Vitamin D Deficiency and Its Association with Inflammatory Markers, Lipid Profile and Regulatory T-cells in Pediatric Sickle Cell Disease Patients.

We investigated vitamin D deficiency in pediatric sickle cell disease patients and its association with selected bone, lipid and inflammatory parameters. The study included 64 patients (33 SS and 31 SB) and 21 carriers (AS). Blood was obtained to assess levels of vitamin D, WBC, CRP, Ca, P, ALP, PTH, triglyceride, total cholesterol, LDL, VLDL, HDL, IL-2, IL-12, TNF-α, IL-4, IL-6, IL-10 and regulatory T cells. The patients were grouped according to their genotype (SS, SB) and vitamin D status (low or normal). Carriers were also grouped as low or normal vitamin D. Laboratory findings were similar between low and normal Vit D groups in SS, SB and AS genotypes except a lower IL-12 in SB-low vitamin D compared SB-normal vitamin D group. Acute chest syndrome was more frequent in SS-low Vit D (63%) compared to SS-normal Vit D (25%), SB-low Vit D (21%) and SB-normal Vit D (33%) (P = 0.045). Both SS and SB with low vitamin D had higher VLDL (P = 0.006 and P = 0.022), TNF-α (P = 0.001) and regulatory T cells (P = 0.000) compared to AS-low vitamin D. Both SS and SB with normal vitamin D had higher levels of regulatory T cells (P = 0.000) compared to AS-normal vitamin D. Vit D was not a modifier of selected inflammation, bone and lipid parameters in sickle cell disease. Acute chest syndrome was comparably more frequent in SS-low vitamin D. Increase of regulatory T cells in the patients was a result of chronic inflammation in sickle cell disease.

Determination of NF-κB and RANKL levels in peripheral blood osteoclast precursor cells in chronic kidney disease patients.

PURPOSE: Chronic kidney disease (CKD) is a progressive condition characterized by irreversible loss of functional nephron mass due to variety of causes; an inevitable complication of CKD is metabolic bone disease, and this pathology is called as renal osteodystrophy (ROD). In this study, we aimed to determine the levels of serum sRANKL and intracellular NF-κB levels in peripheral blood osteoclast precursor cells in patients with stage 3 CKD. MATERIALS AND METHODS: Forty-one male patients aged 35-60 with CKD identified as stage 3 according to GFR calculated on the basis of creatinine values and 27 healthy male subjects with age ranging from 40 to 60 as control group were included in this study. Levels of biochemical parameters, vitamin D3, parathyroid hormone, bone mineral density, sRANKL and NF-κB were determined by using photometric, electrochemiluminescence, HPLC, ELISA and flow cytometric methods in control and patient groups, respectively. RESULTS: When stage 3 CKD patients were compared with controls, patients with stage 3 CKD had statistically significantly higher iPTH levels, but they had statistically significantly lower vitamin D3 levels. However, the other biochemical parameters, bone mineral density, sRANKL and NF-κB levels did not reveal any significance. CONCLUSION: In conclusion, vitamin D3 and iPTH levels seem to be important parameters for evaluating the early stages of ROD. The lack of statistically significant differences in the levels of sRANKL and NF-κB suggests that these parameters are not sufficient in the evaluation of bone metabolism in the early stages of renal failure.

Seasonal variation of asthma control, lung function tests and allergic inflammation in relation to vitamin D levels: a prospective annual study.

