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Toxemia of pregnancy in Jerusalem. II. The role of diet.

A dietary history was obtained from 180 patients with preeclampsia and eclampsia, representing 92% of all cases occurring in the pregnant population of West Jerusalem over a defined period. The intake of nutrients and 78 items of diet was compared for each patient and two healthy control subjects who were matched for country of origin, parity, month of delivery, age, year of immigration and years of schooling. All diagnoses were made by the same research team and dietary histories were elicited by one of two experienced dieticians. Comparisons between the 180 patients and their respective control pairs showed a significantly reduced intake of calories, proteins and fats and an increase in consumption of sugar and sweets by the patients. The food items involved, including cheese, eggs, olives and nuts, did not appear consistently, however, in population subgroups defined by age, period of immigration and country of origin. Sixty-six patients reported not having changed their diets during pregnancy and these showed no significant differences in consumption of any of the foods or nutrients at the 1% level, when compared with their matched control subjects. All differences observed were confined to the 114 patients who, for one reason or another, had changed their diets. It is concluded that the differences in diet between patients and control subjects are the result, and not the cause, of the toxemia of pregnancy. Supporting and contradictory evidence in the literature is analyzed, and possible sources of the discrepancies are pointed out.

Diet↗

[D-dimer in different stages of pregnancy toxemia. A pilot study].

We assayed D-Dimer levels in the different stages of preeclampsia. This test appears to be the most reliable for the probability of abnormal status in patients with disseminated intravascular coagulation. Data were analyzed by dividing all cases in four groups: a.-Healthy non pregnan women (10 cases) 550 ng/ml mean levels. B.-Normal pregnant women (8 cases) 875 ng/ml mean levels. C.-Mild and severe preeclamptic patients (8 cases) 1625 ng/ml mean levels, and D.-Eclampsia and HELLP patients (6 cases) 3000 ng/ml. This results were statistical significant at level p < 0.05. It is believed that pregnancy is associated with "hypercoagulability" that it is enhance in toxemia cases. It is necessary to perform more studies with quantitative elisa techniques of D-Dimer, more cases and other markers of dic and endothelial cell injury.

Adolescent↗

Pre-eclamptic toxemia: potential new therapy based on animal studies.

OBJECTIVE: Pre-eclamptic toxemia (PET) affects 4 to 8% of human pregnancies. Presently, reliable specific therapies to treat this disorder are not available. This study was designed to develop a new therapeutic approach in the management of PET using an animal model. DESIGN: Pregnant rats (5/group) infused with 50 mg L-NAME daily via osmotic mini pumps from day 17 of gestation developed a PET-like syndrome. Systolic blood pressure (BP) was monitored daily during pregnancy and up to 7 days postpartum by the tail cuff method. Pup weight and mortality were recorded immediately after delivery. We examined the effect of CGRP to ameliorate L-NAME-induced hypertension during pregnancy, and the efficacy of CGRP and progesterone in combination to inhibit L-NAME-induced hypertension during the post-partum period. RESULTS: Blood pressure in L-NAME-treated rats was significantly elevated (P < 0.01) throughout pregnancy (141 +/- 3 to 166 +/- 10 mm Hg). CGRP 10 micrograms/day did not cause hypotension, the values being similar to controls which received only saline. On the other hand, CGRP infusion inhibited L-NAME-induced hypertension to normotensive levels (116 +/- 3 to 122 +/- 2) during pregnancy (up to day 22 of gestation), but not during postpartum period (137 +/- 8 to 148 +/- 2). During the post-partum period, neither progesterone nor CGRP by itself was effective in lowering L-NAME-induced hypertension. The combination of CGRP with progesterone decreased BP to control levels in the post-partum period, and also significantly improved foetal mortality and growth (P < 0.05). CONCLUSIONS: CGRP inhibited L-NAME-induced hypertension during pregnancy and not during postpartum period. The same phenomenon was evident in the presence of adequate levels of progesterone in the post-partum period. We believe that CGRP regulates vascular adaptations during pregnancy and these effects may be progesterone-dependent. This combination treatment of CGRP plus progesterone may be a promising therapy in the management of PET in humans.

Animals↗