consequences in overweight people with normal thyroid function

Growth hormone/insulin-like growth factor axis in patients with subclinical thyroid dysfunction

Objective: Our aim was to evaluate serum concentrations of GH, IGF-I, and insulin-like growth factor-binding protein-3 (IGFBP-3) in patients with subclinical thyroid dysfunction before and after normalization of thyroid function. Design and methods: The study included 51 patients (mean age 42.2 ± 1.8 years) with subclinical hypothyroidism and 30 patients (mean age 44.3 ± 2.4 years) with subclinical hyperthyroidism. A group of 37 euthyroid healthy subjects were studied as controls. Serum concentrations of TSH, FT4, FT3, GH, insulin, IGF-I, and IGFBP-3 were measured in all patients before starting therapy and after normalization of thyroid function. The dosage of levothyroxine (LT4) and antithyroid drugs was adjusted in attempt to keep the serum-free thyroxine (FT4) and thyrotropin (TSH) concentrations within the normal range. Main outcome: Baseline growth hormone levels were similar with hypothyroid group and hyperthyroid group in relation to euthyroid control subjects. Fasting serum IGF-I levels were significantly lower in the subclinical hypothyroid group compared with the control group. On the other hand, IGF-I levels of subclinical hyperthyroid patients and control group were similar. After normalization of thyroid function tests, IGF-I concentrations were increased in subclinical hypothyroid subjects, but unchanged in subclinical hyperthyroid subjects. Patients with subclinical hyperthyroidism showed slightly lower mean serum IGFBP-3 concentrations than those found in control group, but the difference was not statistically significant. Serum GH and IGFBP-3 levels were unaltered by treatment. Conclusions: In this study, it was shown that GH-IGF axis was not affected in patients with subclinical hyperthyroidism, while it was affected in patients with subclinical hypothyroidism. That is, investigation of the axis in subclinical hyperthyroidism would not bring any extra advantages, but LT4 replacement therapy could prevent abnormalities related to GH-IGF axis in patients with subclinical hypothyroidism. © 2008 Elsevier Ltd. All rights reserved

Ratlarda metotreksata bağlı oksidatif intestinal hasarda leflunomidinin koruyucu etkisinin araştırılması

ABSTRACT Background and Aims: The aim of this study was to investigate the effects of leflunomide treatment in methotrexate-induced oxidative small intestinal injury in rats. Materials and Methods: Forty rats were randomly divided into 4 groups. Methotrexate-induced intestinal injury was induced by single dose intraperitoneal injection of 20 mg/kg methotrexate. After induction, leflunomide (10 mg/kg/day) was administered intragastrically for 5 consecutive days. On the sixth day, homogenized small intestine tissues were examined for superoxide dismutase activity, myeloperoxidase activity, and glutathione and malondialdehyde levels. Results: Leflunomide treatment significantly decreased tissue myeloperoxidase activity and malondialdehyde levels (3.4;plusmn;0.7, 1.9;plusmn;0.4, p;lt;0.05 and 231;plusmn;199, 94;plusmn;80, p;lt;0.05, respectively). Leflunomide treatment significantly improved the decreased tissue levels of glutathione and superoxide dismutase activity (21;plusmn;0.5, 25;plusmn;3, p;lt;0.05 and 22;plusmn;0.6, 25;plusmn;2, p;lt;0.05, respectively). Conclusions: Leflunomide treatment ameliorated oxidative parameters of methotrexateinduced small intestinal injury.Giriş ve Amaç: Bu çalışmanın amacı metotreksata bağlı oksidatif ince barsak hasarında leflunomid tedavisinin etkisini araştırmaktır. Gereç ve Yöntem: 40 adet rat randomize olarak dört gruba ayrılmıştır. Metotreksata bağlı ince barsak hasarı 20 mg/kg metotreksatın tek doz intraperitoneal injeksiyonu ile oluşturulmuştur. İndüksiyon sonrası leflunomid 10 mg/kg/gün dozunda intra gastrik olarak 5 gün boyunca verilmiştir. İnce barsak dokuları, 6. gün superoksit dismutaz aktivitesi, myeloperoksidaz aktivitesi, glutatyon ve malondialdehit düzeylerinin ölçümü için homojenize edilmiştir. Bulgular: Leflunomid tedavisi doku myeloperoksidaz aktivitesi ve malondialdehit düzeylerini anlamlı ölçüde azaltmıştır (Sırasıyla 3.4±0.7, 1.9±0,4 p0.05 ve 231±199, 94±80 p0.05). Leflunomid tedavisi doku glutatyon düzeyleri ve süperoksit dizsmutaz aktivitesindeki azalmayı anlamlı ölçüde iyileştirmiştir (Sırasıyla 21±0.5, 25±3 p0.05 ve 22±0.6, 25±2 p0.05). Sonuç: Leflunomid tedavisi metotreksata bağlı ince barsak hasarındaki oksidatif parametreleri düzeltmektedir