INTRODUCTION: There are scarce data about the role of vitamin D (vitD) in asthma control related to seasons and other confounders. AIM: To investigate the seasonal relationship between vitD levels and asthma control, lung function tests (LFTs) and cytokines during a 1-year period, among 7-17-year-old asthmatic children. MATERIAL AND METHODS: Thirty patients with asthma with house dust mite monosensitization were evaluated 3 monthly about the previous month's health and vitD related lifestyle factors and asthma control test (ACT), spirometry and bronchial provocation test for a year. Serum vitD, vitD binding protein (VDBP), total IgE levels, absolute eosinophil and Treg counts and cytokine levels were simultaneously measured. The seasonal changes of vitD and other parameters and the relationship between 120 pooled data sets of vitD and major outcomes were evaluated. RESULTS: Mean vitD levels, forced expiratory volume in 1 s (FEV1%) and ACT score were lowest in winter and highest in summer. Pooled vitD levels were positively correlated with pooled ACT scores, Treg counts, FEV1% values and VDBP levels and negatively with total immunoglobulin E (IgE) and interleukin-4 (IL-4) levels and bronchodilator response. VitD levels were positively associated with ACT score, and FEV1% value and negatively with serum IgE level and bronchodilator response after adjusting for confounders. CONCLUSIONS: This study revealed that asthma control measures, LFTs and IgE levels were significantly related to serum vitD levels, independent from age, body mass index, inhaled corticosteroid use, sun exposure and season among asthmatic children. Vitamin D levels showed a positive correlation with Treg counts and a negative correlation with Th2 type cytokines.

A nationwide multicentre study in Turkey for establishing reference intervals of haematological parameters with novel use of a panel of whole blood.

INTRODUCTION: A nationwide multicentre study was conducted to establish well-defined reference intervals (RIs) of haematological parameters for the Turkish population in consideration of sources of variation in reference values (RVs). MATERIALS AND METHODS: K2-EDTA whole blood samples (total of 3363) were collected from 12 laboratories. Sera were also collected for measurements of iron, UIBC, TIBC, and ferritin for use in the latent abnormal values exclusion (LAVE) method. The blood samples were analysed within 2 hours in each laboratory using Cell Dyn and Ruby (Abbott), LH780 (Beckman Coulter), or XT-2000i (Sysmex). A panel of freshly prepared blood from 40 healthy volunteers was measured in common to assess any analyser-dependent bias in the measurements. The SD ratio (SDR) based on ANOVA was used to judge the need for partitioning RVs. RIs were computed by the parametric method with/without applying the LAVE method. RESULTS: Analyser-dependent bias was found for basophils (Bas), MCHC, RDW and MPV from the panel test results and thus those RIs were derived for each manufacturer. RIs were determined from all volunteers' results for WBC, neutrophils, lymphocytes, monocytes, eosinophils, MCV, MCH and platelets. Gender-specific RIs were required for RBC, haemoglobin, haematocrit, iron, UIBC and ferritin. Region-specific RIs were required for RBC, haemoglobin, haematocrit, UIBC, and TIBC. CONCLUSIONS: With the novel use of a freshly prepared blood panel, manufacturer-specific RIs' were derived for Bas, Bas%, MCHC, RDW and MPV. Regional differences in RIs were observed among the 7 regions of Turkey, which may be attributed to nutritional or environmental factors, including altitude.

The effects of selective head cooling versus whole-body cooling on some neural and inflammatory biomarkers: a randomized controlled pilot study.

