Intra-operative testing for parathyroid hormone: the Central Laboratory option.

BACKGROUND: Intra-operative PTH testing in the operating theatre has proven to be an accurate way to verify the removal of all pathological parathyroid tissue in primary hyperparathyroidism. Its limitation is the high cost. An alternative, more cost-effective procedure is proposed: intra-operative PTH dosage at the Central Laboratory. PATIENTS AND METHODS: Fifty-four patients underwent parathyroidectomy with intraoperative dosage of PTH at the Central Laboratory. Three blood samples were taken from each patient: just after the induction of anesthesia, 5 and 10 min after parathyroidectomy. The samples were sent to the Central Laboratory and analysed simultaneously. The results were phoned back to the theatre. The procedure was considered effective when PTH drop was >/=50% from basal value, 10 min after parathyroidectomy. RESULTS: 98.1% of patients proved recovered (average follow- up 31.1 months). The procedure had 3 false negatives, 1 false positive, with sensitivity, specificity, accuracy, positive predictive value and negative predictive value of 94.0%, 75.0%, 92.6%, 97.9%, and 50.0%, respectively. DISCUSSION AND CONCLUSION: The main disadvantage of the presented procedure is the long waiting time. Nevertheless this time is the same as that required for results from intra-operative histological examination, the only alternative to determine surgery effectiveness in centres where portable instrumentation for intra-operative PTH dosage in the operating theatre is not available. The advantage of intra-operative PTH at the Central Laboratory is the very low cost. If results in terms of sensitivity, specificity, accuracy, and cost are taken into consideration, intra-operative dosage of PTH at the Central Laboratory may be deemed a viable alternative to the operating theatre.

Peripheral edema due to increased vascular permeability: a clinical appraisal.

The release of vasoactive substances produces reversible changes of endothelial permeability with consequent edematous syndromes. We present 899 patients referred to our clinic for "non-hydrostatic non-hyponcotic" recurrent edema problems. Personal and family histories were recorded and a complete physical examination was carried out for each patient. In chronic situations laboratory tests [blood cell count, cryoglobulins, thyroid hormones, complement components (C3, C4, C1 inhibitor), total IgE, skin testing] were performed. Four subgroups of angioedema are identified for relevant clinical and etiopathogenetic differences. Seventy-three percent of patients had an urticaria-angioedema syndrome responding to antihistamine and/or corticosteroid treatment (histamine-dependent angioedema). Twenty-three percent had an angioedema related to a deficiency in C1 esterase inhibitor (complement-dependent angioedema). In a minority of patients, angioedema was due to the pharmacological effect of a drug (pharmacological angioedema) or was of a totally unknown origin (idiopathic angioedema). A generalized increase in vascular permeability was reported in 3 patients (systemic capillary leak syndrome). A brief survey of the literature is given with the review of our patients.