Serum myeloperoxidase level is associated with heart-type fatty acid-binding protein but not troponin T in patients with chronic heart failure.

OBJECTIVE: Our aim was to investigate the possible relationship between myeloperoxidase (MPO) and myocardial damage markers such as heart-type fatty acid-binding protein (H-FABP) and troponin T (TnT) in patients with chronic heart failure (HF). MATERIALS AND METHODS: Forty-two consecutive patients (age range: 27-80 years) with chronic HF were enrolled in the study. Serum H-FABP, TnT and MPO levels were measured. Routine biochemical and clinical parameters were recorded. Echocardiographic examinations were performed on all patients. A linear regression analysis was performed to determine the correlates of serum H-FABP. RESULTS: The MPO, H-FABP and TnT levels were 255 ± 227, 60.6 ± 48.5 and 0.07 ± 0.15 ng/ml, respectively. In multiple linear regression analysis, age (ß = -0.36, p = 0.006), creatinine level (ß = 0.3, p = 0.024) and serum MPO level (ß = 0.41, p = 0.009) were significant determinants of H-FABP levels. Bivariate predictors were not significantly associated with TnT levels in linear regression analyses. CONCLUSIONS: The MPO was significantly associated with serum H-FABP levels but not with TnT.

Circulating levels of erythropoietin and its relation to arterial stiffness in patients with hypertension.

BACKGROUND: Emerging experimental and clinical data indicates that erythropoietin (EPO) have significant roles in the cardiovascular system. But the relationship between endogenous EPO levels and arterial stiffness remains unknown. We investigated the EPO levels in relation to arterial stiffness parameters in patients with never treated newly diagnosed hypertension (HT). METHODS: We studied 42 (47.8 ± 10 years) never treated HT patients and age and gender-matched 40 (47 ± 8.6 years) normotensive individuals. Serum EPO levels were determined in all subjects using the chemiluminescence immunoassay kit. We evaluated heart rate-corrected augmentation index (AIx@75), a marker of wave reflections and aortic pulse wave velocity (PWV) as indices of elastic-type aortic stiffness using applanation tonometry (Sphygmocor). RESULTS: The levels of EPO were not significantly different in hypertensive patients and the controls (10.6 ± 5 vs. 11.6 ± 9, mIU/mL, p = 0.5). Aortic PWV (10.3 ± 2.3 vs. 8.7 ± 1.6 m/s, p = 0.0001) and AIx@75 (22.7 ± 10 vs. 15 ± 11, %, p = 0.002) were significantly higher in hypertensive patients than the controls. EPO levels were not correlated with brachial and central pressures. Also EPO level was not significantly correlated with AIx@75 (r = -0.15, p = 0.17) and aortic PWV (r = -0.16, p = 0.13). CONCLUSION: Results from this study indicate that endogenous EPO levels may not be a factor in development of increased arterial stiffness.

The effects of rosiglitazone and metformin on inflammation and endothelial dysfunction in patients with type 2 diabetes mellitus.

Diabetic patients have a markedly increased risk of cardiovascular disease compared with non-diabetics. Two drug groups today target insulin resistance; biguanides and thiazolidinediones. In addition, these may have other effects on cardiovascular risk factors. The aim of this study was to evaluate the effects of metformin and rosiglitazone on non-traditional cardiovascular risk factors. Forty type 2 diabetic patients were randomized into metformin and rosiglitazone groups. After receiving the optimal doses, the patients were monitored for 12 weeks. Biochemical parameters, lipid parameters, CRP, insulin, c-peptide, and HbA1c levels were analyzed. VWF, PAI-1, ICAM-1, TNF-α, IL-6, E-selectin, and fibrinogen levels were measured in order to assess coagulation status and endothelial dysfunction. In the metformin group, body mass index, PPG, HbA1c, IL-6, ICAM-1, and TNF-α levels were significantly decreased after 12 weeks compared with the basal levels. IL-6 levels decreased from 75 pg/ml ± 20 to 42 pg/ml ± 9 (P 0.023) and TNF- α levels from 61 pg/ml ± 31 to 39 pg/ml ± 10 (P 0.018). In the rosiglitazone group, FPG, PPG, HbA1c, insulin, HOMA-IR, IL-6, and TNF-α levels decreased significantly after 12 weeks compared with the basal levels. IL-6 levels decreased from 78 pg/ml ± 21 to 41 pg/ml ± 9 (P 0.028) and TNF-α levels from 62 pg/ml ± 19 to 37 pg/ml ± 10 (P 0.012). At the end of the study, no significant differences were determined between groups. Insulin resistance and type 2 diabetes are strongly associated with low grade inflammation. Both metformin and rosiglitazone were effective in controlling inflammatory markers in addition to metabolic parameters.