BACKGROUND: Therapeutic hypothermia (TH) has become standard care in newborns with moderate to severe hypoxic ischemic encephalopathy (HIE), and the 2 most commonly used methods are selective head cooling (SHC) and whole body cooling (WBC). This study aimed to determine if the effects of the 2 methods on some neural and inflammatory biomarkers differ. MATERIALS AND METHODS: This prospective randomized pilot study included newborns delivered after >36 weeks of gestation. SHC or WBC was administered randomly to newborns with moderate to severe HIE that were prescribed TH. The serum interleukin (IL)-1ß, IL-6, neuron-specific enolase (NSE), brain-specific creatine kinase (CK-BB), tumor necrosis factor-alpha (TNF-α), and protein S100 levels, the urine S100B level, and the urine lactate/creatinine (L/C) ratio were evaluated 6 and 72 h after birth. The Bayley Scales of Infant and Toddler Development-III was administered at month 12 for assessment of neurodevelopmental findings. RESULTS: The SHC group included 14 newborns, the WBC group included 10, the mild HIE group included 7, and the control group included 9. All the biomarker levels in the SHC and WBC groups at 6 and 72 h were similar, and all the changes in the biomarker levels between 6 and 72 h were similar in both groups. The serum IL-6 and protein S100 levels at 6 h in the SHC and WBC groups were significantly higher than in the control group. The urine L/C ratio at 6 h in the SHC and WBC groups was significantly higher than in the mild HIE and control groups. The IL-6 level and L/C ratio at 6 and 72 h in the patients that had died or had disability at month 12 were significantly higher than in the patients without disability at month 12. CONCLUSION: The effects of SHC and WBC on the biomarkers evaluated did not differ. The urine L/C ratio might be useful for differentiating newborns with moderate and severe HIE from those with mild HIE. Furthermore, the serum IL-6 level and the L/C ratio might be useful for predicting disability and mortality in newborns with HIE.

Diagnostic evaluation and risk factors for drug allergies in children: from clinical history to skin and challenge tests.

BACKGROUND: Parent or self-reported drug allergy claims frequently overestimate the real incidence of hypersensitivity reactions. A detailed and algorithmic diagnostic evaluation of drug reactions may allow a proper diagnosis. OBJECTIVE: The aim of this study was to determine the confirmation rates and risk factors for confirmed allergic drug reactions in children. SETTING: Mersin University Hospital in Turkey. METHOD: The study consisted of children between ages of 8 months and 18 years with the history of suspected drug allergy as reported by the clinician or the patients. Parents were interviewed by a clinician to complete questionnaires that included questions about demographic data and characteristics of index drug reaction. Immediate reactions (IRs) were assessed with immediate-reading skin prick (SPT) and intradermal tests (IDT). Nonimmediate reactions (NIRs) were assessed with SPT, both early and delayed reading of IDT and patch tests. In case of negative skin tests, drug provocation tests were performed. The possible risk factors for confirmed drug allergy in univariate analysis (p < 0.1) were entered into the multivariate logistic regression analysis to determine independent predictors. MAIN OUTCOME MEASURE: (1) Confirmation rates of drug allergy (2) Risk factors related to confirmed drug allergy in children. RESULTS: We evaluated a total of 180 suspected drug allergy reactions in 97 children, mainly to antibiotics, non-steroidal anti-inflammatory drugs (NSAIDs) and anticonvulsants. Among all suspected allergic drug reactions, 97 (53.9 %) were immediate type and 83 (46.1 %) were non-immediate type. The average time interval between the reaction and allergologic work-up was 5 months. Drug allergy confirmation rates were 30.1 % for beta-lactams, 27.2 % for non-betalactams, 21.1 % for NSAIDs and 30 % for anticonvulsants. Eight of 54 confirmed NIRs showed positivity on immediate skin tests. Regulatory T cells, TGF-ß and IL-10 levels were not different between groups with and without confirmed drug allergy. A strong family and personal history of drug allergy were found to be significantly related to the confirmed allergic drug reactions. CONCLUSION: Parent or self-reported drug allergy should be evaluated with a standardized diagnostic work-up before strict prohibitions are made. In addition, family and personal histories of drug allergy were significant risk factors related to allergic drug reactions in children.

Effects of venlafaxine and fluoxetine on lymphocyte subsets in patients with major depressive disorder: a flow cytometric analysis.

