Evaluation of boys with daytime incontinence by combined cystourethroscopy, voiding cystourethrography and urodynamics.

Objects: Approximately, 1% of school children have daytime urinary incontinence. The symptoms may be caused by an overactive bladder (OAB). In the evaluation of boys with OAB complaints, one should consider a possible urethral cause. The aim of the study was to evaluate the value of a diagnostic regime with cystourethroscopy, voiding cystourethrography (VCUG) and urodynamic pressure-flow studies in boys with OAB complaints after unsuccessful urotherapy and pharmacological therapy. Materials and Methods: Seventy-five boys (5-14 years old) were investigated with cystourethroscopy and within 24 h thereafter VCUG followed by urodynamic combined cystometry and pressure-flow study. All boys had daytime incontinence and urgency. Results: Sixty-one boys had no suspected urethral valves at cystoscopy or VCUG, and urodynamics showed no obstructed Pdet-Qmax. All 61 boys had detrusor overactivity. Two boys had late diagnosed urethral valves. In four boys, the initial cystourethroscopy was described as normal. The VCUG indicated presence of posterior urethral valves, but urodynamics showed no obstructed Pdet-Qmax. In eight boys, the initial cystourethroscopy was described as normal whereas urodynamics showed obstructed Pdet-Qmax. In four of these boys, VCUG showed abnormalities in the sphincter area but they were not described as suspected urethral valves. At repeat cystourethroscopy, urethral valves could still not be identified. Patient follow-up regarding achievement of continence after investigation guided treatment was in accordance with the literature. Conclusions: Boys can be safely evaluated by cystourethroscopy followed by urodynamics in search for a possible urethral problem. It is our suggestion, that VCUG can be restricted to those boys where urodynamics indicates obstruction or the findings by cystourethroscopy are uncertain.

18F-FDG PET/CT as a diagnostic tool in patients with extracervical carcinoma of unknown primary site: a literature review.

BACKGROUND: Carcinoma of unknown primary (CUP) represents a heterogeneous group of metastatic malignancies for which no primary tumor site can be identified after extensive diagnostic workup. Failure to identify the primary site may negatively influence patient management. The aim of this review was to evaluate (18)F-fluorodeoxyglucose positron emission tomography/computed tomography ((18)F-FDG PET/CT) as a diagnostic tool in patients with extracervical CUP. MATERIALS AND METHODS: A comprehensive literature search was performed and four publications were identified (involving 152 patients) evaluating (18)F-FDG PET/CT in CUP patients with extracervical metastases. All studies were retrospective and heterogeneous in inclusion criteria, study design, and diagnostic workup prior to (18)F-FDG PET/CT. RESULTS: (18)F-FDG PET/CT detected the primary tumor in 39.5% of patients with extracervical CUP. The lung was the most commonly detected primary tumor site (∼50%). The pooled estimates of sensitivity, specificity, and accuracy of (18)F-FDG PET/CT in the detection of the primary tumor site were 87%, 88%, and 87.5%, respectively. CONCLUSIONS: The present review of currently available data indicates that (18)F-FDG PET/CT might contribute to the identification of the primary tumor site in extracervical CUP. However, prospective studies with more uniform inclusion criteria are required to evaluate the exact value of this diagnostic tool.

ADAM12-S stimulates bone growth in transgenic mice by modulating chondrocyte proliferation and maturation.

UNLABELLED: ADAM12-S transgenic mice exhibit a pronounced increase in the length of bones, such as femur, tibia, and vertebrae. The effect of ADAM12-S on longitudinal bone growth involves the modulation of chondrocyte proliferation and maturation, likely through proteolytic activities and altered cell-extracellular matrix interactions in the growth plate. INTRODUCTION: The disintegrin and metalloprotease ADAM12 is expressed in both osteoblasts and osteoclasts, suggesting a regulatory role of ADAM12 in bone. However, thus far, no in vivo function of ADAM12 in the skeleton has been reported. MATERIALS AND METHODS: Transgenic mice expressing the secreted form of human ADAM12, ADAM12-S, or a truncated metalloprotease-deficient form of ADAM12-S in the circulation were used to study the effects of ADAM12 on the skeleton. In addition, murine chondrocyte cultures were used to study the effect of ADAM12-S on cell-extracellular matrix interactions. RESULTS: ADAM12-S transgenic mice exhibit increased longitudinal bone growth. The increased bone length is progressive and age dependent, with a maximum increase of 17% seen in the femur from 6-month-old transgenic mice. The effect is gene dose dependent, being more pronounced in mice expressing higher levels of the transgene than in a lower-expressing line. Histological analysis revealed no alterations in the growth plate organization, but mean growth plate width was increased. Both the cellular incorporation of bromodeoxyuridine and the width of the collagen type X-positive hypertrophic zone were increased in the growth plate of ADAM12-S transgenic mice. Importantly, mice expressing a truncated form of ADAM12-S that lacked the pro- and metalloprotease domains showed no alterations in bone length, suggesting that protease activity is required for the ADAM12-S effect. In vitro studies showed that ADAM12-S inhibits chondrocyte adhesion to fibronectin and collagen type II. CONCLUSIONS: ADAM12-S stimulates bone growth in mice by modulating chondrocyte proliferation and maturation through mechanisms probably involving both metalloprotease and adhesion activities.