The relationship between endothelial damage and aortic augmentation index.

Augmentation index (AIx), a measure of wave reflection, is regulated by a number of factors, including endothelial function and vascular smooth muscle tone. The relationship between local endothelium-derived factors and AIx is well known; however, association between endothelial damage markers and AIx has not been sufficiently studied. This study investigates whether endothelial damage markers-von Willebrand factor (vWF) soluble thrombomodulin (sTM)--are associated with wave reflections. We studied 46 (48.5 +/- 10.6, years) never-treated patients with hypertension (HT) and an age-matched control group of 40 (47 +/- 8.6, years) normotensive individuals. von Willebrand factor and sTM levels were determined in all subjects. We evaluated the aortic AIx of the study population using applanation tonometry (Sphygmocor, AtCor Medical, Sydney, Australia). The heart rate-corrected augmentation index (AIx@75) was estimated as a marker of wave reflections. Endothelial damage markers and AIx@75 were significantly higher in hypertensive patients than in controls. In the whole population, the vWF level (beta = 0.24, p = 0.01) was an independent determinant of AIx@75 in multivariate analysis. However, the sTM level was not associated with AIx@75. We found that the vWF level was an independent determinant of AIx@75. Our results suggest that increased an vWF level contributes significantly to increased wave reflections.

A novel indicator of widespread endothelial damage and ischemia in diabetic patients: ischemia-modified albumin.

Ischemia-modified albumin (IMA) is a novel marker of tissue ischemia. Nowadays, IMA is accepted as a marker of oxidative stress. In this study, we aimed at establishing an association between IMA and hyperglycemia, blood pressure, lipid parameters, microvascular complications, hsCRP, and microalbuminuria in type 2 diabetes patients without overt macrovascular disease and acute ischemia. Fifty type 2 diabetes mellitus patients without a history of macrovascular disease or end-stage renal disease were enrolled into the study. Age-matched 30 healthy individuals were also included in the study as a control group. Plasma IMA (0.329 ± 0.046 and 0.265 ± 0.045 AbsU; P < 0.0001) and hsCRP levels (0.51 ± 0.36 and 0.32 ± 0.17 mg/dl; P < 0.0001) were significantly higher in the diabetic group compared to healthy controls. IMA level was significantly correlated with hsCRP (r = 0.76; P < 0.0001), HbA1c (r = 0.72; P < 0.0001), microalbuminuria (r = 0.40; P = 0.004), systolic blood pressure (r = 0.28; P = 0.049), diastolic blood pressure (r = 0.44; P = 0.005), and HOMA-IR (r = 0.42; P = 0.005) levels in the entire diabetic subjects. In the diabetic patients group, presence of microalbuminuria was associated with a higher plasma IMA level (0.355 ± 0.035 and 0.265 ± 0.0045 AbsU; P < 0.0001, patients with microalbuminuria and control subjects, respectively). In the type 2 diabetes patients with nephropathy, IMA level (0.355 ± 0.035 and 0.311 ± 0.046 AbsU; P = 0.002) was determined higher compared to the diabetes patients without nephropathy. Diabetic patients without an overt cardiovascular disease still have a higher serum IMA level compared to healthy controls. The correlation of high plasma IMA levels with high hsCRP and microalbuminuria levels in diabetic subjects indicates the presence of a chronic ischemic process. Therefore, elevated IMA levels may indicate an underlying subclinical vascular disease in type 2 diabetes mellitus patients.