BACKGROUND: Studies have yielded conflicting results concerning flow cytometric lymphocyte analyses in patients with depression. Data about the effect of antidepressants on lymphocyte subsets are also contradictory. The aim of this study was to determine effects of venlafaxine versus fluoxetine on lymphocyte subsets in depressive patients. METHODS: Sixty-nine patients diagnosed with major depressive disorder (MDD) according to DSM-IV and 36 healthy controls are included in the study. Sixty-nine patients were randomized to take fluoxetine (FLX) (n=33) or venlafaxine (VEN) (n=36). Serum lymphocyte subsets included CD3, CD4, CD8, CD16/56, CD19, CD45, Anti-HLA-DR which were measured by flow cytometric analyses at baseline and 6 weeks after the start of treatment. The severity of depression was evaluated with Hamilton rating scale for depression. RESULTS: At baseline, patients with MDD had significantly lower CD16/56 ratio and higher CD45 ratio compared to the controls. Although numerically higher in the VEN treated patients, treatment response rates between the FLX (53%) and the VEN (75%) groups were not different statistically. CD45 values decreased significantly in the VEN group at the end of the 6 week treatment period whereas no difference was observed in the FLX group. By the 6th week, treatment responders showed a significantly higher CD16/56 ratio than non-responders. Baseline severity of depression and anxiety was positively correlated with baseline CD45 ratio and negatively correlated with baseline CD16/56 ratio. We did not observe consistent changes in the absolute number of circulating B or T cells, nor in the helper/inducer (CD4) or suppressor/cytotoxic (CD8) subsets. CONCLUSIONS: CD16/56 was lower in patients with MDD and increased in treatment responders at 6th week. CD45 ratio was higher in patients with MDD than healthy subjects; it decreased with antidepressant treatment and was positively correlated with the severity of depression. Antidepressant treatment contributes to immune regulation in patients with major depressive disorder.

CD4+CD25+ Treg cells in patients with toenail onychomycosis.

The essential role played by CD25+CD4+ regulatory T (Treg) cells in the control of immunity against some pathogens such as Helicobacter pylori is now well established. But their role in cutaneous fungal infections is still unknown. Onychomycosis is the chronic fungal infection of the nails, which is very common. The aim of this study was to evaluate possible relationship of CD4+CD25+ Treg cells and onychomycosis. Peripheral blood samples were investigated for CD4+CD25+ Treg cells using flow cytometry analysis in 43 toenail onychomycosis patients and in 30 healthy controls. We have found that onychomycosis patients had a higher expression of CD25+CD4+ Treg cells than controls, with values of 8.45 +/- 4.47% versus 4.64 +/- 1.59%, respectively (P = 0.001). The results of this study suggests that increased numbers of CD4+CD25+ Treg cells may play a role in failure of clearance of dermatophytes from skin by preventing the protective inflammation which is leading to development of onychomycosis. Accordingly, we address the possibility that CD4+CD25+ Treg cells may play a role in immune pathogenesis of other superficial fungal infections.

Granulocyte-colony stimulating factor improves the survival of ischaemic skin flaps by the induction of angiogenesis.

In this study the effects of granulocyte-colony stimulating factor (G-CSF) on angiogenesis and the survival of ischaemic skin flaps are evaluated. Thirty adult Wistar rats were equally randomised into three groups. Caudal-based, ischaemic skin flaps of 10 x 3 cm were designed on the back and injected with saline in group 1 and with 100 microg/kg G-CSF in groups 2 and 3. The injections were performed just prior to flap elevation in groups 1 and 2 and 2 days earlier in group 3. Peripheral leukocyte counts, tissue myeloperoxidase enzyme assays, necrotic to total flap area ratio (NA/TA) calculations, flap tissue inflammation gradings, immunohistochemical vessel counts, and electron microscopic evaluation of endothelial cells were performed on the 8th day. No significant difference was encountered between the groups in terms of the leukocyte counts, myeloperoxidase enzyme assays and inflammation gradings (P > 0.05), demonstrating the absence of an increased inflammatory response within the flap tissue. The surviving flap portions were observed to be increased with the application of G-CSF. The mean NA/TA results (when measured in situ) were 0.44+/-0.13 for group 1, 0.30+/-0.17 for group 2, and 0.22+/-0.16 for group 3. The difference between groups 1 and 3 was statistically significant (P = 0.009). The mean vessel count was 3.53+/-1.20 in group 1, 7.36+/-1.41 in group 2 and 7.43+/-0.92 in group 3. The differences between groups 1 and 2 and groups 1 and 3 were statistically significant (P < or = 0.001). Early apoptotic changes were encountered in the endothelial cells of group 1, while activated and proliferating endothelial cells were seen in groups 2 and 3 with electron microscopy. G-CSF promotes angiogenesis by increasing the number of activated and proliferating endothelial cells within the ischaemic flaps by the resettlement of G-CSF-stimulated endothelial progenitor cells into the ischaemic tissue. The overall result is an improved survival of ischaemic skin flaps. These effects are more pronounced when G-CSF is introduced 2 days prior to flap elevation.

