Renal abscess with bacteremia caused by extended-spectrum ß-lactamase-producing Escherichia coli: a case report.

BACKGROUND: Renal abscess in children is a rare and severe form of infectious kidney disease that is responsible for several serious complications. In this report, we describe a previously healthy 5-year-old girl with a renal abscess caused by extended-spectrum ß-lactamase (ESBL)-producing Escherichia coli (E. coli), which led to bacteremia and renal scarring. CASE PRESENTATION: The patient presented to our department with high fever, headache, vomiting for 2 days and high inflammatory response. We diagnosed her with a urinary tract infection and initiated treatment with ampicillin and cefotaxime. Gram-negative bacilli bacteremia was noted on day 3. On day 4, her fever persisted, and a computed tomography (CT) scan revealed a renal abscess in the left kidney. After identifying the bacteria as ESBL-producing E. coli from the blood culture, we switched to the antibiotic meropenem and continued treatment for 3 weeks. The renal abscess was not drained. Although the renal abscess was successfully treated and it disappeared, a low-density area remained in same lesion on subsequent CT scans and a dimercaptosuccinic acid renal scan performed 4 months after onset revealed renal scarring. CONCLUSION: Given the increasing prevalence of ESBL-producing microorganisms, clinicians should be aware of the possibility of renal abscesses caused by community-acquired ESBL-producing organisms even in previously healthy children. Once a renal abscess is suspected, early diagnosis and management are important for reducing the risk of life-threating complications and renal scarring.

Deletion at chromosome 10p11.23-p12.1 defines characteristic phenotypes with marked midface retrusion.

Approximately 3% of the live-born infants have major dysmorphic features, and about two-thirds of which are observed in the maxillofacial region; however, in many cases, the etiology of the dysmorphic features remains uncertain. Recently, the genome-wide screening of large patient cohorts with congenital disorders has made it possible to discover genomic aberrations corresponding to the pathogenesis. In our analyses of more than 536 cases of clinically undiagnosed multiple congenital anomalies and mental retardation (MR) by microarray-based comparative genomic hybridization, we detected two non-consanguineous unrelated patients with microdeletions at 10p11.23-p12.1, which overlapped for 957 kb, including four protein-coding genes: ARMC4, MPP7, WAC and BAMBI. As the two patients had similar phenotypes; for example, MR and multiple maxillofacial abnormalities including midface retrusion, wide mouth and large tongue, we assessed the phenotypes in detail to define the common features, using quantitative evaluations of the maxillofacial dysmorphism. The concordance of the genetic and phenotypic alterations is a good evidence of a new syndrome. Although an interstitial deletion of 10p is rare, the current study is the first trial to examine precisely the craniofacial characteristics of patients with a heterozygous deletion at 10p11.23-p12.1, and presents good evidence to diagnose potential patients with the same genetic cause.

Initial Treatment of Pediatric Graves' Disease with Methimazole: A Retrospective Follow-up Study.

Antithyroid drugs are widely used in the therapy of Graves' disease (GD), and methimazole (MMI) is preferred for treatment of pediatric GD. The recommended initial dosage of MMI is 0.5-1.0 mg/kg/d for pediatric GD, although there are few studies on the optimal MMI dosage for initial treatment in children. We retrospectively compared the efficacy of different doses of MMI in 35 children with GD. Eight children were excluded due to lack of follow-up, etc. The remaining 27 children were divided into a high-dose group (HD; MMI≥0.7 (0.85 ± 0.13) mg/kg/d, n=8) and a low-dose group (LD; MMI<0.7 (0.51 ± 0.12) mg/kg/d, n=19), and we compared the time needed for the serum FT4 levels to normalize (≤1.6 ng/dl) between the groups. There were no significant differences between the FT4 levels (HD: 5.5 ± 2.8 ng/dl; LD: 5.0 ± 2.4 ng/dl p=0.59) or thyroid stimulating hormone receptor antibody levels (HD: 56.2 ± 29.3%; LD: 60.9 ± 27.2% p=0.69) between the groups before treatment. The mean time required to normalize the FT4 levels was 22.5 ± 7.4 d in the HD group and 28.8 ± 16.2 d in the LD group (p=0.30). In addition, no other factor influenced the time to efficacy of MMI. A dose of MMI<0.7 (0.51 ± 0.12) mg/kg/d appears to as effective as a higher dose in normalizing the serum FT4 level in children with mild or moderate GD.