Low total antioxidative capacity levels are associated with augmentation index but not pulse-wave velocity.

It is well known the relationship between oxidative stress and vascular function. However, association between total antioxidative capacity and arterial stiffness was not studied in patients with hypertension (HT). This study investigated whether total antioxidative capacity is associated with arterial stiffness and wave reflections. We studied 46 (age 48.5 +/- 10.6 years) never treated patients with HT and age-matched control group of 40 (age 47 +/- 8.6 years) normotensive individuals. Total antioxidative capacity level was determined in all subjects. We evaluated arterial stiffness and wave reflections of the study population, using applanation tonometry (SphygmoCor). Carotid-femoral pulse-wave velocity (PWV) was measured as index of aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a composite marker of wave reflections and arterial stiffness. Carotid-femoral PWV (10.5 +/- 2.2 vs 8.7 +/- 1.6, m/s, P = 0.0001) and AIx@75 (22.7 +/- 9.5 vs 15 +/- 11, %, P = 0.001) were significantly higher in patients with HT compared with age-matched control subjects. Total antioxidative capacity level (274 +/- 70 vs 321 +/- 56 micromol/l, P = 0.001) was significantly lower in hypertensive patients than controls. In the whole population, total antioxidative capacity level negatively correlated with AIx@75 (r = -0.24, P = 0.02) in univariable analysis, but not with carotid-femoral PWV (r = -0.08, P = 0.43). Also, we found that total antioxidative capacity level (beta = -0.21, P = 0.03) was an independent determinant of AIx@75 in multivariable analysis. Our results suggest that the decrease in the ability of antioxidant defenses contributes significantly to increased wave reflections.

Methyltetrahydrofolate reductase C677T gene mutation and hyperhomocysteinemia as a novel risk factor for diabetic nephropathy.

Hyperhomocysteinemia is a well-defined risk factor for endothelial dysfunction and atherosclerosis. A point mutation (677 C-T) of MTHFR gene results in a significant increase at plasma homocysteine levels. In this study we aimed to evaluate the effects of MTHFR gene mutation and consequent hyperhomocysteinemia on the development of diabetic microvascular complications in comparison with the other defined risk factors. Diabetic patients without a history of macrovascular complication or overt nephropathy enrolled into the study. The presence of MTHFR 677 C-T point mutation was evaluated by Real-Time PCR technique by using a LightCycler. MTHFR heterozygous mutation was present in 24 patients over 52. Patients with diabetes were divided into two groups according to the presence of MTHFR gene mutation. Both groups were well matched regarding age and diabetes duration. Metabolic parameters, plasma homocysteine, microalbuminuria, folic acid, and vitamin B12 levels were also studied. Presence of neuropathy and retinopathy were evaluated by specific tests. Duration of diabetes, BMI, systolic and diastolic blood pressure, plasma CRP, HbA1c, and lipid levels were not different between the two groups. Plasma homocysteine (12.89 +/- 1.74 and 8.98 +/- 1.91 micromol/l; P < 0.0001) and microalbuminuria levels (73.40 +/- 98.15 and 29.53 +/- 5.08 mg/day; P = 0.021) were significantly higher in the group with MTHFR gene mutation while creatinine clearance levels (101.1 +/- 42.6 and 136.21 +/- 51.50 ml/min; P = 0.008) were significantly lower. Sixteen over 22 (73%) of the patients with diabetic nephropathy had MTHFR gene mutation, while this was only 27% (8 over 30) in normoalbuminuric patients (P = 0.017). There was a significant correlation of plasma homocysteine level with microalbuminuria (r = 0.54; P = 0.031) in the patients with diabetic nephropathy who had C677T polymorphism. We did not find any specific association of MTHFR gene mutation and hyperhomocysteinemia with retinopathy or neuropathy.

Comparison of the effect of propofol and N-acetyl cysteine in preventing ischaemia-reperfusion injury.

