Biomedical subjects
Publications and source records attributed to J G Pascalis.
The law of December 20th 1988 provides for the protection of those people who lend themselves to clinical research, both patients and healthy subjects. The ex-expert clinicians are confronted with new drugs and protocols of experimentation enacted by industry. Grey areas still exist, authors try to limit them for want of being able to through light on them, today.
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Voluntary drug ingestion with benzodiazepine represent today the most frequent method of attempt of autolysis. One must note the difficulties the doctor may find in front such problems to judge the reliability of interviews made in such difficult conditions. Residual disturbances of superior functions, more precisely of vigilance during the period with follow the suicidal action must not be overlooked. Thanks to a clinical scale easily used the residual disturbances have been put in evidence on a sample of 20 subjects who had been admitted with this aim in view in a university ward specialized in psychiatric emergencies. The possibility of continuity within middle range care must allow an improvement of minimum care of such pathologies.
Lithium has proved to be a highly effective preventive measure in mood disorders and an increasing number of patients are receiving long-term lithium carbonate therapy. Among other biologically and clinically important effects of lithium, the possible induction of hyperparathyroidism was first suggested in 1973 by Garfinkel et al. About thirty other case reports have since been described, but they could simply have represented the coincidental occurrence of primary hyperparathyroidism and lithium carbonate treatment in the same patients. Eleven cross-sectional studies of calcium metabolism in patients treated with lithium carbonate have been reported. Evidence of a causal relationship of lithium to hyperparathyroidism can lead to a loss of effectiveness of lithium in controlling the affective symptoms. Interestingly, coexistence with hypothyroidism is not uncommon. Low serum phosphate, high serum chloride are also observed. Bone mineral content may decrease. In addition, several studies have shown that lithium treatment increases serum magnesium level. Unusual metabolic features are associated with hyperparathyroidism and long-term lithium treatment: low urinary calcium excretion, absence of nephrolithiasis, and normal urinary cyclic AMP excretion. Lithium inhibition of PTH sensitive adenylcyclase in the kidney would explain these features. In vitro studies suggested that lithium is a potent inhibitor of several hormone responsive adenylcyclase systems. It is possible that the tissue susceptibility to adenylcyclase inhibition in an individual may decide the nature of endocrine dysfunction seen during lithium treatment. Information about the time course with which abnormalities may develop is derived from longitudinal studies. Several months to several years are needed for lithium inducing primary hyperparathyroidism. In vitro studies provide strong evidence that lithium can induce a shift in the set-point for inhibition of PTH secretion by calcium and a direct stimulation of PTH secretion. The extent to which we can extrapolate these data to the clinical situation is discussed. In vivo data from Shen an Seely are compatible with these two mechanisms. These alterations should cause parathyroid hyperplasia. The possibility that a generalized parathyroid stimulus might lead to formation of a single adenima is not proved. Several recommendations regarding parathyroid function in patients receiving lithium have been suggested. Measurement of total calcium and serum proteins or of serum calcium ion values when available should be performed before therapy is begun. If elevated values are obtained, lithium treatment should be deferred and evaluation for hyperparathyroidism performed. Serum calcium should be monitored periodically during lithium treatment. Sustained hypercalcemia or true hyperparathyroidism require parathyroidectomy. If hypercalcemia is mild without complication and psychiatric symptoms well controlled, perhaps surgery should not be employed.
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By four patients hospitalized for a depressive recurrent the favorable element of clinic evolution was a lithotherapy then bring the effect very rapidly (three to seven days) grace using gluconate of lithium. The lithium being antidepressant, the absence of lithotherapy tentative in the course of major depressive status recurrent is a loss of chance for patients.
The definition of treatment-resistant depression is variously interpreted. There is no agreement of different authors on its meaning. The present vagueness of criteria for the diagnosis of a refractory depression contrasts with the many studies reporting potentiation of antidepressants by lithium. De Montigny in 1981, after early works by Zall and by Lingjaerde, initiated this approach that still remains poorly understood in terms of biochemical mechanisms. A review of the controlled studies shows that the delay of antidepressant action varies and the term "lithium potentiation" does not seem totally relevant. From a pharmacological point of view, several types of data suggest a synergic potentiation rather than a true potentiation. This effect applies to all classes of antidepressants and improves about 50% of patients who did not respond positively to an adequate treatment received during 4 to 6 weeks. Many questions remain unanswered particularly concerning the lithium levels, factors predicting a positive response and the strategy for the maintenance treatment. Studies are necessary in order to compare the relevance of this potentiation technique with the mere substitution by another antidepressant and to understand the biochemical mechanisms underlying the synergic effect.