Gene/Protein Disease Symptom Drug Enzyme Compound
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Vascular spasm has been considered to be an important component of the eclamptic state. If this abnormal vascular reactivity affects the coronary arteries in eclampsia, one might expect to find areas of myocardial contraction band necrosis, a lesion secondary to coronary reflow after periods of no flow. We reviewed the cardiac findings in the 34 patients with fatal eclampsia (hypertension, edema, proteinuria, and convulsions without evident cause) autopsied at The Johns Hopkins Hospital since 1899, and compared each with the next pregnant or puerperal nontoxemic autopsied patient. The eclamptic patients were 15-45 years old (average 27 years). Convulsions began antepartum in 21 patients, intrapartum in eight, and postpartum in five. The hearts weighed 200-407 g (average 312 g). One heart had rheumatic valvular disease and one had myocarditis. Histologic study of heart sections showed the presence of contraction band necrosis in 12 cases (35%). The control cases included two patients with rheumatic valvular disease, two with endocarditis, two with myocarditis, two with pericarditis, and one with leukemic infiltration. Only one control patient (3%) had contraction band necrosis (p less than 0.001). The frequent occurrence of myocardial contraction band necrosis suggests that coronary artery spasm may be common in patients who die with eclampsia.
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PMID:Morphologic evidence for coronary artery spasm in eclampsia. 719 18

Sixty-seven cases of eclampsia were managed from 1977 to 1980, for an incidence of 1 in 310 deliveries. Eighty-four percent of patients were nulliparous and 82% had received some prenatal care. Prior to convulsion, 14 patients (21%) had a diastolic blood pressure below 90 mmHg, 39% had no edema, and 21% had no proteinuria. Thirty-seven patients (55%) had their first convulsion in the hospital. Eight patients had convulsions while receiving magnesium sulfate therapy. Convulsions occurred post partum in 25 patients (37%). In 11 patients the onset of eclampsia occurrred 3 to 11 days after delivery. The total perinatal mortality was 8.6% for all cases of eclampsia. Excluding postpartum cases, perinatal mortality was 13.3%, but was only 5% for those fetuses alive on admission to the perinatal center. Abruptio placentae was present in 9 cases and accounted for 4 of the 6 perinatal deaths. The high incidence of eclampsia at the authors' center has not decreased over the past 20 years, but maternal mortality has been reduced from 2.1 to 0%. It was disturbing to find that management error played some role in the development of eclampsia in 50% of the cases. Significant errors--including ineffective magnesium sulfate therapy, failure to treat adequately prior to transport, and lack of communication with a perinatal center--are discussed.
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PMID:Eclampsia. I. Observations from 67 recent cases. 730 Dec 37

A 42-yr-old woman with hypertension and renal involvement due to systemic lupus erythematosus (SLE) developed unilateral headache followed by the sudden onset of confusion and a grand mal convulsion. Cerebral computed tomography was normal. A magnetic resonance imaging angiogram revealed cerebral venous thrombosis and a venous infarct. Nephrotic syndrome had resulted in an acquired protein S deficiency. A review of previous cases suggests that either renal disease with proteinuria or features of the antiphospholipid syndrome are prerequisites for the development of cerebral venous thrombosis in SLE. Low free-protein S levels may be an additional risk factor. Furthermore it is likely that this condition is underdiagnosed.
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PMID:Cerebral venous thrombosis and acquired protein S deficiency: an uncommon cause of headache in systemic lupus erythematosus. 763 1

The maternal mortality rate associated with eclampsia ranges from 100 to 6000 per 100,000, and the perinatal mortality rate ranges from 150 to 400 per 1000. Both eclampsia and its preceding condition, pregnancy-induced hypertension, occur in varying degrees in different parts of India. The warning signs of imminent eclampsia are 1) systolic blood pressure of 160 mmHg or more on two occasions six hours apart when the patient is on bed rest; 2) proteinuria of 5 g or more in 24 hours or 3 + or more by semiquantitative assay; 3) oliguria or anuria; 4) cerebral or visual disturbances; 5) pulmonary edema or cyanosis; and 6) epigastric/right hypochondriac pain, impaired liver function, and thrombocytopenia and coagulation disorders. Eclampsia is classified as the acute fulminating type, which can occur without warning, and the insidious type. Most cases (61%) show onset of eclampsia during the prenatal period. Treatment of eclampsia involves 1) control of convulsions (through an injection of magnesium sulphate or diazepam or the intravenous administration of phenytoin); 2) correction of hypoxia and acidosis; 3) a gradual lowering of blood pressure with hydralazine hydrochloride, nifedipine, atenolol, labetalol, oxprenolol, or metoprolol); and 4) steps to effect delivery. Diagnosis of HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) requires a complete blood count, blood film for platelet count and red blood cell fragmentation, and a coagulation screen for diagnosis of disseminated intravascular coagulation. Efforts to induce delivery in cases of prenatal eclampsia can take place 12-24 hours after convulsions have stopped. There is no reason to prolong pregnancy in the interests of the fetus, and in some cases Cesarean section may be required. Adequate prenatal care should allow the identification of almost every potential case of eclampsia and allow the prompt treatment of pre-eclampsia or termination of pregnancy when necessary. Medical staff must receive proper training to diagnose pre-eclampsia and treat the condition.
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PMID:Eclampsia. 765 39