BACKGROUND AND OBJECTIVE: The aim of this study was to compare the effects of propofol and N-acetyl cysteine (NAC) on tourniquet-induced ischaemia-reperfusion injury by determining malonyldialdehyde, ischaemia-modified albumin, lactate, blood gas and haemodynamic levels in arthroscopic knee surgery. METHODS: Sixty ASA I or II patients were randomized into three groups. Intrathecal anaesthesia was administered using 0.5% heavy bupivacaine in all patients. In group P, propofol was administered in a 0.2 mg kg(-1) bolus, followed by infusion at a rate of 2 mg kg(-1) h(-1); in group NAC, NAC was administered as an infusion at a rate of 5 mg kg(-1) h(-1), and, in group C (the control group), an equal volume of isotonic saline was administered to patients until 30 min after reperfusion. Blood samplings were obtained immediately before intrathecal anaesthesia (t1), 1 min before tourniquet release (t2), 5 min after tourniquet release (t3) and 30 min after tourniquet release (t4). RESULTS: Plasma malonyldialdehyde, ischaemia-modified albumin and lactate levels increased significantly in group C at t3 and t4 compared with the baseline values. Plasma concentrations of malonyldialdehyde, ischaemia-modified albumin and lactate in groups P and NAC were significantly lower than those in group C at t3 and t4. In blood gas analyses, pH, HCO3 and base excess were found to be significantly lower at t3 and t4 compared with t1 and t2 in group C. Comparisons between groups P and NAC revealed no significant differences. CONCLUSION: Small-dose infusions of both propofol and NAC appear to provide similar protection against ischaemia-reperfusion injury in arthroscopic knee surgery.

Circulating levels of relaxin and its relation to cardiovascular function in patients with hypertension.

BACKGROUND: The role of endogenous relaxin on hypertensive cardiovascular damage remains unknown. We investigated the relaxin level and its relation to cardiovascular function in patients with never treated hypertension (HT). METHODS: We studied 42 (47.8+/-10 years) never treated patients with HT and 40 age-matched (47+/-8.6 years) normotensive individuals. Serum relaxin levels were determined in all subjects using enzyme-linked immunosorbent assay. Left ventricular (LV) diameters were evaluated by transthoracic echocardiography. Ejection fraction and LV mass index were measured. Diastolic functions were evaluated with both conventional and tissue Doppler echocardiography. We evaluated central aortic pressures, heart rate-corrected augmentation index (AIx@75), a marker of wave reflections, and aortic pulse wave velocity (PWV) as indices of elastic-type aortic stiffness of the study population using applanation tonometry (SphygmoCor). RESULTS: Relaxin levels were significantly lower in hypertensive patients as compared with controls (36.5+/-7.3 vs 49.7+/-39.8 pg/ml, p=0.03). The relaxin level was negatively correlated with brachial and central aortic pressure. However, serum relaxin was not significantly associated with LV diameters, ejection fraction, LV mass index, LV diastolic function, AIx@75 or aortic PWV in our study. CONCLUSION: Serum relaxin is decreased in patients with HT. However, low endogenous relaxin is not related to cardiovascular function.

Association between serum C-reactive protein elevation and atrial fibrillation after first anterior myocardial infarction.

