The Effect of Udenafil on Stasis Zone in an Experimental Burn Model.

BACKGROUND: Management of the burn injuries is still a problematic issue because the stasis zone may become necrotic. We hypothesized that udenafil, a potent phospodiesterase inhibitor, can be beneficial in burn treatment by enhancing the viability of the stasis zone. METHODS: Fifteen Wistar rats were randomly divided into 3 groups. Comb burn injury model was conducted bilaterally on the back of rats in each subject. Group 1 received 1 mL/d of saline orally for 7 days. Group 2 received 10 mg/kg per day of udenafil for 7 days. Group 3 received 20 mg/kg per day of udenafil for 7 days. At the end of seventh day, gross morphological and histopathological samples of stasis zone survival were evaluated. RESULTS: Histopathological examination of groups 2 and 3 revealed that the stasis zone was mostly viable. The mean necrotic area and severity of inflammation was significantly higher in the control group compared with the treatment groups. Significant differences were determined in treatment groups compared with control group in terms of vital stasis zone area and histopathological parameters. CONCLUSIONS: Udenafil treatment improved tissue survival on zone of stasis in. Future experimental studies should be conducted to develop zone of stasis treatment protocols combining udenafil with potent anti-inflammatory and antioxidant drugs.

Are vitamin D and vitamin D receptor levels different in children with developmental dysplasia of the hip?

INTRODUCTION: Developmental dysplasia of the hip (DDH) is a common disorder and associated with significant morbidity of the hip joint. Several risk factors have been identified for DDH. The aim of this study is to investigate whether vitamin D and vitamin D receptor (VDR) levels differ in children with DDH and whether they have an effect on DDH development. MATERIALS AND METHODS: A total of 40 (17 males, 23 females; 9 right hips, 16 left hips, 15 bilateral hips) children who were treated for developmental dysplasia and 40 (23 males, 17 females) healthy children without any musculoskeletal system and metabolic disorders were included in this study between January and June 2019. Blood samples from the DDH and control groups of children were collected to measure the serum levels of vitamin D, VDR, calcium (Ca), phosphorus (P), and alkaline phosphatase (ALP). The levels of Ca, P, and ALP were analyzed using the automated standard spectrophotometric laboratory method. The levels of vitamin D and VDR in the samples were analyzed using enzyme-linked immunoassay. RESULTS: There were no significant differences in the serum levels of Ca, P, ALP, and vitamin D between the DDH and healthy groups (Ca 9.96 ± 0.47 vs. 9.92 ± 0.48 mg/dL, respectively, p = 0.721; P 5.3 ± 0.94 vs. 4.82 ± 0.88 mg/dL, respectively, p = 0.23; ALP 252.22 ± 170.15 vs. 245.3 ± 130.93 U/L, respectively, p = 0.839). However, serum VDR levels were significantly lower in children in the DDH group (5.77 ± 3.51 ng/mL) than in the healthy control group (9.25 ± 6.43 ng/mL) (p = 0.004). CONCLUSIONS: In conclusion, we believe that low VDR levels can affect DDH regardless of the serum levels of Ca, P, ALP, and vitamin D. More comprehensive studies involving parents are needed to understand whether VDR levels mediate genetic transmission in DDH or not.

Serum amphiregulin and cerebellin-1 levels in severe preeclampsia.

PURPOSE: Preeclampsia is a form of hypertensive disorders of pregnancy and defined as the presence of new-onset hypertension and proteinuria or other end organ damage occurring after 20-week gestation. Preeclampsia can be a destructive process that can cause maternal and infant mortality. The exact etiopathogenesis of preeclampsia is still undefined. We aimed to compare serum amphiregulin and cerebellin-1 levels of severe preeclampsia patients with healthy pregnant women and healthy control subjects. MATERIALS AND METHODS: A total of 88 women were enrolled in this study. Patients diagnosed with severe preeclampsia were group 1 (n = 28), healthy non-pregnant normotensive women group 2 (n = 30), and healthy pregnant women group 3 (n = 30). The participants in each group were matched for age. Pregnant women in groups 1 and 3 were also matched for gestational age. Serum amphiregulin and cerebellin-1 levels were measured using ELISA. RESULTS: Serum amphiregulin levels were 3413 ± 1.38 ng/ml (1748-7739), 8510 ± 7213 ng/ml (2019-24,000), and 6580 ± 5360 ng/ml (2484-24,000) in preeclampsia patients, controls and healthy pregnant women, respectively. Amphiregulin levels were significantly lower in preeclampsia patients than healthy pregnant women (p=.008) and controls (p = .015). Amphiregulin levels were similar between healthy controls and healthy pregnant women (p = 1.00). Cerebellin-1 levels were 222.039 ± 92.681 pg/ml (138,580-557,757) in preeclamptic patients, 537.043 ± 525.117 pg/ml (150,432-1,600,000) in controls and 415.091 ± 436.580 pg/ml (137,284-1,600,000) in healthy pregnant women. Cerebellin-1 levels were similar among groups (p = .272). Serum amphiregulin and cerebellin-1 levels were significantly and positively correlated with each other in preeclampsia patients (r = 0.693, p < .001), controls (r = 0.882, p < .001), and healthy pregnant women (r = 0.591, p = .001). Serum level of amphiregulin ≤3590 pg/ml had a sensitivity of 67.9% and specificity of 63.3% in the diagnosis of preeclampsia (AUC: 0.751; p = .001). CONCLUSIONS: Serum amphiregulin decreases in severe preeclampsia patients.

