ABSTRACT
The role of insufficient pyridoxine as an etiologic factor in the development of carpal tunnel syndrome (CTS) has been reported and has led to the empirical use of pyridoxine to treat CTS. Previous studies have not employed standardized electrodiagnostic criteria to objectively determine the presence of CTS or to rule out peripheral neuropathy (PN). The present study categorized subjects with symptoms suggestive of CTS into four groups by standardized electrodiagnostic criteria: (1) CTS, (2) PN, (3) CTS and PN, (4) normal. At least seven subjects were in each group. Erythrocyte glutamine oxaloacetic acid transaminase (EGOT) activity with and without in vitro enhancement with pyridoxal phosphate was used as a means of identifying subjects with and without pyridoxine metabolic abnormalities. A significant difference in pyridoxine metabolic activity (PMA) was found between groups by both chi square (p less than 0.05) and analysis of variance (p less than 0.05). Further evaluation showed that this difference was associated with the presence or absence of PN (p less than 0.05). There was no difference in PMA when groups were separated on the basis of CTS. Results showed that a PMA abnormality was a factor highly correlated with the presence of PN but not CTS. This finding suggested that the positive response reported previously in subjects with CTS taking supplemental pyridoxine may actually be related to an unrecognized PN, which was compounding the symptomatology.
Subject(s)
Carpal Tunnel Syndrome/blood , Peripheral Nervous System Diseases/blood , Pyridoxine/blood , Aspartate Aminotransferases/blood , Carpal Tunnel Syndrome/diagnosis , Electromyography , Erythrocytes/enzymology , Female , Humans , In Vitro Techniques , Male , Middle Aged , Neurologic Examination , Peripheral Nervous System Diseases/diagnosis , Pyridoxal Phosphate , Skin Temperature , Vitamin B 6 Deficiency/blood , Vitamin B 6 Deficiency/diagnosisABSTRACT
Prolonged immobilization may result in hypercalcemia, hypercalciuria, and osteoporosis. Although bone resorption is central to this syndrome, the mechanism of resorption is uncertain. In particular, the role of systemic calcium-regulating hormones remains unclear. In 14 immobilized subjects we measured fasting calcium excretion, 24-hour urinary calcium excretion during restricted calcium intake, the renal phosphorus threshold, plasma 1,25-dihydroxyvitamin D, nephrogenous cyclic AMP, and immunoreactive parathyroid hormone. Mean serum calcium levels were normal, but fasting and 24-hour calcium excretion were markedly elevated (0.28 mg per deciliter of glomerular filtrate and 314 mg per 24 hours, respectively). The mean levels of serum phosphorus (4.8 mg per deciliter) and the renal phosphorus threshold (4.3 mg per deciliter) were elevated. Mean plasma 1,25-dihydroxyvitamin D was strikingly reduced (9.9 pg per milliliter), as were nephrogenous cyclic (0.64 nmol per deciliter of glomerular filtrate) and immunoreactive parathyroid hormone in both assays. These findings indicate that the parathyroid--1,25-dihydroxyvitamin D axis is suppressed in patients with immobilization-induced hypercalciuria, as would be predicted by a model of resorptive hypercalciuria.