BACKGROUND: Elevated inflammatory markers have been found to correlate with higher risk for cardiac events in patients with acute myocardial infarction (AMI). It has been suggested that C-reactive protein (CRP) may be involved in the initiation process of atrial fibrillation (AF). However, the role of CRP levels in the occurence of AF in patients with AMI has not been studied. This study investigated whether CRP is a risk factor for AF in patients with acute anterior MI. METHODS: We prospectively evaluated 92 consecutive patients (25 women and 67 men; aged 58 +/- 11 y) with a first acute anterior wall MI. Blood samples were obtained at the time of admission to the hospital, and serum CRP levels were measured by an ultrasensitive immunonephelometry method. All patients were evaluated by echocardiography to measure the left ventricular (LV) diameter and functions. All patients were monitored continuously for the detection of AF in the coronary care unit. RESULTS: Atrial fibrillation occured in 19 (20%) of 92 patients. Univariate analysis showed that patients with AF had an advanced age (63 +/- 9.9 versus 56.7 +/- 11.7 y, p = 0.034), higher serum CRP level (2.95 +/- 2.5 versus 1.71 +/- 2.12 mg/dL, p = 0.034), larger LV end-systolic volume (74 +/- 15 versus 63 +/- 19, mL p = 0.02), higher LV ejection fraction (31.1 +/- 6.2 versus 38.4 +/- 10%, p = 0.001), and larger left atrial (LA) diameter (37.1 +/- 4.2 versus 34.7 +/- 3.3 mm, p = 0.01). In multivariate analysis, only age (odds ratio [OR]: 1.05, 95% confidence interval [CI]: 1-1.11, p = 0.036) and CRP levels (OR: 1.27, 95% CI: 1-1.59, p = 0.039) were independent predictors of AF. CONCLUSION: These results suggest that CRP may be a risk factor for AF in patients with acute anterior wall MI.

Relationship between arterial stiffness and myocardial damage in patients with newly diagnosed essential hypertension.

BACKGROUND: Arterial stiffness increases in hypertensive individuals. Arterial stiffness is associated with impairment of systolic and diastolic myocardial function in hypertension (HT). However, the relationship between arterial stiffness and serum heart-type fatty acid-binding protein (H-FABP) levels, a sensitive marker of myocardial damage, has not been previously examined in patients with HT. We investigate the relationship between serum H-FABP levels and arterial stiffness in patients with newly diagnosed HT. METHODS: We studied 46 (48.5 +/- 10.6, years) never-treated patients with HT and age-matched control group of 40 (47 +/- 8.6, years) normotensive individuals. H-FABP levels were determined in all subjects. We evaluated arterial stiffness and wave reflections of study population, using applanation tonometry (Sphygmocor). Carotid-femoral pulse wave velocity (PWV) was measured as indices of elastic-type, aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a marker of wave reflections. RESULTS: Carotid-femoral PWV (10.5 +/- 2.2 vs. 8.7 +/- 1.6, m/s, P = 0.0001) and AIx@75 (22.7 +/- 9.5 vs. 15 +/- 11, %, P = 0.001) were significantly higher in patients with HT than control group. H-FABP levels were increased in hypertensive patients compared with control group (21.1 +/- 14.8 vs. 12.9 +/- 8.5, ng/ml, P = 0.002). In multiple linear regression analysis, we found that the body mass index (beta = 0.42, P = 0.0001) and carotid-femoral PWV (beta = 0.23, P = 0.03) were significant determinants of H-FABP levels. CONCLUSION: Arterial stiffness is associated with serum H-FABP levels, a sensitive marker of myocardial damage, in patients with newly diagnosed HT.

Reference values of cord blood transferrin, ceruloplasmin, alpha-1 antitrypsin, prealbumin, and alpha-2 macroglobulin concentrations in healthy term newborns.

Acute phase proteins are sensitive markers of tissue necrosis and inflammatory process. These markers may be especially useful in the neonatal period, in which mortality and morbidity rates are high, because fetus and baby are subjected to numerous metabolic, genetic, physiologic and environmental injuries such as neonatal asphyxia and septicemia. The purpose of the present study was to establish normal cord blood levels of some acute phase proteins in healthy term neonates. Umbilical cord blood was obtained at the time of vaginal delivery in 60 newborn infants (30 girls, 30 boys). Specific protein concentrations were measured by nephelometric assay. Transferrin, ceruloplasmin, alpha-1 antitrypsin, prealbumin, and alpha-2 macroglobulin concentrations [arithmetic mean (+/- SD)] were found to be 199.7 (+/- 34.6) mg/dl, 14.6 (+/- 4.0) mg/dl, 160.2 (+/- 23.6) mg/dl, 11.9 (+/- 2.2) mg/dl, and 284.6 (+/- 44.4) mg/dl, respectively. Prealbumin levels for girls [12.9 (+/- 2.2)] were found to be significantly higher than those of boys [10.9 (+/- 1.8)] (p < 0.001), while there were no significant differences between the other proteins. We conclude that these results may be used as reference values for the diagnosis of pathological conditions in newborns.

