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High serum homocysteine (HCY) and indirectly deficiency of folate and/or vitamin B(12) stimulate bone resorption and adversely affect collagen cross-linking. The aim of this study was the evaluation of serum levels of HCY, folate and vitamin B(12) in patients with Paget's disease of bone (PDB) and the effect of zoledronic acid (ZOL) on their serum levels. Nine consecutive patients with polyostotic PDB (median age 66 years) received a single 5-mg ZOL infusion. Blood samples for HCY, folate, vitamin B(12), 25-hydroxyvitamin D (25-OH-D), total serum alkaline phosphatase (TSAP), bone-specific serum alkaline phosphatase (BSAP) and C-terminal cross-linking telopeptide of type I collagen (CTX) were obtained at baseline and 3, 6 and 12 months after ZOL infusion. Twelve age-, gender- and BMI-matched healthy individuals were recruited for the control group at baseline assessment. Patients with PDB had significantly higher serum HCY (p = 0.028), folate (p < 0.001) and bone markers [TSAP (p < 0.001), BSAP (p < 0.001) and CTX (p < 0.001)] compared with the control group at baseline. In the pagetic group, serum HCY significantly decreased 3 months after ZOL infusion and remained essentially unchanged up to the end of the study (p = 0.005). Serum vitamin B(12) and folate remained unaffected throughout the study. Our data suggest that serum HCY levels are increased in patients with PDB. A single ZOL infusion results in a decrease in HCY levels that might represent another mechanism for the reduction of the activity of PDB achieved by ZOL.

BACKGROUND AND PURPOSE We present the clinical, electrophysiological, and nerve ultrasound findings in cases of persistent carpal tunnel syndrome (PCTS). METHODS Eighteen PCTS patients underwent evaluation with the Boston Carpal Tunnel Syndrome Questionnaire (BCTSQ), electrophysiology, and nerve ultrasound with a mean of 3.5 months (SD ± 1.4) after open surgery. RESULTS PCTS patients showed a mean symptom severity scale score of 3.1 (SD ± 1.1) and functional severity scale score of 3.2 (SD ± 0.9) in BCTSQ. Nerve conduction studies revealed axonal affection of the median nerve in 13/18 patients, ultrasound showed disturbed echogenicity in all patients, a pathological wrist to forearm ratio in 16/18 patients, and cross‐sectional area enlargement of the median nerve at the distal wrist crease in 12/18 patients. Ultrasound documented scar tissue formation (in 12/18 patients), incomplete release of retinaculum flexorum (in 4/18 patients), and neuroma of the median nerve (in 2/18 patients) as PCTS cause. CONCLUSION Our data show significant functional disability, axonal nerve damage, and scar tissue formation as common PCTS causes.

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