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Postoperative (PO) complications after transsphenoidal surgery (TSS) are rare when performed in pituitary referral centers. Partial hypopituitarism is more frequent and somewhat expected. Meningitis, cerebrospinal fluid leaks, and visual deficits are unusual. Cerebrovascular complications, including cerebral vasospasm are rare, usually under-appreciated and not mentioned to the patient prior to the surgery. This is a report of a 51-year-old male with a non-functioning pituitary macroadenoma presenting with partial hypopituitarism and visual field loss. The patient was submitted to an uneventful TSS. On the first PO day, he developed a left palpebral ptosis with unequal pupils and impaired consciousness (12 points on Glasgow Coma Scale). CT scan revealed a perimesencephalic subarachnoid hemorrhage (SAH) grade 1 according to the modified Fisher scale. High-dose dexamethasone (16 mg/day) was initiated and the patient became more alert (Glasgow 14). On the fifth PO day, due to progression of the neurological deficits (left III, IV, and VI cranial nerves palsy, ataxia, dysdiadochokinesia, right dysmetria, and dysarthria), a magnetic resonance angiography was obtained and revealed a recent mesencephalic infarct without evident vasospasm. Nevertheless, nimodipine 60 mg 4/4 h was initiated. No improvement was seen after 3 days of treatment. The patient was discharged and put on rehabilitation, returning to normal gait and balance after 7 months. This, therefore, is a case of an unexpected mesencephalic infarct probably due to vasospasm induced by minor SAH. Although exceptionally rare, informing the patient about this event prior to TSS is important due to its significant neurological impact. More data are needed considering preventive treatment with nimodipine as soon as SAH is detected after TSS and whether it would improve neurological outcomes.

Objective: To investigate the impact of early exposure to androgen excess on gonadotropin-dependent puberty (GDP) and final height (FH) of patients with androgen-secreting adrenocortical tumors (ACT) in childhood. Methods: Retrospective cohort study. Occurrence of GDP and achievement of FH were evaluated. Central precocious puberty (CPP) and early fast puberty (EFP) were considered pubertal disorders. Patients with normal puberty and pubertal disorders were compared. Results: The study included 63 patients (44F), followed in a single institution from 1975 until 2017. At diagnosis of ACT, median age was 25.8 month s; duration of signs, 6 months; stature SDS, 0.5 (−3.6 to 3.9) and bone age advancement, 14.7 months (−27.9 to 85.4). To date, 37 patients developed GDP: 26 had normal puberty; one, precocious thelarche; seven, CPP and three, EFP. GnRHa effectively treated CPP/EFP. Tall stature and older age at diagnosis of ACT were associated with risk of CPP alone (RR 4.17 (95% CI 1.17–14.80)) and CPP/EFP (RR 3.0 (95% CI 1.04–8.65)). Recurrence/metastasis during follow-up were associated with risk of CPP alone (RR 4.17 (95% CI 1.17–14.80)) and CPP/EFP (RR 3.0 (95% CI 1.12–8.02)). Among the 19 patients that reached FH, stature SDS dropped from 1.4 to −0.02 since diagnosis of ACT (P = 0.01). Seventeen achieved normal FH. There was no difference in FH SDS between patients with norm al puberty and pubertal disorders (P = 0.75). Conclusions: Gonadotropin-dependent pubertal disorders are common in patients with androgen-secreting ACT in childhood. FH is usually not impaired. The study reinforces the importance of close follow-up after surgery to identify and treat consequences of early exposure to androgen excess.

The present study was designed to evaluate the relationship between bone traits [bone mineral density (BMD) and trabecular bone score (TBS)] and the accumulation of fat in adipose tissues [abdominal subcutaneous (SAT), visceral (VAT), marrow (MAT) and intrahepatic lipids (IHL)], as well as insulin resistance, in subjects with Cushing's disease (CD). The study included control (C = 27), paired (P = 16) and Cushing's disease (CD = 10) groups, which underwent biochemical assessment, dual X-ray absorptiometry, TBS, and magnetic resonance imaging to determine fat deposits. The CD group showed higher serum levels of glucose and insulin, as well as HOMA-IR values, but lower circulatory levels of osteocalcin, in comparison to C and P. The CD group exhibited lower L1-L4 BMD than P (P = 1.059 ± 0.141 vs CD = 0.935 ± 0.093 g/cm2, p < 0.05) (Fig 1A). The lumbar spine BMD from the C group was similar to the other groups. TBS was lower in CD than in P and C (C = 1.512±0.077 vs P = 1.405±0.150 vs CD = 1.135±0.136; p