The effects of increased intraabdominal pressure on testicular blood flow, oxidative stress markers, and morphology.

BACKGROUND: This study was carried out to evaluate the effects of increased intraabdominal pressure (IAP) on testicular blood flow (TBF), oxidative stress markers, and morphology. METHODS: Twenty-four Sprague-Dawley rats weighing 300 to 350 g were allocated randomly into 3 groups consisting of 8 animals each: A, gasless (control); B, 10 mm Hg IAP with CO(2) pneumoperitoneum for 60 minutes; and C, 20 mm Hg IAP with CO(2) pneumoperitoneum for 60 minutes. Testicular blood flow was studied using the Doppler technique. In the 10 and 20 mm Hg IAP groups, time points of TBF measurements were defined as follows: TBF(baseline), 10 minutes before insufflation; TBF(10min), 10 minutes after pneumoperitoneum; TBF(50min), 50 minutes after pneumoperitoneum; and TBF(reperfusion), 10 minutes after pneumoperitoneum deflation. To evaluate the changes in oxidative stress, we assayed the malondialdehyde (MDA) levels of testicular tissues. A 4-level grading scale was used to quantify histologic injury. RESULTS: For both testes of each rat, TBF(10min), TBF(50min), and TBF(reperfusion) values of each group were separately evaluated according to their TBF(baseline) value percentages. The results revealed no significant differences for each time point of TBF measurements between the right and left testes in any group. Pneumoperitoneum caused a significant decrease in TBF at the 10th and 50th minutes of pneumoperitoneum, both in the 10 and 20 mm Hg IAP groups, compared with their baseline values. TBF(reperfusion) values in both groups were also lower than their baseline values. We determined that mean TBF(10min) and TBF(50min) values decreased significantly in the 20 mm Hg IAP group compared with the 10 mm Hg IAP group, despite there being no significant difference in their mean TBF(reperfusion) values. Mean MDA levels were significantly increased in both the 10 and 20 mm Hg IAP groups compared with those of the control group for the right and left testes. However, there was no significant difference between the mean MDA levels in these first 2 groups. The histologic injury score was significantly increased in both the 10 and 20 mm Hg IAP groups compared with the control group; however, there was no difference in the scores between these first 2 groups. CONCLUSIONS: We demonstrated in an animal model that abdominal deflation after IAP of 10 and 20 mm Hg for 60 minutes causes testicular hypoperfusion, free radical production, and subsequent testicular damage.

Effects of melatonin on suppression of renal scarring in experimental model of pyelonephritis.

OBJECTIVES: To determine the effects of melatonin combined with antibiotic administration on the suppression of renal scarring in an experimental pyelonephritis model. METHODS: The control group underwent a sham operation without infection. In the other groups, treatment began 72 hours after direct bacterial inoculation. In the no-treatment group, rats received daily intraperitoneal injections of saline. In the antibiotic-only group, the rats were treated only with ceftriaxone intramuscularly at a dose of 50 mg/kg once daily for 5 days. In the melatonin-only group, only 20 mg/kg of melatonin once daily was given by intraperitoneal injection for 5 days. In the antibiotic plus melatonin group, melatonin and ceftriaxone were administered at the same dosages and duration as for the single-modality treatment groups. After 6 weeks, the kidneys were removed for malondialdehyde measurements and histopathologic examination (inflammatory response and cicatrization). RESULTS: Melatonin only (134.25 +/- 13.42) and antibiotic plus melatonin treatment (122.62 +/- 8.91) caused a marked reduction in the mean malondialdehyde values compared with no treatment (214.12 +/- 17.77) and antibiotic-only treatment (161.37 +/- 16.03), with no significant difference compared with that of the control group (120.75 +/- 9.83). Histopathologically, in the no-treatment group, the severity of scarring correlated directly with the severity of inflammation (r = 0.93). No significant differences were found in the renal scarring scores in rats receiving no treatment and those treated only with antibiotic or melatonin. In the antibiotic plus melatonin treatment group, the cicatrization score was not statistically different from that of the control group. CONCLUSIONS: When combined with antibiotics, melatonin causes a significant inhibition of malondialdehyde production and neutrophil infiltration caused by acute pyelonephritis in an experimental rat model, and these are responsible for the protective effect of melatonin against renal damage, preventing renal scarring formation.

