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Background: Granulomatous disease secondary to cosmetic injection of silicone is an uncommon cause of hypercalcemia. Transgender persons with limited access to appropriate surgery commonly use this procedure as an alternative, which can cause serious complications. Clinical Case: Forty year old transgender women with a 7-year history of nephrolithiasis treated with lithotripsy, pyelotomy and requiring the installation of a pig tail. She is admitted at the emergency room due to renal failure. Non-contrast CT rules out acute obstruction and lab tests conclude terminal kidney failure so she is started with dialysis and discharged. Two months later she returns with fever, she is diagnosed with central venous catheter-related bloodstream infection associated to the dialysis catheter and is started with antibiotics. Physical exam reveals pigmented, indurated nodular areas in her buttocks, hips and legs. The patient is re-interrogated and admits to have had injections of industrial silicone at the age of 22 in the described nodular areas. Regarding her transition process she had a vaginoplasty at 25 years old and was started with estrogens at that time but abandoned controls thereafter. Laboratory: Calcium 10, 8 (8,6-10,2 mg/dl), P 6 (2,5-4,5 mg/dl), PTH 17 (12-88 pg / ml), 25OHVD 3 (30ng / ml). Abdominal and thorax CT showed multiple pulmonary nodules, hilar, axillar and retroperitoneal adenopathies, hepatosplenomegaly, and subcutaneous granulomas with calcification in the buttocks and lumbar areas. HVB, HVC, VDRL and HIV serologies were negative as were ANA, pANCA and Rheumatoid Factor. Myelogram was normal. Biopsy of the involved skin and axillary lymph nodes revealed foreign body granulomatous reaction. Real Time PCR determination of the CYP27B1 mRNA showed a positive expression of this gene in the lesions confirming increased 1 alpha-hydroxylase activity as the cause of hypercalcemia. Tc-99m MDP scintigraphy showed increased activity in the soft tissue of the hips, buttocks and legs. Currently she maintains dialysis with normal values of calcium and is following regular controls in our gender program. Conclusion: Granulomatous disease due to cosmetic injection of silicone is a cause of hypercalcemia that should be suspected in the appropriate context. It is important to educate the transgender community about the possible severe adverse effects of these not authorized procedures.

Obesity reduces maternal insulin sensitivity and alters sex steroid serum concentrations. However, it is not clear if these changes are reflected in the fetal circulation. On the other hand, similar to other metabolic tissues, modifications in sex steroid concentrations and metabolic parameters could modify the transport and metabolism of fatty acids (FA) in the placenta increasing their availability for the fetus. Therefore, we aimed to study, in pregnant women with normal-weight and obesity, sex steroid serum concentrations in cord blood and their relationship with the gene expression of FA transporters and of molecules related with FA metabolism in the placenta. We included 26 pregnant women with normal-weight and 26 pregnant women with obesity without pregnancy complications. At term of pregnancy, mixed cord blood and placenta samples were collected and stored at -80°C. Serum concentrations of dehydroepiandrosterone (DHEA), DHEA sulfate (DHEAS), androstenedione, testosterone, estrone, estradiol, estriol, insulin and TNF-α were measured by RIA or ELISA. Glycemia and lipid profile were also analyzed. In placental samples, the gene expression of MFSD2A, CD36, FABP4, SLC27A4, PPARG, LPL and DGAT were determined by quantitative PCR. No differences were observed in sex steroid concentrations and metabolic parameters between groups. On the other hand, the gene expression of MFSD2A, CD36 and FABP4 were higher in placentas from women with obesity compared to women with normal-weight (P = 0.050, P = 0.037 and P = 0.038, respectively). When distributed according to fetal sex, cholesterol levels were higher in cord blood of women with obesity and female fetuses (P = 0.005), whereas glycemia was lower in women with obesity and male fetuses (P = 0.045). In turn, the gene expression of CD36 and FABP4 were higher (P = 0.024 and P = 0.034, respectively), whereas MFSD2A tended to be higher (P = 0.092) only in placentas from women with obesity and male fetuses. Moreover, in women with obesity and male fetuses, glycemia was positively correlated with MFSD2A (r = 0.650; P = 0.022), and in women with obesity and female fetuses FABP4 was inversely correlated with triglyceride levels (r = -0.580; P = 0.048). In conclusion, these data suggest that modifications in placental steroidogenesis do not affect sex steroid serum concentrations in the fetal circulation. On the other hand, metabolic parameters in cord blood of pregnant women with obesity are associated with an abnormal expression of FA transporters in placental tissue.

Polycystic ovary syndrome (PCOS) is a familial endocrine-metabolic dysfunction, increasingly recognized in adolescent girls with hyperandrogenism. However, it is difficult to establish whether the metabolic abnormalities described in PCOS are present before the onset of hyperandrogenism. In children, a strong association of adiponectin levels with metabolic parameters of insulin resistance has been described.The objective of the study was to evaluate adiponectin serum concentrations and metabolic parameters in prepubertal and pubertal daughters of women with PCOS to identify girls with increased metabolic risk.Fifty-three prepubertal and 22 pubertal (Tanner stages II-V) daughters of PCOS women (PCOSd) and 32 prepubertal and 17 pubertal daughters of control women (Cd) were studied. In both groups, an oral glucose tolerance test was performed with measurement of glucose and insulin. Adiponectin, leptin, C-reactive protein, SHBG, sex steroids, and lipids were determined in the fasting sample.Both groups had similar chronological ages, body mass index sd score, and Tanner stage distribution. In the prepubertal girls, 2-h insulin was higher (P = 0.023) and adiponectin levels were lower (P = 0.004) in the PCOSd group, compared with the Cd group. In the pubertal girls, triglycerides (P = 0.03), 2-h insulin (P = 0.01), and serum testosterone concentrations were higher (P = 0.012) and SHBG lower (P = 0.009) in PCOSd, compared with Cd, but adiponectin levels were similar in both groups.Some of the metabolic features of PCOS are present in daughters of PCOS women before the onset of hyperandrogenism. Adiponectin appears to be one of the early markers of metabolic derangement in these girls.