The benefits of the proposed study include mid-term effects in weight reduction for overweight and obese adolescents. The current proposal will contribute to fill a gap in the literature on the mid-term effects of gamification-based interventions to control weight in adolescents. This trial is a well-designed RCT that is in line with the Consolidated Standards of Reporting Trials statement.

SUMMARYThe XX male syndrome -Testicular Disorder of Sexual Differentiation (DSD) is a rare condition characterized by a spectrum of clinical presentations, ranging from ambiguous to normal male genitalia. We report hormonal, molecular and cytogenetic evaluations of a boy presenting with this syndrome. Examination of the genitalia at age of 16 months, showed: penis of 3.5 cm, proximal hypospadia and scrotal testes. Pelvic ultrasound did not demonstrate Mullerian duct structures. Karyotype was 46,XX. Gonadotrophin stimulation test yielded insufficient testosterone production. Gonadal biopsy showed seminiferous tubules without evidence of Leydig cells. Molecular studies revealed that SRY and TSPY genes and also DYZ3 sequences were absent. In addition, the lack of deletions or duplications of SOX9, NR5A1, WNT4 and NROB1 regions was verified. The infant was heterozygous for all microsatellites at the 9p region, including DMRT1 gene, investigated. Only 10% of the patients are SRY-negative and usually they have ambiguous genitalia, as the aforementioned patient. The incomplete masculinization suggests gain of function mutation in one or more genes downstream to SRY gene. Arq Bras Endocrinol Metab. 2010;54(8):685-9 SUMÁRIO A síndrome do homem XX é uma condição rara na qual o fenótipo da genitália externa pode variar de uma genitália ambígua até uma genitália masculina normal. Este estudo tem por objetivo relatar a avaliação hormonal, molecular e citogenética de um menino com essa síndrome. O exame da genitália externa na idade de 16 meses mostrava: pênis medindo 3,5 cm, hipospadia proximal e testículos tópicos. A ultrassonografia pélvica não visualizou estruturas mullerianas. Cariótipo foi 46,XX. A testosterona sérica não se elevou após o teste de estímulo com gonadotrofina. Biópsias gonadais mostraram túbulos seminíferos, sem evidência de células de Leydig. Estudos moleculares revelaram ausência dos genes SRY, TSPY e DYZ3, bem como ausência de deleção ou duplicação das regiões SOX9, NR5A1, WNT4 e NROB1. A criança era heterozigótica para todos os microssatélites da região 9p, incluindo o gene DMRT1. Apenas 10% dos pacientes com a síndrome do homem 46,XX são SRY-negativos. Nesses casos, a genitália geralmente é ambígua, como corroborado pelo paciente do presente relato. A masculinização incompleta sugere ganho de mutação funcional em um ou mais genes a jusante do gene SRY. Arq Bras Endocrinol Metab. 2010;54(8):685-9

Chronic inflammatory demyelinating polyradiculopathy (CIDP) is an immune-mediated disorder for which specific clinical cerebrospinal fluid (CSF), electrophysiologic and histological criteria have been proposed 1 . CIPD is an uncommon cause of childhood polyneuropathy. Descriptions of children with CIPD are scarce. Therefore, this article intends to report a case about an adolescent with type 1 diabetes mellitus (T1DM) with a satisfactory therapeutic response to immunoglobulin and methylprednisolone.This presentation highlights the importance of investigating diabetic patients, including children, with polyneuropathy in an attempt to identify the ones with demyelinating polyneuropathy, because of the likelihood of these patients to benefit from immumodulatory and/or immunossupressive treatment. CaSeMale, 14 year-old, with a seven year history of T1DM and one year history of diabetic nephropathy. Under insulinotherapy and captopril with unsatisfactory glycemic control. Nine months before the initial evaluation he presented pain, paresthesia and a progressive, symmetric muscular weakness, in both lower limbs. After five months of therapeutic failure under carbamazepine and amytryptiline, he was referred to our service. The initial evaluation showed a mild and symmetric, proximal and distal lower limb weakness (the upper limbs were not affected). The proximal compromise was worse than distal. There were patellar and Achilles tendon hyporeflexia, with absence of Babinski sign. Pain, vibratory and position stimulus modalities were normal, although tactile sensory tests evidenced paresthesias. Anal and vesical sphincter function and muscular tone were preserved.Complete blood count, erythrocyte sedimentation rate, urea, creatinine, electrolytes, AST, ALT, GGT, alkaline phosphatase, prothrombine time, total proteins, albumin, creatinekynase (CK), CK-MB, thyroid function tests, lipid profile and cerebrospinal fluid evaluation were normal.The first electromyography (EMG), done five months after the beginning of the neurologic symptoms (Nihon Khoden Electromyography, 4 channels), evidenced decreased conduction velocities with normal amplitude in the median, ulnar, left fibular and posterior tibial nerves, except in the deep right fibular nerve, where although the amplitude was 75% of the lower limit of the normal range (LLNR), the conduction study was 80% lower than LLNR. The distal motor latencies of the median, left ulnar, superficial fibular and sural nerves were prolonged (above 120% of the normal range). The F waves presented prolonged latencies in the ulnar and posterior tibial nerves. The examination with monopolar needle showed decrease in the recruitment of action potentials of the motor unit.The patient was initially treated with human immunoglobulin (400 mg/Kg/day, IV, 5 days), improving the sensory symptoms for about a month, with subsequent relapse, in smaller intensity. There was not improvement of the lower limb weakness. A second EMG, performed 2 months after therapy with immunoglobulin, evidenced increment...