Pregabalin versus gabapentin in the treatment of neuropathic pruritus in maintenance haemodialysis patients: A prospective,crossover study

Aim: Pruritus is common in dialysis patients. Peripheral neuropathy is also prevalent in this patient population. However, the role of neuropathy in the genesis of uraemic itch has not been adequately studied to date. Therefore, we aimed to investigate the effects of gabapentin and pregabalin on uraemic pruritus along with neuropathic pain in patients receiving haemodialysis. Methods: This is a 14 week long randomized, prospective, cross‐over trial. Haemodialysis patients with established neuropathy and/or neuropathic pain were included. Fifty patients were randomly assigned to gabapentin 300 mg after each haemodialysis session and pregabalin 75 mg daily. After 6 weeks of treatment, cross‐over was performed and patients received the other drug for another 6 weeks. Short Form of McGill Pain Questionnaire and Visual Analogue Scale were used to evaluate pain and pruritus, respectively. At each week's visit, patients were interrogated in terms of adverse effects of study drugs. Baseline laboratory data and demographic characteristics were recorded from patient charts. Results: Forty (12 males, 28 females) out of 50 patients completed the study. Mean age was 58.2 ± 13.7. Overall, 29 out of 40 patients (72.5%) had pruritus symptoms at baseline evaluation. Fifteen patients (37.5%) were diabetic. Thirty‐one out of 40 patients (77.5%) had electromyography (EMG)‐proven peripheral neuropathy. Twenty three patients (57.5%) had both EMG‐proven neuropathy and pruritus. Gabapentin and pregabalin improved both neuropathic pain and pruritus significantly. There was no difference between the study drugs in terms of efficacy against pain and pruritus. Conclusion: Treatment of neuropathic pain with either pregabalin or gabapentin effectively ameliorates uraemic itch.     

Implantable Cardioverter Defibrillator Lead Endocarditis Causing Diffuse Right Atrial Abscess and Pulmonary Artery Embolism

Implantation of electrophysiological cardiac devices such as pacemakers and implantable cardioverter defibrillators has become a widely available and routine procedure in cardiovascular medicine. One of the most feared complications of device implementation is infection. Infection rates for these devices are reported to vary between 0.7% and 7.0%. Cardiac thromboembolic event is a recognized complication of permanent cardiac rhythm devices with an incidence of 0.6%–3.5%, unrelated to lead size or number. These complications are associated with high morbidity and mortality rates. In this case report, right atrial mass, right atrial abscess, perforation of tricuspid septal leaflet, and pulmonary embolism secondary to ICD lead endocarditis is presented. (PACE 2011; 34:e115–e117)     

Sialic acid in childhood renal diseases: Correlation with clinical and laboratory indices

There are many kinds of glycoproteins that have sialic acid residues and it has been reported that these are elevated in some renal diseases and their significance in the pathogenesis of several renal diseases has been investigated. In the present study the serum and urine levels of sialic acid were measured in healthy controls and in children with either poststreptococcal acute glomerulonephritis (PSAGN) or minimal change nephrotic syndrome (MCNS) to test if there is any correlation with clinical and laboratory indices. In PSAGN and MCNS patients the serum and urine sialic acid concentrations at onset and relapse were significantly different from healthy controls (Mann-Whitney U-test P < 0.005). There was not a significant correlation between the clinical severity, serum creatinine and complement C₃ levels and serum sialic acid concentrations in PSAGN patients. Also there was not a significant correlation between edema, serum albumin, IgG, transferrin, α-1-antitrypsin and serum sialic acid concentrations in MCNS patients. Although high serum and urine sialic acid levels were found in both PSAGN and MCNS patients, it does not have any clinical significance nor is it important as a diagnostic or prognostic marker.     

