Total or subtotal parathyroidectomy is considered the treatment of choice for multiple endocrine neoplasia type I (MEN-I)-associated primary hyperparathyroidism (HPT). However, persistent or recurrent HPT is frequently observed. The development of a rapid two-site immunoradiometric assay (IRMA) method for measuring intact parathormone (PTH) has provided a valuable tool for recognizing possible surgical failures. Our experience includes 16 MEN-I patients (10 females, 6 males) of mean age 35.5 years operated on between 1990 and 1996. Total parathyroidectomy (TPTX) with autotransplantation of parathyroid tissue was the standard treatment. Blood samples for PTH measurement were drawn at the induction of anesthesia (basal value), 10 and 20 minutes after the removal of each gland, and 60 minutes after TPTX. Rapid PTH measurement, which required only 15 minutes of incubation at 37 degrees C, showed a highly significant correlation (p < 0.0001) with the standard method. Circulating PTH levels exhibited a stepwise decrease during TPTX, reaching a mean value of 22.3% of the baseline 20 minutes after removal of the last gland. Two patients showed a prompt decrease of PTH after removal of the single enlarged gland, featuring the kinetics observed in the adenomas. One of these two patients was successfully treated with more conservative surgery. None of the patients showed persistence or recurrence of HPT. In our experience, intraoperative measurement of PTH seems to be a valuable adjunct in both the diagnosis of multiglandular involvement and the prediction of surgical treatment in patients with primary parathyroid hyperplasia.
Dual site antibody-base immunoassays are commonly used in clinical laboratories to quantify the CT serum concentrations as a specific and sensitive marker of medullary thyroid carcinoma (MTC). Heterophile antibodies can interfere with these assays, however, and cause erroneous results. In order to avoid this interference, immobilized and conjugated antibodies from two different animal species or immunoreactive antibody fragments, as well as the addition of non-immune globulins, are generally included among the assay reagents. We describe the case of a 73-year-old man affected by a multinodular goiter, who showed high basal CT plasma levels as measured by a monoclonal antibody based IRMA. The finding of negative results for the presence of MTC at fine needle aspiration (FNA) and the mild increase observed in plasma CT during a pentagastrin (Pg) stimulation test, suggested that the high CT levels might depend on a cross-reaction with heterophilic antibodies. In fact, after the addition of the heterophilic blocking tube (HBT) to each specimen, the CT levels markedly decreased by more than 80% (average decrease+/-SE= 87.6+/-2.668%). Such a decrease strongly suggests that in our case the routinely used F(ab')2 fragments were unable to eliminate all of the interference and that the elevated serum CT levels might have been caused by human heterophilic antibodies. In conclusion, these results indicate a novel cause of CT false positivity, suggesting that high serum CT levels, when combined with a slight increase during Pg stimulation, should be critically interpreted in view of the possible presence of heterophilic antibodies in the specimens.
Beta-endorphin (RIA method, previous chromatographic extraction) was evaluated in plasma of migraine sufferers in free periods and during attacks. Decreased levels of the endogenous opioid peptide were found in plasma sampled during the attacks but not in free periods. Even chronic headache sufferers exhibited significantly lowered levels of beta-endorphin, when compared with control subjects with a negative personal and family history of head pains. The mechanism of the hypoendorphinaemia is unknown: lowered levels of the neuropeptide, which controls nociception, vegetative functions and hedonia, could be important in a syndrome such as migraine, characterized by pain, dysautonomia and anhedonia. The impairment of monoaminergic synapses ("empty neuron" condition) constantly present in sufferers from serious headaches, could be due to the fact that opioid neuropeptides, because of a receptoral or metabolic impairment, poorly modulate the respective monoaminergic neurons, resulting in imbalance of synaptic neurotransmission.
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