Does sensorimotor training influence neuromuscular responses, balance, and quality of life in diabetics without a history of diabetic distal polyneuropathy?

OBJECTIVE: To evaluate the effect of supervised and home sensorimotor training on static postural balance (SPB), quality of life (QL), and neuromuscular responses of Type 2 Diabetics (DM-2). DESIGN: Randomized controlled blind study with DM-2 patients, between 45 and 64 years old, of both sexes, divided into 3 groups: Control Group - CG (n = 27), Home Training Group - HTG (n = 27), and Supervised Training Group - STG (n = 26). The subjects were evaluated before and at the end of 3 months of treatment, with a four-week follow-up. The intervention was held twice a week, for 45 min, divided into three phases: warm-up, sensorimotor training, and cool-down. The primary outcome was SPB, using the force platform. Secondary outcome: questionnaires and clinical measures related to diabetic foot and knee flexor-extensors using isokinetic dynamometry. RESULTS: In the baseline, the characteristics were similar between groups and between times. Tactile and vibratory sensitivity demonstrated the absence of symptoms of peripheral neuropathy in diabetic patients. In the intra-group comparison, there was a significant increase in the classification without symptoms of diabetic distal polyneuropathy in the HTG and STG groups (p < 0.05) and there were no significant effects on other clinical outcomes and QL and SPB, muscle strength, and sense of knee joint position. CONCLUSION: The intervention showed no improvement in SPB, QL, and other clinical outcomes of DM-2 patients. Thus, no differences were found between the groups, considering that the patients did not present clinical characteristics of diabetic distal polyneuropathy.

Do all infants need vitamin D supplementation?

A high prevalence of vitamin D deficiency (VDD) in children has been observed worldwide, but there are few studies on the nutritional status of vitamin D (VD) in healthy infants. The main cause of deficiency in healthy children is breastfeeding without supplementation and lack or insufficiency of sun exposure. The aims of this study were to determine serum concentrations of 25(OH)D and verify its association with parathyroid hormone (PTH) concentrations and use of VD supplementation in healthy infants aged ≥ 6 to ≤ 24 months attended at two Primary Health Care Units in Ribeirão Preto city, São Paulo, Brazil. A cross-sectional, observational and analytical study was performed in which serum concentrations of 25(OH)D, PTH, alkaline phosphatase (AP), calcium (Ca), phosphorus (P) and albumin were determined in 155 healthy infants. Information on sun exposure, sociodemographic aspects of mothers and clinical and nutritional characteristics of infants were obtained through interviews with responsible infants's legal representatives. Ten infants (6%) presented deficient 25(OH)D serum concentration (≤20ng/ml) and 46 (30%), insufficient (21 to 29ng/ml). No changes in serum P, Ca and albumin concentrations were detected. Only one infant had an increase in PTH serum concentrations. 35% (55/155) of infants had high AP e 40% (22/55) presented insufficient serum concentrations of 25(OH)D but none presented deficient ones. There was a weak association between serum concentrations of 25(OH)D and PTH and an association between serum concentrations of 25(OH)D and P when adjusted for sex, age and BMI. There were no associations between inadequate serum concentrations of 25(OH)D (deficient ou insufficient), sun exposure and VD supplementation. This study found a low prevalence of deficient 25(OH)D serum concentration and high prevalence of insufficient ones which was not associated with changes in serum PTH, AP, P, Ca and albumin concentrations, VD supplementation and the formula volume intake.

High-fat diet induces site-specific unresponsiveness to LPS-stimulated STAT3 activation in the hypothalamus.

