PERORAL ENDOSCOPIC DUODENAL BIOPSY IN INFANTS AND CHILDREN

ABSTRACT. Peroral endoscopic duodenal biopsy was used in the diagnosis and follow-up of forty-nine infants and children with suspected small intestine disease. Their ages ranged between one month and 12 years. Fifty-four upper gastrointestinal endoscopy procedures were performed and 139 biopsies were taken. The mean procedure time was 3.2 min with a range of 1.5–5.5 min. There were no complications. Tissue adequate for histopathologic examination was obtained in all but one of the fifty-four procedures. On the basis of this experience we think that peroral endoscopic duodenal biopsy is faster, safer and as diagnostic as conventional suction biopsy in infants and children. It is also more informative when other diseases of the upper gastrointestinal tract are suspected.     

TINEA VERSICOLOR AND VISCERAL LEISHMANIASIS

Background. Visceral leishmaniasis (VL) is endemic in several areas in the Sudan. The disease is associated with depressed cellular immunity. Tinea versicolor is a normal commensal of the skin which can become pathogenic particularly in patients with depressed cell-mediated immunity. Patients with VL have a high prevalence of tinea versicolor. Methods. One hundred and thirty patients with parasitologic confirmation of VL were screened for tinea versicolor infection. In the suspected cases the diagnosis was made by demonstrating the fungal hyphae and spores in skin scrapings. All patients were treated with sodium stibogluconate. Results. Of the 130 patients with VL, 10.8% were found to have severe tinea versicolor. The fungal infection developed or became worse with the start of VL. After successful treatment of VL, the tinea lesions disappeared completely or decreased in severity. Conclusions. Depressed cell-mediated immunity that is a feature of VL is the probable underlying cause for fungal infection. Tinea infection during the course of VL is to be distinguished from lesions of post-kala-azar dermal leishmaniasis.     

Interlead Distance and Left Ventricular Lead Electrical Delay Predict Reverse Remodeling During Cardiac Resynchronization Therapy

Background: Both anatomic interlead separation and left ventricle lead electrical delay (LVLED) have been associated with outcomes following cardiac resynchronization therapy (CRT). However, the relationship between interlead distance and electrical delay in predicting CRT outcomes has not been defined. Methods: We studied 61 consecutive patients undergoing CRT for standard clinical indications. All patients underwent intraprocedural measurement of LVLED. Interlead distances in the horizontal (HD), vertical (VD), and direct (DD) dimensions were measured from postprocedure chest radiographs (CXR). Remodeling indices [percent change in left ventricle (LV) ejection fraction, end‐diastolic, end‐systolic dimensions] were assessed by transthoracic echocardiogram. Results: There was a positive correlation between corrected LVLED and HD on lateral CXR (r = 0.361, P = 0.004) and a negative correlation between LVLED and VD on posteroanterior (PA) CXR (r =?0.281, P = 0.028). To account for this inverse relationship, we developed a composite anatomic distance (defined as: lateral HD—PA VD), which correlated most closely with LVLED (r = 0.404, P = 0.001). Follow‐up was available for 48 patients. At a mean of 4.1 ± 3.2 months, patients with optimal values for both corrected LVLED (≥75%) and composite anatomic distance (≥15 cm) demonstrated greater reverse LV remodeling than patients with either one or neither of these optimized values. Conclusions: We identified a significant correlation between LV–right ventricular interlead distance and LVLED; additionally, both parameters act synergistically in predicting LV anatomic reverse remodeling. Efforts to optimize both interlead distance and electrical delay may improve CRT outcomes. (PACE 2010; 575–582)     

Catheter Ablation of Atrial Fibrillation and Risk of Asymptomatic Cerebral Embolism

Recent studies have suggested that a significant minority of patients undergoing atrial fibrillation catheter ablation (AFCA) develop evidence of acute, asymptomatic cerebral emboli (ACE) detected by brain magnetic resonance imaging. Although the prognostic significance of ACE associated with AFCA remains unclear, given the heightened risk of dementia associated with asymptomatic chronic infarcts on brain imaging, it is imperative to understand the pathogenesis of ACE and identify methods to mitigate the risk of emboli associated with AF ablation. In this paper, we review the incidence of ACE associated with AFCA and discuss patient‐ and procedure‐specific markers of risk for asymptomatic embolism. We also review the data to support strategies, which have been proposed to reduce the incidence of ACE.     

Bartter's syndrome in Arabic children: review of 13 cases

BACKGROUND: Bartter's syndrome (BS) is an inherited disease of renal potassium wasting characterized by hypokalemic alkalosis, normal blood pressure, vascular insensitivity to pressor agents and elevated plasma concentrations of renin and aldosterone. It is caused by generalized hyperplasia of the juxtaglomerular apparatus at the site of renin production caused by mutations in the Na-K-2Cl cotransporter gene, NKCC2. The objective of our study is to establish the prevalence and incidence of BS in Kuwait and to assess treatment modalities for it. METHODS AND RESULTS: Bartter's syndrome was diagnosed in 13 Kuwaiti children over a 14 year period (1981-1995) with the estimated incidence of 1.7/100,000 live births. The mean age at diagnosis was 9.3 months (range 2-32 months). There were five males and eight females (ratio 1:1.6). The mean duration of follow up was 5.6 years (1-14 years). Both consanguinity and familial history among our patients were high (69 and 54%, respectively). All patients had hypokalemia, hypochloremia with metabolic alkalosis, hyperreninemia and were normotensive. Clinical presentation was essentially similar to that in other series. Eleven patients (85%) had growth failure, two had nephrocalcinosis (15%) and one had renal failure. All patients were treated with supplemental potassium, an aldosterone antagonist (spironolactone) and a prostaglandin synthetase inhibitor (indomethacin or aspirin) sequentially. Significant catch-up of growth (four patients) and increases in serum potassium (eight patients) were recorded after administration of indomethacin therapy. One patient died of severe pneumonia with respiratory failure from hypokalemic myopathy. Clinical presentation, inheritance, complications and therapy of BS are briefly discussed. CONCLUSION: Bartter's syndrome is a rare disease, but should be considered in the differential diagnosis of other disorders with growth failure and/or hypokalemia. Early diagnosis, close follow up and compliance with treatment may lead to appropriate growth and development.