Are glutathione S-transferase gene polymorphisms linked to neonatal jaundice?

Glutathione S-transferases (GSTs) are a major group of phase II detoxification enzymes involved in the metabolism of both endogenous and xenobiotic compounds. In addition to their catalytic function in detoxification, GSTs participate in binding to nonsubstrate ligands such as bilirubin. Ligandin, which is one of the principal hepatic-binding proteins, is also a member of the GST family. The aim of the present study was to investigate the possible relationship between neonatal jaundice and the GST gene polymorphisms. The study cohort consisted of a patient group of 116 newborns (plasma bilirubin levels > or = 15 mg/dl) and a control group of 54 newborns (plasma bilirubin levels <13 mg/dl). In the patient group, the null genotype frequencies in GSTM1 and GSTT1 were 52.6 and 19%, respectively; in the control group, these were 63 and 27.8%, respectively. The frequencies of GSTM1 and GSTT1 were similar in the patient and control groups (p > 0.05). Total bilirubin levels were found to be significantly higher in patients with the GSTM1 null genotype than in patients with the GSTM1 wild genotype (p = 0.042). There was no statistically significant difference in total bilirubin levels between patients with the null GSTT1 genotype and those with the wild GSTT1 genotype. It is conceivable that there is a relation between GSTM1 gene polymorphism and total bilirubin levels in neonatal jaundice. We suggest that GSTM1 gene polymorphisms may affect ligandin functions in hepatocytes, which are important in bilirubin transportation. Consequently, patients with the GSTM1 null genotype may have higher total levels of bilirubin.

The frequency of UDP-glucuronosyltransferase 1A1 promoter region (TA)7 polymorphism in newborns and it's relation with jaundice.

Increased bilirubin formation and decreased bilirubin conjugation play an important role in the pathogenesis of the newborn jaundice. Although physiologic jaundice is seen in most of the newborns, there are many risk factors that affect the severity and duration of hyperbilirubinemia. The latest studies showed that the frequency and severity of neonatal jaundice have been increased when mutations of the gene coding UDP-glucuronosyltransferase(UGT)1A1 coexist with other risk factors. Healthy term newborns weighing over 2500 g. were included in this study. The patient group consisted of 107 newborns either with total bilirubin level over 15 mg dl(-1) within 7 days or 5 mg dl(-1) after 15 days of age. The control group consisted of 55 newborns with bilirubin levels in physiological ranges. We investigated the frequency of promoter region [thymine-adenine(TA)]7 polymorphism in UGT1A1 gene. Factors which might cause pathologic and prolonged jaundice with coexisting polymorphism were also investigated. UGT1A1 6/7 genotype was found to be 11% in patient group and 13% in the control group. The difference between patient and control groups was not statistically significant. (TA)7 allele frequency was 0.069 and it is concluded that UGT1A1 promoter region polymorphism was not a risk factor for neonatal jaundice.

Serum leptin levels in patients with allergic rhinitis.

