Effect of low-level laser therapy and zoledronic acid on bone repair process.

This study aimed to evaluate, through histomorphometric analysis, the bone repair process in the tibia of rats treated with zoledronic acid and submitted to 808-nm low-level laser therapy (LLLT) by using arsenide aluminum gallium laser. For this purpose, 20 rats were used and distributed according to treatment: group 1-saline administration; group 2-treated with LLLT; group 3-treated with zoledronic acid; and group 4-treated with zoledronic acid and LLLT. The zoledronic acid was administered at a dose of 0.035 mg/kg every 2 weeks for 8 weeks. Subsequently, bone defects of 2 mm were prepared in the tibias of all groups. The bone defects in groups 2 and 4 were irradiated with LLLT in the immediate post-operative period. After 14 and 28 days of application, the animals were submitted and euthanized for histomorphometric analysis. The results were submitted to statistical analysis (α = 5%), and the intragroup comparison was performed using the t test. On the other hand, for intergroup comparison, the ANOVA test was performed, and to the groups presenting statistically significant difference, the Student-Newman-Keuls test was used. In intergroup comparison, group 1 (mean ± SD= 45.2 ± 18.56%) showed a lower bone formation compared with groups 2 (64.13 ± 3.51%) (p = 0.358) and 4 (15.2 ± 78.22%) (p = 0.049), at the 14-day period. Group 3 (20.99 ± 7.42%) also presented a lower amount of neoformed bone tissue, with statistically significant difference when compared with groups 1 (p = 0.002), 2, and 4 (p ≤ 0,001). After 28 days, group 1 presented a lower amount of neoformed bone tissue compared with the other groups, with p = 0.020. Thus, it was concluded that LLLT associated with zoledronic acid is effective for stimulating bone formation in surgically created defects in rats, at the periods studied.

Levels of bioavailable, and free forms of 25(OH)D after supplementation with vitamin D3 in primary hyperparathyroidism.

The 25 hydroxyvitamin D [25(OH)D] is the major metabolite for ascertaining vitamin D status, which circulates bound to a specific carrier (vitamin D-binding protein - VDBP). A portion that circulates unbound vary according to the VDBP genotype. This study evaluates the behavior of different forms of 25(OH)D, before and after supplementation with 14,000 IU of vitamin D3, weekly for 12 weeks, in individuals with primary hyperparathyroidism and controls. Fifty-six patients with active primary hyperparathyroidism (PHPT) and 64 paired controls (CTRL), not taking vitamin D3 for the last three months, were enrolled. The genetic isotypes of VDBP were determined to calculate bioavailable and free 25(OH)D. A p < 0.05 was considered significant. There were no statistical differences in free, bioavailable, and total 25(OH)D levels between PHPT and CTRL groups at baseline. The distribution of VDBP haplotypes 1s/1s, 1f/1f, 1s/1f, 2/2, 1s/2, and 1f/2 was similar between groups. After supplementation, all three forms of 25(OH)D proportionally increased within each group, although the percentage increment was lower in the PHPT group (p < 0.05). Total 25(OH)D is better correlated with PTH in the PHPT group than bioavailable and free 25(OH)D (r = -0.41; p < 0.05). The concentrations of total, free, and bioavailable 25(OH)D were similar in both PHPT and CTRL groups, and all forms increased proportionally after supplementation, although this increment percentage was higher in the CTRL group, with a subsequent reduction of PTH and AP. Total 25(OH)D correlated better with PTH than other forms, suggesting no advantages in measuring free or bioavailable 25(OH)D in these situations.

An approach to the diagnosis and management of a case presenting with recurrent hypomagnesemia secondary to the chronic use of a proton pump inhibitor.

PURPOSE: Magnesium is an important electrolyte for very many cell functions and its deficiency may lead to a wide spectrum of diseases. We report a clinical case of hypomagnesemia resulting from the chronic use of a proton pump inhibitor (PPI). PPIs are drugs widely used in medical practice, and a growing number of cases of PPIs causing hypomagnesemia have been described. Our aim was to monitor the clinical and electrolyte findings during recovery from hypomagnesemia caused by long-term PPI use. RESULTS: A 65-year old female who had been using omeprazole for 10 years, presented with arrhythmia and paresthesia of the lower and upper limbs that had been attributed to severe hypomagnesemia, hypocalcemia, and hypoparathyroidism. Her laboratory tests revealed the following results: magnesium 0.6 mg/dL (NR: 1.5 to 2.5 mg/dL), calcium 7.3 mg/dL (NR: 8.5 to 10.2 mg/dL), parathyroid hormone (PTH) 13.3 pg/mL (NR: 15 to 65 pg/mL), and low urinary calcium and magnesium excretion. Her electrocardiogram disclosed typical, prolonged QT interval, ST depression, and U waves. We discuss the differential diagnoses, pathophysiology, and reversibility of symptoms after effective treatment of the hypomagnesemia. CONCLUSION: this report emphasizes that even if long-term PPI users appear largely asymptomatic, life-threatening arrhythmias can present very suddenly. Long-term PPI users should be monitored for otherwise unexplained hypomagnesemia, hypocalcemia, functional hypoparathyroidism and associated symptoms.