The serum level of soluble CXCL16 is increased in preeclampsia and associated with hepatic/renal damage.

OBJECTIVE: To compare the serum level of the chemokine, CXCL 16, in preeclamptic and healthy pregnant patients. METHODS: This prospective case control study was conducted between January and December 2018 in a tertiary level hospital. The study group was formed of 70 pregnant women diagnosed with preeclampsia, and the control group was formed of 70 healthy pregnant women matched to the study group in respect of age, gestational week and body mass index (BMI). The study group was separated into two subgroups of mild preeclampsia (n = 35) and severe preeclampsia (n = 35). The groups were compared in terms of demographic and clinical parameters and the levels of serum CXCL 16. RESULTS: No statistically significant difference was determined between the study and control groups in respect of maternal age, gravida, parity, BMI, and gestational age at sampling. Neonatal birth weight was significantly lower in the study group than in the control group. Mean serum alanine aminotransferase (ALT), aspartate amino transferase (AST) and creatinine levels of the study group were significantly higher than those of the control group (p < .05 for all). There was a statistically significant difference between the study and control groups regarding the mean platelet count. Compared to the control group, the severe and mild preeclampsia groups had a significantly higher serum level of CXCL 16. The serum level of CXCL 16 was significantly higher in patients with severe preeclampsia than in patients with mild preeclampsia (2.94 ± 3.89 pg mL-1 vs. 1.08 ± 1.87 pg mL-1, p = .14). Correlation analysis revealed a significant positive correlation of serum CXCL 16 level with serum ALT level (r = 0.320, p ≤ .001) and serum AST level (r = 0.373, p ≤ .001) and serum creatinine level (r = 0.279, p = .01) in both groups. High values indicated presence of preeclampsia, with a diagnostic cut-off point of 0.225, sensitivity of 75.7% and specificity of 72.9% for CXCL 16 (area under curve: 0.820, p < .001 CI: 0.753-0.888). CONCLUSIONS: This is the first study in literature to show a significantly higher level of CXCL 16 in patients with severe preeclampsia compared to those with mild preeclampsia. The study can also be considered of value in respect of showing that CXCL 16 could play a role in the etiopathogenesis of preeclampsia and the emergence of renal-hepatic damage. Blocking the CXCL 16/CXCR six axis in preeclampsia treatment could lay the ground for the development of new drugs which could be used in the treatment of preeclampsia.

Relationship of leptin, growth hormone, and insulin-like growth factor levels with body mass index and disease severity in patients with fibromyalgia syndrome.

OBJECTIVE: A high prevalence of obesity in fibromyalgia syndrome (FMS) predisposes patients to metabolic changes. It is not clear how the clinical manifestations of the disease affect metabolism. This study aimed to investigate leptin, growth hormone (GH), and insulin-like growth factor (IGF-1) levels in FMS, and their relationship with body mass index (BMI) and disease severity. METHOD: This case-control study included 60 patients with FMS and 42 age- and sex-matched healthy controls. BMIs were recorded for all participants. The disease severity was assessed using the Fibromyalgia Impact Questionnaire (FIQ) and a visual analog scale (VAS). The serum levels of leptin, GH, and IGF-1 of all participants were measured using specific enzyme-linked immunosorbent assays. RESULTS: Both groups had similar age (p = 0.058), sex (p = 0.25), and BMI (p = 0.29) distribution. The mean age of the FMS and the control groups was 40.7 ± 10.8 years and 36.2 ± 13.6 years, respectively. The mean BMI was 26.7 kg/m2 in the FMS group. The GH (p = 0.037) and IGF-1 (p = 0.002) levels were statistically lower, and leptin (p = 0.002) levels were considerably higher in the FMS group than in the control group. The leptin values were positively correlated with age (p = 0.001; r = 0.386) and BMI (p < 0.001; r = 445). Insulin-like growth factor levels were negatively correlated with age (p < 0.001; r = - 0.605) and BMI (p < 0.001; r = - 0.564). Similarly, GH levels were negatively correlated with age (p = 0.040; r = - 0.243) and BMI (p < 0.001; p = - 0.420). None of the three hormones were associated with FIQ and VAS. CONCLUSION: We found that leptin (high), GH (low), and IGF-1 (low) levels were statistically different, together with being independent of disease severity (FIQ, VAS), and correlated with BMI in the FMS group. These findings may be related with hypothalamo-pituitary axis dysfunction, BMI, and energy metabolism.

