[Preeclampsia: physiopathology and prospects for early detection]. / La prééclampsie: physiopathologie et perspectives de dépistage précoce.

Preeclampsia is a complication of pregnancy characterized by hypertension, edema and proteinuria, beginning after 20 weeks of gestation. Six percent of the pregnant women in North America develop this disease, which is associated with increased morbidity and mortality for the mother and her baby. The physiopathology remains uncertain despite many research efforts. Actual hypotheses seek to explain the vasospasm that characterizes the disease. Among the many factors influencing vascular reactivity and possibly implicated are: the renin-angiotensin system, prostaglandins, progesterone and its metabolites, calcium, magnesium, digoxin-like immunoreactive substance(s), auricular natriuretic factor, substances secreted by platelets and leukotrienes. Prevention of the disease is limited by the absence of a biological or clinical marker with good sensitivity and appropriate specificity. Many biochemical or hematological parameters have been reported: uric acid, calcium, magnesium, proteinuria, blood iron, hematocrit, platelet count, antithrombin III, estrogen and progesterone. The combination of several tests could be superior to the use of each test individually, providing a better sensitivity and improving the positive predictive value. With early detection, new therapies for the prevention of the disease could be experimented on the higher risk women before the apparition of clinical symptoms or signs. Furthermore, those tests could be used in the study of the pathophysiology and in the choice of the best therapy.

On the pathogenesis and therapy of dementia of the Alzheimer type: some neuropathological, biochemical, genetic and pharmacotherapeutic considerations.

The extensive literature on dementia of Alzheimer type (DAT) testifies to the enormous progress achieved in the clinical and biochemical delineation of this disease. Newly developed laboratory and imaging techniques are also being applied to the diagnosis of DAT. Nevertheless, unequivoval diagnosis still relies primarily on morphological data from biopsy or autopsy. An overview is presented of major morphological changes occurring at different levels of organization in the central nervous system (CNS) in DAT. Currently formulated etiopathogenic hypotheses of DAT are reviewed and discussed in the context of morphological alterations. Some of the recombinant DNA methods, that are currently available for gene analysis, are described. Some approaches for studying Alzheimer specific genes using the above methods have been suggested. Finally, a critical overview of the current pharmacotherapeutic armamentarium used in DAT and senile dementia is presented. The efficacy, side effects, and the main mechanisms of action of the two categories of drug therapy -supposed etiopathogenic and symptomatic- are presented.