After 1 mg DST, 25 major depressive patients (DSM-III) received at random either a specific inhibitor of noradrenaline reuptake (Maprotiline) or an inhibitor of serotonin reuptake (Indalpine or Citalopram). After at least 3 weeks of treatment, no difference was found in treatment response between suppressors and non suppressors. This study is unable to confirm the usefulness of the DST in selection of treatment according to its central activity on serotonin or noradrenaline-reuptake.

Two lithium intoxication cases due to an association with acetazolamide and niflumic acid are reported. They confirm the necessity of plasma lithium monitoring when a new drug is added.

For the last few years, many clinical investigators have tried to prove that the lithium intraglobular determination is to be preferred to plasma lithium determination for monitoring lithium treatment.

Different Li, Na and K transport pathways were assessed in erythrocytes from manic-depressive patients. No alteration in the Li-Na countertransport, Na,K cotransport or passive permeabilities was observed in either unipolar or bipolar manic-depressive patients. In addition, acute or chronic lithium treatment did not alter the maximal velocity of either the Li-Na countertransport or the Na,K cotransport. A two-fold reduction of the ouabain-sensitive Na efflux was observed among manic-depressive patients without alteration in the affinity of the Na pump for internal Na.

One night sleep deprivation in 10 healthy volunteers was performed: none of them presented an abnormal dexamethasone suppression test (DST) during the following afternoon. In this experimentation, a short deprivation of sleep does not alter DST. Etiopathogenic hypothesis of DST abnormalities (and other factors) have been discussed.

From the plasma and red cell kinetics of lithium in 43 patients having received lithium therapy for at least 15 days, the authors try to establish a correlation between intolerance and a variety of parameters examined. Statistical analysis reveals that: intra-erythrocytic concentration is a more reliable biological index than the lithium level; it can be modified by associated drug therapy; measuring the erythroplasmic ratio at different times of the day shows important variation within individuals. This type of kinetic study can identify biologically the 2 sub-groups distinguished by clinical examination: tolerant subjects (those on lithium therapy without any neurological signs) and poorly tolerant subjects.

THe correlation between red cell lithium concentration and signs of neurotoxicity have been reported in the literature by a great majority of authors. A deficiency in the lithium-sodium counter-transport mechanism may be responsible. Measurement of blood lithium levels only is not always sufficient to identify in the laboratory patients showing signs of intolerance. The three cases reported here indicate the limitations of the measurement of plasma lithium levels and the perfect correlation between neurological signs and erythrocyte levels. In vitro studies of transmembrane ion exchanges should make it possible to undertake an investigation before starting treatment in order to identify the risks of cellular toxicity.