We studied the impact of blood coagulation and fibrinolysis on the clinical features of eclamptic patients (n = 20) in Bangladesh. The variables used were edema, proteinuria, blood pressure, number of convulsions, level of consciousness at the time of admission, thrombin antithrombin complexes (TAT), antithrombin (AT) III (%) activity and antigen, D dimer fibrin degradation product and alpha 2-plasmin inhibitor-plasmin complex (PIC) in plasma. Canonical correlation analysis was made to obtain clinical index, eclampsia index and two coagulation indices. On admission, the mean values of coagulation parameters were AT III activity: 83.2% (range 57-108), TAT complex: 47.6 ng/ml (range 11.5-60), D dimer: 1,693 ng/ml (range 417-8,276) and PIC 1.4 mg/ml (range 0.4-3.3). We found a significant correlation between the eclampsia index and clinical index (r = 0.601; p = 0.01). Gestosis index, clinical index, and eclampsia index have also a strong correlation with the coagulation index (r = 0.695, p < 0.005; r = 0.871, p < 0.0001 and r = 0.805, p < 0.0001, respectively). Coagulation and fibrinolysis were markedly activated in eclampsia. The correlation between the clinical status and coagulation status in this study suggested a close relation between the coagulation and the development and progression of the disease.
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PMID:Blood coagulation and fibrinolysis in eclamptic patients and their correlation with the clinical signs. 777 98

The rate of progression of renal failure was analyzed in 19 patients with biopsy-proven chronic primary glomerular diseases, by the slope (regression coefficient) of the linear regression of reciprocal serum creatinine on time. The relative importance of proteinuria, sex, underlying disease and components of arterial pressure (systolic, diastolic and mean) was tested using stepwise multiple linear regression, the dependent variable being the slope of progression. We found that the only variable significantly related with slopes of progression was arterial pressure. Hypertension was found in 14 of the 19 patients. There was a significant linear relationship (p < 0.05) between mean arterial pressure and slopes of progression. Notwithstanding, the best fit to the data follows a quadratic function (p < 0.001 for mean arterial pressure), which corresponds to a negative parabolic curve. Therefore, either low or high values of mean arterial pressure were associated with faster mean progression rates. Thus, an accurate approach of this relationship fits a nonlinear regression model.
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PMID:Progression of renal failure in chronic primary glomerular diseases. 799 Oct 38

In an attempt to identify causes of perinatal mortality and thence devise preventative strategies on the island of Jamaica, a study was made of the 1847 singleton perinatal deaths occurring over the 12-month period between 1 September 1986 and 31 August 1987. Complications of the pregnancy were elicited by questioning the mother as well abstracting data from the antenatal and clinical obstetric records. The deaths were classified using the Wigglesworth categorisation and the three largest groups were chosen for special study: antepartum fetal deaths, deaths of live birth from immaturity and deaths from intrapartum asphyxia. The medical features of the pregnancies were compared with data similarly obtained from 9919 women delivering singletons in the 2 months of September and October 1986 and who survived the first week of life. Unadjusted statistically significant associations were found with maternal syphilis, vaginal infection or discharge, bleeding in the first two trimesters, bleeding in the third trimester, lowest haemoglobin, highest diastolic and first diastolic blood pressures, highest level of proteinuria, diabetes and antenatal eclampsia. Logistic regression taking account of social, environmental and health behaviour variables showed the following significant relationships. Antepartum fetal death was associated with adjusted odds ratio (AOR) for syphilis 2.88 [95% confidence interval (CI): 1.91, 4.32], bleeding in third trimester 3.86 [2.73, 5.44], highest diastolic blood pressure (P < 0.0001), highest level of proteinuria (P < 0.0001), lowest Hb (P < 0.0001) and antenatal eclamptic fits AOR 4.62 [1.47, 14.50]. Deaths from immaturity were independently associated with bleeding < 28 weeks AOR 3.50 [2.39, 5.13], bleeding 28 + weeks AOR 1.93 [1.16, 3.22], highest diastolic blood pressure (P < 0.01) and highest level of proteinuria (P < 0.0001). Infection featured in deaths associated with intrapartum asphyxia, with syphilis AOR 2.17 [1.44, 3.26] and vaginal infection/discharge (P < 0.01) independently associated; other strong associations were bleeding < 28 weeks AOR 2.10 [1.57, 2.81], bleeding 28 + weeks AOR 2.32 [1.62, 3.33], highest diastolic blood pressure (P < 0.0001), first diastolic blood pressure (P < 0.0001) and antenatal eclampsia AOR 6.70 [2.63, 17.13]. For all perinatal deaths combined, independent features were syphilis AOR 2.06 [1.49, 2.85], vaginal infection/discharge (P < 0.001), bleeding < 28 weeks AOR 2.01 [1.60, 2.53], bleeding 28 + weeks AOR 2.65 [2.02, 3.48], highest diastolic blood pressure (P < 0.0001), first diastolic blood pressure (P < 0.0001), proteinuria (P < 0.0001) and antenatal eclampsia AOR 4.22 [1.76, 10.14]. The results help identify areas for monitoring and identifying pregnancies at highest risk.
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PMID:Medical conditions present during pregnancy and risk of perinatal death in Jamaica. 807 3