Night work has become necessary in our modern society. However, sleep deprivation induces a circadian misalignment that effectively contributes to the development of diseases associated with metabolic syndrome, such as obesity and diabetes. Here, we evaluated the pattern of circadian clock genes and endoplasmic reticulum stress (ERS) genes in addition to metabolic and anthropometric measures in subjects that work during a nocturnal period compared with day workers. We study 20 night workers (NW) and 20 day workers (DW) submitted to a work schedule of 12 h of work for 36 h of rest for at least 5 years in a hospital. The present report shows that NW have increased fasting blood glucose, glycated hemoglobin (HbA1c), triglycerides, and low-density lipoprotein (LDL)-cholesterol levels, and lower high-density lipoprotein (HDL)-cholesterol levels compared to DW. In addition, we observed that waist circumference (WC), waist–hip ratio (WHR), and systemic blood pressure are also increased in NW. Interestingly, gene expression analysis showed changes in CLOCK gene expression in peripheral blood mononuclear cells (PBMC) samples of NW compared to the DW, evidencing a peripheral circadian misalignment. This metabolic adaptation was accompanied by the up-regulation of many genes of ERS in NW. These findings support the hypothesis that night shift work results in disturbed glycemic and lipid control and affects the circadian cycle through the deregulation of peripheral CLOCK genes, which is possibly due to the activation of ERS. Thus, night work induces important metabolic changes that increase the risk of developing metabolic syndrome.

ABSTRACT Objective: Feeding restriction in rats alters the oscillators in suprachiasmatic, paraventricular, and arcuate nuclei, hypothalamic areas involved in food intake. In the present study, using the same animals and experimental protocol, we aimed to analyze if food restriction could reset clock genes ( Clock, Bmal1 ) and genes involved in lipid metabolism ( Pgc1a, Pparg, Ucp2 ) through nutrient-sensing pathways ( Sirt1, Ampk, Nampt ) in peripheral tissues. Materials and methods: Rats were grouped according to food access: Control group (CG, food ad libitum ), Restricted night-fed (RF-n, food access during 2 h at night), Restricted day-fed (RF-d, food access during 2 h in the daytime), and Day-fed (DF, food access during 12 h in the daytime). After 21 days, rats were decapitated at ZT3 (0900-1000 h), ZT11 (1700-1800 h), or ZT17 (2300-2400 h). Blood, liver, brown (BAT) and peri-epididymal (PAT) adipose tissues were collected. Plasma corticosterone and gene expression were evaluated by radioimmunoassay and qPCR, respectively. Results: In the liver, the expression pattern of Clock and Bmal1 shifted when food access was dissociated from rat nocturnal activity; this phenomenon was attenuated in adipose tissues. Daytime feeding also inverted the profile of energy-sensing and lipid metabolism-related genes in the liver, whereas calorie restriction induced a pre-feeding increased expression of these genes. In adipose tissues, Sirt1 expression was modified by daytime feeding and calorie restriction, with concomitant expression of Pgc1a , Pparg , and Ucp2 but not Ampk and Nampt . Conclusion: Feeding restriction reset clock genes and genes involved in lipid metabolism through nutrient-sensing-related genes in rat liver, brown, and peri-epididymal adipose tissues.

OBJECTIVES: Idiopathic central precocious puberty and its postponement with a (gonadotropin-releasing hormone) GnRH agonist are complex conditions, the final effects of which on bone mass are difficult to define. We evaluated bone mass, body composition, and bone remodeling in two groups of girls with idiopathic central precocious puberty, namely one group that was assessed at diagnosis and a second group that was assessed three years after GnRH agonist treatment. METHODS: The precocious puberty diagnosis and precocious puberty treatment groups consisted of 12 girls matched for age and weight to corresponding control groups of 12 (CD) and 14 (CT) girls, respectively. Bone mineral density and body composition were assessed by dual X-ray absorptiometry. Lumbar spine bone mineral density was estimated after correction for bone age and the mathematical calculation of volumetric bone mineral density. CONEP: CAAE-0311.0.004.000-06. RESULTS: Lumbar spine bone mineral density was slightly increased in individuals diagnosed with precocious puberty compared with controls; however, after correction for bone age, this tendency disappeared (CD = -0.74 + 0.9 vs. precocious puberty diagnosis = -1.73 + 1.2). The bone mineral density values of girls in the precocious puberty treatment group did not differ from those observed in the CT group. CONCLUSION: There is an increase in bone mineral density in girls diagnosed with idiopathic central precocious puberty. Our data indicate that the increase in bone mineral density in girls with idiopathic central precocious puberty is insufficient to compensate for the marked advancement in bone age observed at diagnosis. GnRH agonist treatment seems to have no detrimental effect on bone mineral density.