Urinary enzyme changes in newborns with unconjugated hyperbilirubinemia

Various changes in renal function caused by unconjugated hyperbilirubinemia in newborns have been suggested in previous reports. Disclosing an injury in renal tubulus epithelium is feasible by measurement of urinary enzymes. Thus, renal function tests and urinary enzymes in 25 term newborns with unconjugated hyperbilirubinemia were evaluated before and after phototherapy. Ten healthy term newborns without hyperbilirubinemia formed the control group. Mean values of the variables obtained before and after phototherapy in the study group and in the controls were, respectively: urine osmolality (osm/kg H₂O); 0.147 ± 0.009, 0.174 ± 0.011, and 0.153 ± 0.018; endogenous creatinine clearance (mL/min per 1.73 m²): 45.7 ± 2.15, 46.0 ± 1.6 and 46.7 ± 3.9; fractional excretion of sodium (%): 1.27 ± 0.30, 0.79 ± 0.19 and 1.24 ± 0.07; tubular phosphorus reabsorption (%): 85.8 ± 3.3, 87.8 ± 2.8 and 86.6 ± 1.7; urinary N-acetyl-β-D glucosaminidase/creatinine (IU/mg): 0.617 ± 0.226, 0.574 ± 0.214 and 0.619 ± 0.210; fractional excretion of alkaline phosphatase (%): 0.422 ± 0.103, 1.001 ± 0.374 and 0.596 ± 0.201; fractional excretion of lactic dehydrogenase (LDH; %): 0.102 ± 0.019, 0.121 ± 0.023 and 0.119 ± 0.041; fractional excretion of AST (%): 0.433 ± 0.127, 0.530 ± 0.113 and 0.502 ± 0.074; fractional excretion of alanine aminotransferase (ALT; %) 0.856 ± 0.413, 1.619 ± 1.076 and 1.066 ± 0.366. No significant difference was found between these values before and after phototherapy in the study group, or between the values before phototherapy in hyperbilirubinemic neonates and in the control group. In conclusion, unconjugated hyperbilirubinemia up to a serum level of 18.4 mg/dL in term neonates does not seem to result in injury of normal tubulus epithelium as shown by urinary enzyme levels.     

Plasma and urinary platelet activating factor concentrations and leukotriene releasing activity of leukocytes in steroid sensitive nephrotic syndrome of childhood

Platelet activating factor (PAF) is synthesized and secreted by glomerular mesangial and endothelial cells. It increases glomerular basement membrane permeability and induces proteinuria. Leukotrienes (LT) are mediators released by either leukocytes or glomerular cells under the PAF effect. The possible role of PAF in steroid sensitive nephrotic syndrome (SSNS) of childhood was studied in 8 children with SSNS in the acute stage, 5 children in remission and 8 healthy controls. The PAF concentrations in urine and plasma were determined. Leukocytes were stimulated in vitro and the LT release in response to stimulation was determined. The urinary and plasma concentrations of PAF were significantly higher in the acute phase than in remission and in control patients. Children with SSNS were found to have peripheral leukocytes with increased LT releasing activity in vitro. These results are in accordance with clinical and experimental observations indicating that PAF originates in the kidney and plays a role in normal kidney physiology. Urinary PAF concentrations may be related to proteinuria because they were strongly correlated in the present study. Elevated plasma PAF concentrations in the acute stage of SSNS could result from either its secretion from the circulating leukocytes or decreased acetyl hidrolase activity needed for its hydrolysis in plasma. The increased LT release in vitro suggests that these cells might have been activated by PAF secreted from glomeruli. It is proposed that PAF and different LT in systemic and glomerular circulation are important mediators in childhood SSNS.     

Cerebral hemiatrophy (Dyke–Davidoff–Masson syndrome) in childhood: Clinicoradiological analysis of 19 cases

BACKGROUND: The purpose of this study was to emphasize the clinical and imaging findings of 19 child cases of cerebral hemiatrophy. METHODS: A total of 11 male and eight female patients underwent assessment with computed tomography and magnetic resonance imaging. The patients ranged from 1 to 17 years in age. The evaluated parameters were: location of the lesions, midline structural shift effect, ipsilateral calvarial and parenchymal changes. RESULTS: Left cerebral hemiatrophy was seen in 14 of the cases while right cerebral hemiatrophy was observed in five cases. Unilateral calvarial thickening was seen in 11 cases, hyperpneumatization of paranasal sinuses in five, and hypoplasia of the middle frontal cranial fossa in three patients. Cerebral peduncle atrophy was noted in seven cases. In total, 11 patients had thalamic atrophy and lentiform nucleus hypoplasia. In one case, cerebral hemiatrophy was associated with ipsilateral large schizencephalic cleft and absence of the septum pellucidum, whereas in another case, there was diffuse cerebellar atrophy associated with cerebral hemiatrophy. CONCLUSION: Computed tomography and, in particular, magnetic resonance imaging are the procedures of choice with respect to assessment of the etiology and extent of cerebral parenchymal involvement in cerebral hemiatrophy.