Eye dosimetry and protective eyewear for interventional clinicians.

Doses to the eyes of interventional clinicians can exceed 20 mSv. Various protective devices can afford protection to the eyes with the final barrier being protective eyewear. The protection provided by lead glasses is difficult to quantify, and the majority of dosimeters are not designed to be worn under lead glasses. This study has measured dose reduction factors (DRFs) equal to the ratio of the dose with no protection, divided by that when lead glasses are worn. Glasses have been tested in X-ray fields using anthropomorphic phantoms to simulate the patient and clinician. DRFs for X-rays incident from the front vary from 5.2 to 7.6, while values for orientations reminiscent of clinical practice are between 1.4 and 5.2. Results suggest that a DRF of two is a conservative factor that could be applied to personal dosimeter measurements to account for the dose reduction provided by most types of lead glasses.

Assessment of eye and body dose for interventional radiologists, cardiologists, and other interventional staff.

A dose limit for the eye of 20 mSv, as proposed by the ICRP, could be exceeded by interventional clinicians. Data on eye dose levels for interventional radiologists and cardiologists provided by medical physicists from hospitals around the UK have been collated. The results indicate that most hospitals would require one or more interventional clinicians to be classified and several would have exceeded a 20 mSv limit. Dose data in the literature have been reviewed to derive factors that might be used to predict eye dose levels based on dose per procedure or kerma-area product workload. These could be used in prior risk assessments to establish monitoring practice. An alternative approach to personnel dose monitoring in radiology applications using a collar dosimeter worn outside the lead apron as the first dosimeter is proposed. The collar dosimeter would provide an assessment of eye dose in terms of Hp(3) and body dose in terms of Hp(10), which could be divided by ten to provide an assessment of effective dose. If Hp(3) exceeded 1 mSv per month, regular monitoring with a head dosimeter would be recommended, and if Hp(10) exceeded 2 mSv per month, then an under-apron dosimeter should also be worn.

A detailed evaluation of oral phosphate therapy in selected patients with primary hyperparathyroidism.

Recent studies have emphasized the pathophysiological importance of circulating 1,25-dihydroxyvitamin D ((1,25-(OH)2D] in the pathogenesis of hypercalciuria and renal stone formation in primary hyperparathyroidism. Reasoning that phosphate administration might be capable of reducing the plasma concentration of 1,25-(OH)2D in patients with a prominent 1,25-(OH)2D-mediated absorptive component to their disease, 10 carefully selected patients were treated with oral phosphate (1500 mg elemental phosphorus daily) for 1 yr. Phosphate treatment significantly reduced circulating 1,25-(OH)2D levels (84 to 56 pg/ml), the calciuric response to an oral calcium tolerance test (0.30 to 0.21 delta mg calcium/dl GF), and calcium excretion on an unrestricted calcium diet (438-269 mg/day), in essence reversing the absorptive pattern of abnormalities observed before treatment. This response, however, was accompanied by an increase in biochemical hyperparathyroidism, as assessed by circulating immunoreactive PTH and nephrogenous cAMP excretion. In patients with biochemical evidence of an increase in bone resorption before therapy, histomorphometric, radiographic, and biochemical data revealed a trend toward a reduction in bone turnover during phosphorus therapy, with an apparent maintenance of coupled bone resorption and bone formation. This trend, however, was of marginal statistical significance in the patient group as a whole. It is concluded 1) that phosphate therapy represents a viable medical alternative in selected patients with primary hyperparathyroidism, 2) that the net response in treated patients is multifaceted and complex, and 3) that the efficacy of phosphate therapy will ultimately depend upon its long term effects on skeletal homeostasis.