Hypophagia induced by inflammation is associated with Janus kinase (JAK)-2/signal transducer and activator of transcription (STAT) 3 signaling pathway, and leptin-mediated hypophagia is also mediated by JAK2-STAT3 pathway. We have previously reported that lipopolysaccharide (LPS) did not reduce food intake in leptin-resistant high-fat diet (HFD) rats but maintained body weight loss. We investigated whether changes in p-STAT3 expression in the hypothalamus and brain stem could account for the desensitization of hypophagia in HFD animals after a low LPS dose (100 µg/kg). Wistar rats fed standard diet (3.95 kcal/g) or HFD (6.3 kcal/g) for 8 wk were assigned into control diet-saline, control diet-LPS, HFD-saline, and HFD-LPS groups. LPS reduced feeding in the control diet but not HFD. This group showed no p-STAT3 expression in the paraventricular nucleus (PVN) and ventromedial hypothalamic nucleus (VMH), but sustained, though lower than control, p-STAT3 in the nucleus of the solitary tract (NTS) and raphe pallidus (RPa). LPS decreased body weight in HFD rats and increased Fos expression in the NTS. LPS increased body temperature, oxygen consumption, and energy expenditure in both control diet and HFD rats, and this response was more pronounced in HFD-LPS group. Brown adipose tissue (BAT) thermogenesis and increased energy expenditure seem to contribute to body weight loss in HFD-LPS. This response might be related with increased brain stem activation. In conclusion, LPS activates STAT3-mediated pathway in the hypothalamus and brain stem, leading to hypophagia, however, LPS effects on food intake, but not body weight loss, are abolished by leptin resistance induced by HFD. The preserved STAT3 phosphorylation in the brain stem suggests that unresponsiveness to LPS on STAT3 activation under HFD might be selective to the hypothalamus.

Primary hyperparathyroidism as the first clinical manifestation of multiple endocrine neoplasia type 2A in a 5-year-old child.

BACKGROUND: Primary hyperparathyroidism occurs in only 10%-30% of patients with multiple endocrine neoplasia type 2A (MEN2A), rarely as the sole clinical manifestation, and is usually diagnosed after the third decade of life. SUMMARY: A 5-year-old girl was referred for prophylactic thyroidectomy as she carried the p.C634R RET mutation. She was clinically asymptomatic, with a normally palpable thyroid and with the cervical region free of lymphadenopathy or other nodules. Preoperative tests revealed hypercalcemia associated with elevation of parathyroid hormone (PTH) (calcium = 11.2 mg/dL, calcium ion = 1.48 mmol/L, phosphorus = 4.0 mg/dL, alkaline phosphatase = 625 U/L, parathyroid hormone (PTH) PTH = 998 pg/mL). A thyroid ultrasound was normal and parathyroid scintigraphy with (99m)Tc-Sestamibi revealed an area of radioconcentration in the upper half of the left thyroid lobe suggesting hyperfunctioning parathyroid tissue. She underwent total thyroidectomy and parathyroidectomy and developed hypocalcemia. The anatomopathological examination showed no histopathological changes in the thyroid tissue and an adenoma of the parathyroid gland, confirming the diagnosis of hyperparathyroidism. CONCLUSIONS: Primary hyperparathyroidism can be a precocious manifestation of MEN2A. This case report highlights that asymptomatic hypercalcemia should be scrutinized in children related to patients with MEN2A who carry a mutation in the RET proto-oncogene, especially mutations in the codon 634, before the currently recommended age of 8 years.

Evaluation of bone and mineral metabolism in patients recently diagnosed with leprosy.

This study was conducted to evaluate patients recently diagnosed with the tuberculoid and lepromatous forms of leprosy for bone mass, bone remodeling, and hormones related to mineral control. Eleven normal control individuals (CG) and 12 patients with leprosy (LG) matched for physical characteristics were submitted to evaluation of bone mass density (BMD) and to the determination of serum levels of PTH, 25-hydroxyvitamin D [25(OH)D], testosterone, LH, FSH, osteocalcin (OC), and urinary levels of deoxypyridinoline (DPD). The T score of lumbar spine and total radius (mean +/- SD) were significantly lower in leprosy patients (L1-L4: CG = -0.7 +/- 1.5 vs LG = -1.8 +/- 1.0 SD, P < 0.04, and total radius: CG = -1.43 +/- 0.6 vs LG = -2.1 +/- 0.8 SD, P <0.02), whereas no significant differences were observed in total hip or femoral neck T score. However, at all sites, the rate of low bone mass (T score < -1.0) was higher in LG (femoral neck: CG = 18% vs LG = 50%, total hip: CG = 27% vs LG = 42%). There was a significant difference in albumin and PTH levels between groups but not in serum 25(OH)D and OC levels or urinary DPD levels. The present results indicate that bone mass loss is an early event in leprosy patients and frequently is already present at diagnosis. Its etiopathogenesis is multifactorial, and further studies are needed to determine the most efficient way to prevent fractures in this condition. The data obtained in the present study need confirmation by the evaluation of a larger sample.