Insulin resistance prevalence varied according to the diagnostic method employed, with no statistical difference between them. The proportion of IR diagnoses was statistically higher in obese women than in women with normal BMI. We observed a significant association between IR and WC, BMI, LAP, as well as dyslipidemia and AH in a high proportion of patients.

BackgroundIn women, during embryologic development, the paired Müllerian (paramesonephric) ducts fuse distally and develop into the uterus, cervix, and upper vagina. If the Wolffian ducts persist in vestigial form, they can lead to Gartner’s cysts, mainly located in the right wall of the vagina. This is one of the few studies of Gartner’s cysts with a series of consecutive cases over a long period of time who were exclusively subject to clinical observation. Although Gartner’s cysts are found in approximately 0.1 to 0.2 % of women, controversy exists regarding the course of action to be taken.Case presentationWe describe the cases of four women who were 38-years old, 53-years old, 37-years old, and 49-years old at their first appointment and who were of mixed ethnicity, mixed ethnicity, black, and mixed ethnicity respectively. The follow-up of these patients ranged from 2 to 17 years. In these four cases the location of the cysts was the right wall of the vagina. Transvaginal ultrasound was the test of choice for diagnostic confirmation. In the cases presented in this study, the women were asymptomatic and chose to be observed clinically.ConclusionsThis is the first study reporting long-term clinical observation of these lesions. This study shows that conservative treatment can be a safe option for asymptomatic patients with vaginal Gartner’s duct cysts.

Objetivo: Investigar a prevalência de PNDS (polineuropatia distal simétrica) e/ou dor neuropática entre indivíduos com obesidade e fatores metabólicos. Métodos: Estudo transversal, descritivo, observacional, realizado em hospital público do DF. Incluídos indivíduos com IMC ≥ 30 kg/m², ≥ 18 anos. Os testes para o diagnóstico de PNDS foram realizados por meio de aplicativo que verifica sintomas neuropáticos, testes clínicos para fibras nervosas finas e grossas e uso da escala visual analógica (EVA). Resultados: O estudo envolveu 31 participantes, idade média 44,19 (±12,88), 27 mulheres (87,1%), IMC 42,44 (±5,89), 22 (71%) com pré-DM ou DM. Observou-se correlação significativa com a presença de PNDS em indivíduos mais velhos (p<0.001), maior tempo de obesidade (p = 0.004), presença de pré-DM ou DM2 (p = 0.045), uso de estatina (p = 0.0001) e valor mais elevado da EVA (8 versus 6, p=0,046). Conclusão: Foi encontrado associação de PNDS e obesidade em indivíduos mais velhos e mais longa duração da doença, pré-DM ou DM2, em tratamento para dislipidemia e com escore mais alto para dor neuropática. O estudo alerta, pela primeira vez em nosso meio, para a necessidade de rastreamento de PNDS em pessoas com obesidade mesmo sem alteração da glicemia.

Background: Hypophosphatemic rickets (HR) is usually an inherited disorder, but it may also occur in several clinical settings as an acquired condition due to phosphate absorption and internal distribution issues. Recently it was described the association between the use of the elemental amino-acid based formula (AAF) and HR. Herein we report two male twins presenting this condition. Clinical case: Two monozygotic preterm (28 weeks + 5 days) brothers, born with extremely low birth weight (895 and 995 grams, -1,4 SDS and -0.9 SDS, respectively), received total parental nutrition from the 1st to the 7th day of life. Afterwards they started oral diet with milk and human milk fortifier FM85 for preventing metabolic bone disease of prematurity. After some weeks they developed abdominal distension, vomiting and hematochezia. Allergy to cow milk protein was suspected and the infants started receiving extensively hydrolyzed milk formula. So, FM85 was suspended and they were put on tricalcium phosphate (12.9%) supplementation from the 4th week of life on. As the gastrointestinal symptoms persisted, the formula was exchanged for elemental formula Neocate at 2 months of age, with improvement of those symptoms. After the 5th week of life the patients developed hypophosphatemia (2.8 mg/dL, reference 4.8-7.4 mg/dL), hyperphosphatasemia (1,619 IU/L and 2,173 IU/L; reference 70-350 IU/L) and low urinary phosphate excretion, keeping normal calcium and PTH ser um levels. Radiographic skeletal inventory showed under mineralized bones with irregular metaphyseal margins, but no signs of fractures. Calcium and phosphate supplementation doses were increased in attempt to correct the metabolic disturbances, and calcitriol was also started. Nevertheless, hypophosphatemia, hyperphosphatasemia and hypophosphaturia persisted. At 4 months of age, Neocate was switched to Alfamino, still an AAF. After that, phosphate serum levels went up until normalization and alkaline phosphatase started to decrease. Calcium and phosphate supplementation were decreased to keep their serum levels at the normal range for age. The boys were then discharged from hospital when they were 4 months old (45 days of life of corrected age), but the family could not afford Alfamino, switching back to Neocate. After that their phosphate serum levels went below normal range again. Conclusion: To our knowledge, this is the first report on monozygotic twins presenting AAF Neocate-related HR. The underlying mechanisms of Neocate induced hypophosphatemia is still elusive, since its content of phosphate and calcium:phosphate ratio are similar to other AAFs. These cases reinforce the importance of evaluating phosphate metabolism in infants receiving AAF while the pathophysiology of this condition is not entirely understood.