Serum SUR1 and TRPM4 in patients with subarachnoid hemorrhage

Neurosurgical Review - Neuroinflammation plays an important role in neuronal injury after aneurysmal subarachnoid hemorrhage (aSAH). Sulfonylurea receptor 1 (SUR1) and transient receptor potential...     

Neutrophil gelatinase associated lipocalin as an indicator of acute kidney injury and inflammation in burned children

Introduction

Neutrophil gelatinase associated lipocalin (NGAL) is a novel predictor of acute kidney injury (AKI), which increases with inflammation. We aimed to assess whether serum NGAL (SNGAL) and urine NGAL (UNGAL) can predict AKI in burned children.

Methods

Patients were referred within the 12 h of burn to our center. Serum samples for SNGAL, C-reactive protein (CRP), procalcitonin (PCT) and urine for UNGAL, microalbumine (Umalb), creatinine (Ucr) were obtained at both admission and the 5th day after burn. Blood urea nitrogen (BUN) and serum creatinine (Scr) were examined daily.

Results

Twenty-two subjects were enrolled and six (27.2%) of them developed AKI within the 48 h of injury. Burn size and abbreviated burn severity index (ABSI) were significantly increased in patients with AKI. CRP, PCT, SNGAL and UNGAL levels at admission and day 5 were significantly higher in patients with AKI than in those without AKI and controls. Scr was not significant between AKI and non-AKI groups at hospital days 1 and 5. A SNGAL level of 315 ng/ml and a UNGAL level of 100 ng/ml were determined as predictive cut-off values of AKI at admission (sensitivity and specificity: 71.4%, 83.3% and 93.3%, 93.7%, respectively). SNGAL and UNGAL were positively correlated with CRP, PCT, ABSI and Umalb/Ucr.

Conclusion

SNGAL and UNGAL are good early predictors of AKI in children with severe burn. NGAL might reflect the severity of burn insult and also could be used as an indicator of inflammation in burn children.     

Circulating levels of cytokines are increased in restless legs syndrome

Background

Restless legs syndrome [RLS] is known as a disease of iron and dopaminergic dysregulation but inflammatory processes might also have a role in the pathogenesis. In this study, we compared the circulating levels of hsCRP, IL-1β, IL-6, and TNF-α in patients with primary restless legs syndrome [RLS] and healthy control subjects.

Methods

We prospectively included 29 patients with primary RLS and 65 healthy controls [HC], all age-sex matched. The diagnosis of RLS was established using international guidelines. IRLSSG Severity Scale was used to evaluate the severity of RLS. Plasma levels of hsCRP, IL-1β, IL-6, and TNF-α were measured in all participants.

Results

The mean age of patients was 37.8?±?11.3 and 52% of RLS group were women. Serum IL-1β, IL-6, and TNF-α levels of the patient group were statistically significantly higher compared to HC [p?<?0.001 for all variables]. Plasma levels of hsCRP did not differ between groups. There were 8 patients with mild RLS [28%], 13 patients with moderate RLS [45%], and 8 patients with severe RLS [28%]. Only IL-6 values were significantly different between the groups. In the severe group, the value of IL-6 was significantly higher than in the other groups [p: 0.03].

Conclusion

These results showing higher circulating levels of inflammatory cytokines in patients with RLS support the notion that inflammation may be involved in the pathogenesis of primary RLS. However, it is necessary to perform further studies to determine if this finding is a cause or an effect.

     

Change in amputation rate in a Turkish diabetic foot population

Diabetic foot, an important cause of morbidity and mortality, is an important economic problem in all countries. We examined the duration of diabetes, ratio of hospitalization, and the amputation rates of our diabetic foot patients between 1996 and 2002 and compared the results with those obtained between 1985 and 1995. Medical reports of 117 patients with diabetic foot referred to Gazi University Medical Faculty between 1996 and 2002 were retrospectively analyzed. The mean age was 61.09+/-10.87 years and mean duration of diabetes was 16.14+/-9.44 years. Sixty-one patients were hospitalized and 56 patients were followed in our outpatient clinic. The mean duration of hospitalization was 45.00+/-18.74 (20-74) days in amputees and 28.95+/-11.61 (10-47) days in the nonamputees (P=.023). The mean age and duration of diabetes were significantly higher in amputees in the present group than that in the previous group. The amputation rate was significantly lower in the group studied between 1996 and 2002 compared to the group followed between 1985 and 1995 (9.4% vs. 21%, respectively, P<.001). Appropriate diabetes education and systematic follow-up in an outpatient clinic may delay preventable diabetic foot lesions and reduce the amputation rate.     