The Clinical Importance of the Plasma Atherogenic Index, Other Lipid Indexes, and Urinary Sodium and Potassium Excretion in Patients with Stroke.

OBJECTIVE: Cardiovascular complications are still the primary reason for high mortality rates worldwide. The determination of risk factors is important to prevent stroke. The aim of the present study was to analyze the importance of serum lipid indexes and urinary sodium (Na)/potassium (K) excretion in patients with stroke together with sex differences. MATERIALS AND METHODS: A total of 50 (28 male and 22 female, mean age 65.9±14.6 years) patients with acute stroke were included in the study group, and 32 body mass index-matched healthy subjects were included in the control group. Lipid profiles [(cholesterol, triglyceride, very low-density lipoprotein, low-density lipoprotein, and high-density lipoprotein (HDL)], serum creatinine (Cre), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and Na, K, and Cre excretion in spot urine samples of the patients were recorded. RESULTS: Systolic blood pressure (p=0.021), ESR (p=0.044), and CRP (p=0.042) were significantly higher in all patients in the stroke group; urinary Tanaka (K) (p=0.033), Kawazaki (K) (p=0.028), urinary spot Cre (p=0.012), and Na excretion (p=0.036) levels were found to be significantly lower in only male patients with stroke. The mean plasma atherogenic indexes were 0.57±0.24 in the study (stroke) group and 0.54±0.22 in the control group (p=0.61). Other lipid indexes, such as Castelli's risk index (CRI)-I (p=0.29), CRI-II (p=0.24), atherogenic coefficient (p=0.29), and non-HDL cholesterol (p=0.69), were not statistically different from the controls. CONCLUSION: Urinary Na, K, and Cre excretion was significantly lower in male patients with stroke, and acute phase reactants were significantly higher in the entire stroke group than in controls. These parameters can be used as auxiliary biomarkers in the risk assessment of stroke.

The Importance of G-protein Coupled Estrogen Receptor in Patients With Fibromyalgia.

OBJECTIVES: This study aims to analyze the G-protein coupled estrogen receptor (GPER/GPR30) activity in patients with fibromyalgia syndrome (FMS). PATIENTS AND METHODS: We enrolled 40 female patients with FMS (mean age 42.9±11.2 years; range, 18 to 64 years) diagnosed according to the 2010 American College of Rheumatology classification criteria and 30 age- and body mass index-matched female healthy controls (mean age 43.7±13.6 years; range, 19 to 64 years). Sex hormones of patients (morning) including estradiol, follicle stimulating hormone, luteinizing hormone, and prolactin (PRL) were recorded. FMS severity was assessed by Fibromyalgia Impact Questionnaire (FIQ). Serum GPER levels were measured by using a quantitative sandwich enzyme-linked immunosorbent assay method with a commercial kit. RESULTS: G-protein coupled estrogen receptor levels were 0.11 (0.02-0.9) ng/mL in the FMS patients and 0.059 (0.01-0.13) ng/mL in controls, with a statistically significant difference (p=0.037). GPER levels were positively correlated with age and negatively correlated with PRL, while they were not correlated with FIQ. Differential diagnosis for FMS with receiver operating characteristic (ROC) analysis for the serum GPER levels was statistically significant (area under the ROC curve: 0.653, confidence interval: 0.522-0.785, p=0.029). High values indicated FMS, with a threshold of >0.075, sensitivity of 60%, and specificity of 60%. CONCLUSION: The GPER levels of FMS patients were higher than those of the controls. Thus, GPER levels may be considered as a biomarker in the diagnosis of FMS independent of disease severity.