Recurrent herpes labialis in the pediatric population: Prevalence, therapeutic studies, and associated complications.

Recurrent herpes labialis (RHL) is an incredibly common condition, though the medical literature evaluating pediatric aspects is limited. This paper assesses prevalence and therapeutic studies of pediatric RHL as well as disease complications. A comprehensive literature search of English-language citations based on PubMed queries of selected terms was performed, with exclusion if methodology was not discussed, or if studies had 10 or fewer patients. RHL prevalence in pediatrics has been assessed by measures of point and periodic prevalence, though methodologic limitations may under- or over-estimate the true prevalence of RHL. Studies have been conducted to evaluate therapeutic safety, tolerability, and efficacy of antivirals in the pediatric population. Pediatric RHL point prevalence ranges from 0.72% to 5.2% depending on the population study and the methodologies used. Pediatric RHL carries a significant public health burden and is often implicated in patients with eczema herpeticum, erythema multiforme, reactive infectious mucositis eruptions, and hypersensitivity reactions. There are few studies that evaluate the rates of occurrence of these sequelae associated with pediatric RHL.

Atypical Café-au-Lait Macules in a Patient with Koolen-de Vries Syndrome (17q21.31 Microdeletion Syndrome).

Koolen-de Vries syndrome (KdVS), also referred to as the 17q21.31 microdeletion syndrome, is a rare genetic disorder characterized by developmental delay, typical facial dysmorphism, and congenital defects. Associated anomalies include many cutaneous findings. Here, we report a 17-year-old boy with KdVS (17q21.31 microdeletion syndrome) who presented with diffuse freckling and multiple pigmented lesions, found to be most consistent with atypical café-au-lait macules (CALMs) on biopsy. We review the cutaneous findings commonly associated with KdVS (17q21.31 microdeletion syndrome) and propose the addition of diffuse freckling and atypical CALMs, histologically similar to those that may be found in neurofibromatosis type 1, to the cutaneous findings associated with KdVS (17q21.31 microdeletion syndrome).

Hand-foot-skin reaction related to use of the multikinase inhibitor sorafenib and hard orthotics.

Hand-foot-skin reaction is a distinct clinical condition arising in association with the use of multikinase inhibitors, including sorafenib. Because multikinase inhibitors are increasingly being used in children with cancer, recognition of this previously unfamiliar condition is of importance to pediatric dermatologists. We describe the diagnosis and successful treatment of a case of hand-foot-skin reaction in a child taking sorafenib for an unresectable desmoid tumor.

Are antibiotics necessary during routine cystoscopic stent removal?

BACKGROUND: The 2008 American Urological Association (AUA) Best Practice Statement on antimicrobial prophylaxis states that prophylaxis is not warranted for subjects with normal risk profile undergoing cystourethroscopy unless manipulation such as ureteral stent removal is performed. To date no studies have specifically assessed the need for antimicrobial prophylaxis during cystoscopic ureteral stent removal. We sought to determine the risk of infectious complications following cystoscopic stent removal with and without antimicrobial prophylaxis. METHODS: A retrospective review identified 70 subjects who underwent cystoscopic ureteral stent removal following kidney stone treatment, under the care of two separate urologists with differing practice patterns. Each cohort consisted of 35 subjects: with and without prophylactic antibiotics. Clinical variables assessed included demographics, type of stone intervention, prior urinary tract infection (UTI) history, immunocompromising comorbidities, antimicrobial class at time of stone intervention, and antimicrobial administration at cystoscopic stent removal. The primary outcome assessed was development of symptomatic UTI within 4 weeks after stent removal. RESULTS: Overall, 35 patients (50%) received antimicrobial prophylaxis at the time of stent removal and 35 (50%) did not receive antimicrobial prophylaxis, with no demographic or clinical differences between cohorts. Two patients in the antimicrobial cohort (6%) developed a UTI and none of the patients who did not receive antimicrobial prophylaxis developed a UTI (P=0.15). CONCLUSIONS: In our cohort study antimicrobial prophylaxis at the time of cystoscopic stent removal did not appear to provide a significant benefit in UTI prevention. Prospective studies would assist in validating these findings.

Sab (Sh3bp5) dependence of JNK mediated inhibition of mitochondrial respiration in palmitic acid induced hepatocyte lipotoxicity.

BACKGROUND & AIMS: Sustained c-Jun N-terminal kinase (JNK) activation by saturated fatty acids plays a role in lipotoxicity and the pathogenesis of non-alcoholic steatohepatitis (NASH). We have reported that the interaction of JNK with mitochondrial Sab leads to inhibition of respiration, increased reactive oxygen species (ROS), cell death and hepatotoxicity. We tested whether this pathway underlies palmitic acid (PA)-induced lipotoxicity in hepatocytes. METHODS: Primary mouse hepatocytes (PMH) from adeno-shlacZ or adeno-shSab treated mice and HuH7 cells were used. RESULTS: In PMH, PA dose-dependently up to 1mM stimulated oxygen consumption rate (OCR) due to mitochondrial ß-oxidation. At ⩾1.5mM, PA gradually reduced OCR, followed by cell death. Inhibition of JNK, caspases or treatment with antioxidant butylated hydroxyanisole (BHA) protected PMH against cell death. Sab knockdown or a membrane permeable Sab blocking peptide prevented PA-induced mitochondrial impairment, but inhibited only the late phase of both JNK activation (beyond 4h) and cell death. In PMH, PA increased p-PERK and its downstream target CHOP, but failed to activate the IRE-1α arm of the UPR. However, Sab silencing did not affect PA-induced PERK activation. Conversely, specific inhibition of PERK prevented JNK activation and cell death, indicating a major role upstream of JNK activation. CONCLUSIONS: The effect of p-JNK on mitochondria plays a key role in PA-mediated lipotoxicity. The interplay of p-JNK with mitochondrial Sab leads to impaired respiration, ROS production, sustained JNK activation, and apoptosis.