OBJECTIVE: To investigate the serum leptin levels in patients with allergic rhinitis during the symptomatic period. STUDY DESIGN AND SETTING: A randomized, prospective study was performed on 26 adult patients with allergic rhinitis and 20 control subjects with similar age, sex and body mass index in a tertiary otolaryngology center. RESULTS: Leptin levels were 28.8 +/- 14.1 ng/mL in the patients with allergic rhinitis, and 20.8 +/- 13.5 ng/mL in the control group respectively. The difference between the groups was statistically significant (p = 0.04). CONCLUSION: Serum leptin levels were found to be significantly higher in patients with allergic rhinitis in symptomatic period. SIGNIFICANCE: Apart from its primary role in the regulation of body weight and energy expenditure, leptin may have a role in the inflammatory process of the allergic rhinitis.

The role of factor V Leiden and prothrombin G20210A mutations in sudden sensorineural hearing loss.

OBJECTIVES: To investigate the incidence of factor V Leiden and prothrombin G20210A in sudden sensorineural hearing loss patients. STUDY DESIGN: The patient group for this study was selected prospectively in the case of 28 patients and retrospectively in the case of another 28. SETTING: Tertiary referral center. PATIENTS: Fifty-six patients (29 female, 27 male) with sudden sensorineural hearing loss (SSHL) and 95 control subjects (48 female, 47 male) were enrolled in this study. The age of the control subjects were between 26 and 76 (38 +/- 16.7), and that of the patients were between 10 and 87 (42.6 +/- 18.2). INTERVENTION: The factor V Leiden and prothrombin G20210A mutations were detected by rapid polymerase chain reaction amplification of genomic DNA extracted from the SSHL patients' peripheral blood cells. MAIN OUTCOME MEASURE: Thrombotic microangiopathic disorders are characterized by widespread microvascular thrombosis leading to end-organ injury. The mutations of factor V Leiden and prothrombin gene are known as genetic risk factors for thrombotic microangiopathy in normal patients. SSHL may occur with occlusion of the cochlear blood supply by microthromboangiopathy. RESULTS: Factor V Leiden mutation was found to be higher in SSHL patients when compared with control subjects (16.1% vs 5.3%). The difference between the two groups was found to be statistically significant (p = 0.02). However, statistical significance was not found between the groups in regard to prothrombin G20210A mutation. Factor V Leiden and prothrombin gene mutations were heterozygous in all of the subjects. CONCLUSION: A significant association between factor V Leiden mutation and idiopathic SSHL could be shown in this study. There was no correlation, however, between the occurrence of idiopathic SSHL and prothrombin mutation.

Liver and kidney toxicity in chronic use of opioids: an experimental long term treatment model.

In this study, histopathological and biochemical changes due to chronic usage of morphine or tramadol in liver and kidney were assessed in rats. Thirty male Wistar rats (180-220 g) were included and divided into three groups. Normal saline (1 ml) was given intraperitoneally as placebo in the control group (n = 10). Morphine group (n = 10) received morphine intraperitoneally at a dose of 4, 8, 10 mg/kg/day in the first, second and the third ten days of the study, respectively. Tramadol group (n = 10), received the drug intraperitoneally at doses of 20, 40 and 80 mg/kg/day in the first, second and the third ten days of the study, respectively. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatinin, blood urea nitrogen (BUN) and malondialdehyde (MDA) levels were measured in the serum. Liver and kidney specimens were evaluated by light microscopy. Serum ALT, AST, LDH, BUN and creatinin levels were significantly higher in morphine group compared to the control group. Serum LDH, BUN and creatinin levels were significantly increased in the morphine group compared to the tramadol group. The mean MDA level was significantly higher in morphine group compared to the tramadol and control groups (P < 0.05). Light microscopy revealed severe centrolobular congestion and focal necrosis in the liver of morphine and tramadol groups, but perivenular necrosis was present only in the morphine group. The main histopathologic finding was vacuolization in tubular cells in morphine and tramadol groups. Our findings pointed out the risk of increased lipid peroxidation, hepatic and renal damage due to long term use of opioids, especially morphine. Although opioids are reported to be effective in pain management, their toxic effects should be kept in mind during chronic usage.