Necrotizing enterocolitis increases the bone resorption in premature infants.

BACKGROUND: Necrotizing enterocolitis is a common neonatal gastrointestinal disease that affects approximately 10% of premature infants less than 1500 g. The average mortality is 20-40% and survivors may present with diarrhea or malabsorption, intestinal strictures and fistulas, feeding abnormalities and failure to thrive. It is not clear whether the higher incidence of this gastrointestinal disease in premature infants contributes to the risk of osteopenia of prematurity. AIM: To examine bone turnover state in premature infants who had a necrotizing enterocolitis attack during postnatal period. STUDY DESIGN AND SUBJECTS: We examine the bone turnover markers in infants with necrotizing enterocolitis and compare them with infants with sepsis. Forty-one premature infants participated in the study and were divided into three groups. In group I, there were 14 premature infants who developed necrotizing enterocolitis with negative blood culture during their hospitalization. In group II, there were 12 premature infants who developed sepsis during their hospitalization. Age-matched 15 premature infants who were given parenteral nutrition served as control group (group III). Blood samples and 6-h urine samples were obtained for bone turnover markers and calcium, phosphorous, creatinine and 25-hydroxy vitamin D between the day 20 and 25. Bone osteoblastic activity was assessed by measurement of serum osteocalcin. Bone resorption was assessed by measurement of serum levels of beta-CrossLaps and urinary deoxypyridinoline. RESULTS: There were no significant differences in bone osteoblastic activity among the groups, but bone resorption markers were significantly higher in infants with necrotizing enterocolitis compared to other groups (p < 0.016). CONCLUSION: Necrotizing enterocolitis increases the bone resorption in premature infants. It may be related with reduced glucagon like peptide-2 levels, a new intestinal hormone that is primary secreted from distal small intestine.

Screening for gestational diabetes mellitus in northeastern Turkey (Trabzon City).

OBJECTIVE: The purposes of this study were to determine the prevalence of gestational diabetes mellitus (GDM) in Trabzon city of Turkey and to identify appropriate risk factors for gestational diabetes in pregnant mothers. RESEARCH DESIGN AND METHODS: Eight hundred and seven adult pregnant women were screened for GDM with a 1-hour, 50 g oral glucose challenge test (GCT). Three-hour, 100 g oral glucose tolerance tests (GTTs) were performed on screen-positive women. RESULTS: Of the 807 pregnancies screened, 59 (7.3%) had an initial oral GCT result of > or = 140 mg/dl. Diagnostic testing with the oral GTT was performed on the 59 screen-positive gravid women. Of those tested, 10 were diagnosed with GDM on the basis of greater > or = 2 criteria over 3 hours, for a prevalence of 1.23%. Significant associations were found between age, body mass index (BMI) and GDM positivity (p < 0.01 and p < 0.05; respectively). The prevalence of GDM was associated with diastolic blood pressure (DBP) and weeks' gestation (p < 0.05). There was no significant association between increased BMI, systolic blood pressure, number of pregnancies and GDM positivity. In addition, the birth weights of the babies born to mothers with GDM were significantly higher than those of the non-diabetic healthy mothers' babies (p < 0.001). CONCLUSIONS: The prevalence of GDM in a Turkish population was low. The prevalence of GDM showed an increase with the ages of pregnant women, gestational age and DBP. This study demonstrates that the universal screening for GDM is not mandatory in our pregnant population. The cost of universal screening may be prohibitive in our population. Large prospective studies are needed to better analyze outcome data and efficacy of screening in adult pregnancies.