This review on hypertension in pregnancy focuses mainly on the pathophysiology and prevention of pregnancy induced hypertension which, when associated with proteinuria, is usually called preeclampsia. Rather than a genuine hypertensive disease, preeclampsia is mainly a systemic endothelial disease causing activation of platelets and diffuse ischemic disorders whose most obvious clinical manifestations involve the kidney (hence the proteinuria, edema and hyperuricemia), the liver (hence the hemolytic elevated liver enzymes and low platelets, or HELLP syndrome), and the brain (hence eclamptic convulsions). Hypertension is explained by increased vascular reactivity rather than by an imbalance between vasoconstrictive and vasodilating circulating hormones. This increased reactivity is due to endothelial dysfunction with imbalance between prostacyclin and thromboxane A2 and possibly dysfunction of NO and endothelin synthesis. The aggressive substances for endothelium are thought to be of placentar origin and the cause of their release is explained by placentar ischemia related to a defect of trophoblastic invasion of the spiral arteries. The etiology of this latter defect is unknown but involves immunologic mechanisms with genetic predisposition. The only effective treatment for PIH is extraction of the baby with the whole placenta. The decision for extraction is often a very delicate obstetric problem. Antihypertensive drugs are mainly indicated in severe hypertension (> 160-100 mm Hg), with the aim of preventing cerebral hemorrhage in the mother, but have not been shown to improve fetal morbidity or mortality. Eclamptic seizures can be prevented and treated more effectively with magnesium sulfate than with diazepam or phenytoin. Prevention of preeclampsia remains the main challenge. Whereas antihypertensive drugs are ineffective, calcium supplementation and low dose aspirin have proven effective but mainly in selected populations with a relatively high incidence of preeclampsia (> 8-10%). In multiparas the selection of such a high risk population is relatively easy when at least 2 (or 1?) previous pregnancies were complicated with early preeclampsia and/or intrauterine growth retardation. In nulliparas the selection of the high-risk population is still a subject of research. The 2 most promising criteria are abnormal Doppler velocimetry of the uterine arteries at around 20 weeks of amenorrhea, and abnormally high plasma levels of beta HCG at 17 weeks of amenorrhea.
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PMID:[Hypertension and pregnancy. Diagnosis, physiopathology and treatment]. 853 76

Diabetes mellitus (or type 1) is a long-lasting disease (even twenty years or more) which causes kidney disease and, in the event of pregnancy, it can make differential diagnostic difficult even fort the most expert clinician. Metabolic changes caused by this type of diabetes (e.g., hypoglycemia, hyperglycemia, ketoacidosis) and their difficult compensation can often lead to the onset of eclampsia or convulsion. The diagnostic suspicion of diabetes is supported by the finding of proteinuria, edema and hypertension that are strictly correlated with the evolution of diabetic disease and sometimes exist prior to pregnancy. This cas report focuses on the diagnostic importance of clotting tests, especially in clarifying diagnostic doubts.
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PMID:[Diabetic nephropathy and pregnancy]. 854 41

A 50-year-old Japanese female with a long history of Raynaud's phenomenon presented with progressive dyspnea due to pulmonary hypertension. The diagnosis of systemic lupus erythematosus was confirmed by proteinuria, lymphocytopenia, bilateral pleurisy, and a seizure of convulsion which was consistent with neurological manifestations of systemic lupus erythematosus, whereas the antinuclear antibody showed a low titer. Despite improvement in the activity of systemic lupus erythematosus, steroid treatment did not alter the progression of pulmonary hypertension, which increased in severity, eventually resulting in her death. We believe pulmonary hypertension to be an unusual but critical complication of systemic lupus erythematosus.
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PMID:Systemic lupus erythematosus with pulmonary hypertension. 865 23


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