Apolipoprotein E polymorphism and lipoprotein compositions in patients with Behçet's disease.

BACKGROUND: Behçet's disease (BD) is a multisystemic disease of unknown etiology characterized by chronic relapsing oral-genital ulcers and uveitis. Some abnormalities in lipoprotein metabolism have been described in patients with BD. METHODS: In this study, apolipoprotein E (apo E) polymorphism and lipoprotein cholesterol concentrations in 30 patients with BD were compared with those of 27 control subjects. RESULTS: Both patients and controls were found to be normolipidemic. Patients with BD had significantly higher concentrations of high-density lipoprotein (HDL) cholesterol than those of controls (P < 0.05); however, there was no difference in serum triglyceride, low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) cholesterol concentrations. The distribution of apo E genotypes and alleles was the same in both groups. There were slight differences in allele frequency between the groups, but this was not statistically significant. CONCLUSIONS: The high HDL cholesterol levels observed in our patients were not related to abnormalities in apo E alleles.

Malondialdehyde and antioxidant enzymes in children with obstructive adenotonsillar hypertrophy.

OBJECTIVE: Free radical induced tissue damage has been implicated in the pathogenesis of several diseases. We aimed to investigate the role of free radicals and scavenging enzymes in children with obstructive adenotonsillar hypertrophy. MATERIALS AND METHODS: The study consisted of 29 children with obstructive adenotonsillar hypertrophy and 51 control subjects with similar age and sex. All the patients and/or their parents had complaints of snoring, mouth breathing, and pausing of breath during sleep for at least 6 months. All patients underwent an adenotonsillectomy operation under general anesthesia with curettage and cold dissection methods. Venous blood was taken preoperatively and 4 weeks postoperatively. After collection of blood samples into citrate (3.5 mg/ml blood) containing glass tubes, erythrocyte sediments were prepared for the analyses. Then malondialdehyde (MDA) level, and superoxide dismutase (SOD), glutathione peroxidase (GSHPx), and catalase (CAT) activities were measured. RESULTS: The levels of MDA and activities of SOD and GSHPx were significantly higher in the pre-tonsillectomy period than in the post-tonsillectomy period. However, CAT activity was not different in pre- and postoperative period. CONCLUSION: Our study supports the notion that oxidant and antioxidant defense mechanisms are altered in children with obstructive adenotonsillar hypertrophy, and this alteration improves after tonsillectomy.

Apolipoprotein E gene polymorphism and serum lipids in patients with superficial fungal disease.

Superficial mycosis, including dermatophytic infections, tinea versicolor, and cutaneous candidiasis is mostly limited to the outer layers of the skin, nails, and mucous membranes. In this study, Apolipoprotein E (ApoE) polymorphism and lipoprotein cholesterol concentrations were compared between 42 patients with superficial fungal disease and 27 control subjects. Both the patients and controls were found to be normolipemic. The patients with superficial fungal disease had significantly higher concentrations of high-density cholesterol (HDL) compared to the control group (p=0.0462). However, there was no difference in the serum triglyceride, low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) cholesterol concentrations. A significantly higher incidence of heterozygosity E2/3 was found in the patients (p=0.0228), and significantly lower incidence of homozygosity E3/3 in all patients, and those with candidiasis and dermatophytosis (p=0.0139, 0.0194 and 0.0337, respectively) compared to the control group. The E3/4 genotype differences between patients and controls were not statistically significant. There were slight differences in the allele frequencies between the two groups, but these did not reach statistically significant levels. It was concluded that the presence of apoE2/3 genotype, high HDL-cholesterol levels and the absence of apoE3/3 genotype can be regarded as risk factors for superficial fungal disease, especially dermatophytosis.

In vivo effects of meloxicam, celecoxib, and ibuprofen on free radical metabolism in human erythrocytes.