Os critérios diagnósticos dos distúrbios do metabolismo de glicose foram estabelecidos pela Organização Mundial de Saúde (OMS)/National Diabetes Data Group (NDDG) no início da década de 1980. Em 1997, a American Diabetes Association (ADA) sugeriu novos critérios diagnósticos, baseados na interpretação da glicemia de jejum. Neste estudo, 56 indivíduos foram submetidos ao teste de tolerância à glicose oral (oGTT) (75g) e aplicamos ambos os critérios diagnósticos para estimar a prevalência de distúrbios de metabolismo de glicose. Dos 56 indivíduos, 11 (19,6% - grupo 1) foram considerados intolerantes pelos critérios da OMS/NDDG e seis (10,7% - grupo 2), como glicemia de jejum alterada (GJA) pelos novos critérios da ADA. Comparamos variáveis clínicas e bioquímicas (idade, índice de massa corporal, pico de insulina durante o oGTT, área sob a curva de insulina durante o oGTT e concentrações séricas basais da proteína carreadora dos fatores de crescimento insulina-símiles 1 (IGFBP-1) entre ambos os grupos, não observando diferença significativa em nenhuma das variáveis (43 ± 13 x 46 ± 4,4 anos, 29,5 ± 3,2 x 27,2 ± 2,6kg/m², 153,7 ± 100,7 x 171,3 ± 145,6µUI/ml, 12.040 ± 8.488 x 13.970 ± 12.170 e 14,4 ± 9,3 x 19,4 ± 11,8ng/ml, respectivamente, p = NS). Entretanto, quando comparamos estas mesmas variáveis entre o grupo de indivíduos considerados normais pelos critérios da ADA e intolerantes pelos critérios da OMS/NDDG (n = 8, grupo 3) e o grupo de indivíduos considerados normais por ambos os critérios (n = 42, grupo 4), observamos que não houve também diferença em relação à idade (42 ± 15 x 38 ± 10 anos, respectivamente, NS); entretanto o grupo 3 apresenta índice de massa corporal (IMC) (29,5 ± 3,9 x 24,5 ± 3,5kg/m², respectivamente, p < 0,02), pico de insulina durante o oGTT (115,2 ± 29,1 x 84,4 ± 56,5µUI/ml, respectivamente, p < 0,02) e área sob a curva de insulina durante o oGTT (9.112 ± 2.323 x 6.649 ± 4.438, respectivamente, p < 0,007) com valores médios superiores ao grupo 4. O grupo 3 apresentou ainda concentrações séricas basais de IGFBP-1 com valores em média inferiores ao grupo 4 (14,9 ± 10,1 x 28,9 ± 17,6ng/ml, respectivamente, p < 0,03).The diagnostic criteria of the glucose metabolism disorders had been established by the World Health Organization (WHO)/National Data Group (NDDG) in the beginning of the 1980's. In 1997, the American Diabetes Association (ADA) suggested new criteria, based upon the interpretation of the fasting glucose. In this study, 56 subjects underwent an oral glucose tolerance test (oGTT), and we have applied both criteria to estimate the prevalence of the glucose metabolism disorders. Out of 56 subjects, 11 (19,6% - Group 1) had been considered glucose intolerants by the criteria of the WHO/NDDG and 6 (10,7% - Group 2) as impaired fasting glycemia (IFG) by the ADA new criteria. We have compared clinical and biochemical variables (age, BMI, insulin peak during oGTT, area under the insulin curve during oGTT and serum concentrations of IGFBP-1) between both groups, not observing differences in any of the variables (43 ± 13 x 46 ± 4.4 years, 29.5 ± 3.2 x 27.2 ± 2.6kg/m², 153.7 ± 100.7 x 171.3 ± 145.6µUI/ml, 12,040 ± 8,488 x 13,970 ± 12,170 e 14.4 ± 9.3 x 19.4 ± 11.8ng/ml, respectively, p = NS). However, when we compare these same variables between the subjects considered normal by the ADA criteria and intolerants by the WHO/NDDG (n = 8, Group 3) and the subjects considered normal by both criteria (n = 42, Group 4), we observed that it also did not have difference in relation to age (42 ± 15 x 38 ± 10 years, respectively, NS), however, Group 3 presents BMI (29.5 ± 3.9 x 24.5 ± 3.5kg/m², respectively, p < 0.02), insulin peak (115.2 ± 29.1 x 84.4 ± 56.5µUI/ml, respectively, p < 0.02) and area under the insulin curve (9,112 ± 2,323 x 6,649 ± 4,438, respectively, p < 0.007)with higher values than Group 4. Group 3 still presented serum concentration of IGFBP-1 with lower values than Group 4 (14.9 ± 10.1 x 28.9 ± 17.6ng/ml, respectively, p < 0.03).