Diurnal leptin secretion is intact in male hypogonadotropic hypogonadism and is not influenced by exogenous gonadotropins

Circulating leptin shows a pulsatile secretory pattern along with a nocturnal rise. We have previously shown that circulating leptin concentrations are high in males with untreated idiopathic hypogonadotropic hypogonadism (IHH). However, circadian leptin secretion in IHH before and after gonadotropin treatment is not known. Thus, we studied 14 adult males with IHH who had no history of previous hormonal therapy, and 12 age- and body mass index-matched healthy men. Plasma leptin concentrations were measured with 1-h intervals for 24 h before and 6 months after gonadotropin treatment. The 24-h mean leptin concentration showed a significant decrease, from 11.78 +/- 1.908 microg/liter at baseline to 10.85 +/- 1.939 microg/liter after 6 months of therapy (z = 3.107; P = 0.002). Before and after treatment, 24-h mean leptin concentrations were also significantly higher in the patient group when compared with controls (4.275 +/- 0.711 microg/liter) (z = 5.938; P = 0.0001). Hourly leptin levels demonstrated a diurnal pattern in hypogonadal patients, a surge in the midday, and a peak just after midnight, and this pattern did not differ before and after treatment. We observed a similar diurnal pattern in the control subjects too. Leptin levels were negatively and significantly correlated with free testosterone and total testosterone levels both before (r = -0.656, P = 0.011; and r = -0.639, P = 0.014, respectively) and after (r = -0.537, P = 0.048; and r = -0.563, P = 0.036, respectively) gonadotropin administration. Our observations suggest that the diurnal rhythm of leptin is intact in males with IHH, and short-term gonadotropin treatment does not effect its diurnal rhythm. Moreover, testosterone produced under the influence of the gonadotropin treatment led to decreases in the leptin levels.     

A new surgical technique for adenoid cystic carcinoma involving tracheal carina

Reported is the successful treatment of a 24-year-old male with adenocystic carcinoma involving the tracheal carina, in which the tumor extended along the right main bronchus across the orifice of the right upper lobe. The patient underwent a carinal resection plus right upper lobectomy and reconstruction of the carina, resulting in neither anastomotic complication nor recurrence of disease during 28 months of follow-up.     

The inhibition of growth hormone secretion presented in obesity is not mediated by the high leptin levels: a study in human leptin deficiency patients

GH secretion is regulated by hypothalamic and peripheral hormones under a very complex interplay. Superimposed on this regulation, signals of a metabolic nature connect GH secretion with the metabolic and energetic homeostasis of a given individual. GH secretion is enhanced in malnutrition and is severely impeded in obesity, but no information is available to explain why GH secretion is severely impeded or blocked in excess adiposity. Obesity is associated with high plasma levels of leptin, and leptin participates at the hypothalamic and pituitary levels in the regulation of GH secretion. Thus, it has been postulated that the inhibitory action of obesity on GH discharge may be mediated by excess leptin levels. The only situation in which obesity does not parallel leptin values is the rare case of morbid obesity due to leptin deficiency caused by missense mutation of the leptin gene. To understand the causes of GH blockade presented in obesity, patients with both homozygous and heterozygous mutations of the leptin gene and matched controls for both sex and body mass index (BMI) were studied. Three homozygous and 5 heterozygous patients with leptin gene mutations as well as 13 control subjects were studied. In all subjects basal levels of leptin and GH values stimulated by the combined administration of GHRH plus GH-releasing peptide-6 (GHRP-6) were analyzed. To analyze the effects of obesity and leptin levels, 5 groups were designed, all them matched by sex and adiposity. The number of subjects (n), leptin levels in micrograms per liter, and adiposity in BMI were as follows: nonobese subjects: n = 5, BMI = 22.1 +/- 0.9 kg/m2, leptin = 5.4 +/- 0.9; heterozygous patients: n = 5, BMI = 27.0 +/- 1.0 kg/m2, leptin = 2.3 +/- 0.1; controls for the heterozygous group: n = 5, BMI = 24.7 +/- 1.1 kg/m2, leptin = 5.7 +/- 1.2; homozygous patients: n = 3, BMI = 54.4 +/- 0.2 kg/m2, leptin = 1.0 +/- 0.2; and controls for the homozygous group: n = 3, BMI = 50.3 +/- 2.0 kg/m2, leptin = 35.0 +/- 6.6. In these matched groups, the GHRH- and GHRP-6-stimulated GH secretion (mean peak +/- SE; micrograms per liter) was: nonobese, 86.8 +/- 8.9 [significantly higher than heterozygous (28.6 +/- 4.9) and control for heterozygous (39.9 +/- 10.4)]; homozygous group, 9.4 +/- 3.0; control for homozygous, 9.3 +/- 1.0 (significantly lower than the heterozygous, control for heterozygous, and nonobese groups). Hence, it appeared that GH discharge was negatively conditioned by adiposity and was not influenced by leptin levels. To further analyze this observation, a correlation analysis showed that GH peaks were negatively correlated with BMI in the 13 control subjects as well as in the 8 leptin-deficient patients. On the contrary, the GH peaks were negatively correlated with leptin levels in controls, but showed the opposite pattern in homo- and heterozygous patients. In conclusion, the GH secretion blockade, which is characteristic of obese states, is due to adiposity or some factor linked to adiposity, but not to elevated plasma leptin levels.