One of the major groups of chemical mediators involved in the inflammatory response is the prostaglandins, which are synthesized from arachidonic acid by the enzyme cyclooxygenase. The aim of this study is to compare the in vivo effects of celecoxib, meloxicam, and ibuprofen on the activities of catalase (CAT), glutathione peroxidase (GSHPx), superoxide dismutase (SOD) as well as malondialdehyde (MDA), and antioxidant potential levels (AOP) in human erythrocytes. Patients diagnosed as osteoarthritis were included in the study. Patients were treated with Celecoxib (200 mg/d) (n = 12), Meloxicam (15 mg/d) (n = 12), and Ibuprufen (1200 mg/d) (n = 9) for 21 days. SOD, CAT, GSHPx activities, MDA, and AOP levels were investigated in human erythrocyte haemolysates. SOD activity and AOP levels were significantly decreased in all NSAID groups when we compared the values before and after 21 days of celecoxib, meloxicam, ibuprofen treatment. There were no significant difference in CAT, GSHPx activities, and MDA levels before and after treatment in each group. Decreased SOD activities are thought to be related with the increased superoxide anion. Decreased AOP levels may indicate impairment in the total antioxidant defence system. These NSAIDs have similar effects on free radical metabolism on human erythrocytes; despite some difference in action mechanisms.

Comparison of ischemic and chemical preconditioning in jejunal flaps in the rat.

Jejunum is one of the most frequently used free flaps in esophagus reconstruction. However, the sensitivity of intestinal tissue to ischemia decreases the margin of safety of this donor site while increasing the risk of postoperative complications such as fistula formation and stenosis. Ischemic preconditioning can increase the tolerance of jejunal tissue to ischemia. In this study, the authors investigated the effects of chemical preconditioning with adenosine infusion on ischemia reperfusion injury in the rat jejunum, and evaluated the presence of any additive effects of adenosine administration when used together with ischemic preconditioning. Forty Sprague-Dawley rats weighting 200 to 250 mg were used in the study. Rats were randomly divided into five groups. In group I (sham-operated controls), only laparotomy was performed. In group II (ischemia-reperfusion injury), the superior mesenteric artery was clamped for 40 minutes to induce ischemia in the small bowel, followed by 60 minutes of reperfusion. In group III (ischemic preconditioning), two cycles of 5-minute ischemia and 5-minute reperfusion were performed before implementation of the ischemia-reperfusion protocol used in group II. In group IV (chemical preconditioning), adenosine (1000 microg/kg) was infused into the internal jugular vein before the group II ischemia-reperfusion schedule was implemented. In group V (adenosine-enhanced ischemic preconditioning), adenosine (1000 microg/kg) was infused into the internal jugular vein before ischemic preconditioning, followed by 40 minutes of ischemia and 60 minutes of reperfusion. At the end of the reperfusion period, samples from the jejunum were harvested and myeloperoxidase activity was determined as a measure of leukocyte accumulation. Malondialdehyde levels were measured to assess lipid peroxidation. Histopathologic sections stained with hematoxylin-eosin were evaluated for the presence of mucosal damage according to the Chiu scoring method. Immunohistochemical staining by M30 monoclonal antibodies was performed to quantify the number of ischemia-induced apoptotic cells in the intestinal mucosa. The myeloperoxidase and malondialdehyde levels were significantly lower in groups I, III, IV, and V when compared with group II. Although there were no significant differences among myeloperoxidase and malondialdehyde levels in groups III, IV, and V, group I had significantly lower levels of activity compared with the other three groups. Histological scoring reflected significantly less damage in groups I, III, IV, and V compared with group II. Similarly, the number of apoptotic cells was significantly lower in groups I, III, IV, and V when compared with group II. However, no difference was detected among these four groups with regard to either histopathological scoring or apoptosis numbers. This is the first study showing that adenosine administration is as effective as ischemic preconditioning in inducing ischemic tolerance in the rat jejunum. However, there was no enhancement of ischemic preconditioning with prior adenosine infusion.