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Thermal trauma impaired the functional state of liver microsomes. Impairment of the monooxygenase system was due to activation of lipid peroxidation during the early period of burns toxemia.
Curative plasmapheresis was used in 10 critically burned patients at the stage of acute burn toxemia with the delirious syndrome with the unfavourable prognosis. Good immediate results were obtained in all the patients: psychic disorders were arrested by the end of the procedure. Clinico-laboratory data have shown the curative plasmapheresis to be an effective detoxicating method resulting in the elimination of various toxic substances from the organism.
Accumulation of biologically active peptides, distinctly affecting the respiration and enzymatic activity of mitochondria, may be responsible for deterioration of oxidative phosphorylation occurring in mitochondria within the early period of burn toxemia.
A 31-year-old captive male African elephant (Loxodonta africana) of 5,000-kg body weight died suddenly in ventral recumbency. Lesions seen at necropsy were bilateral purulent pulpitis and periodontitis of both tusks, serous atrophy of coronary groove fat, Grammocephalus cholangitis, myocardial and skeletal lipofuscinosis, and scattered segmental necrosis in the pectoral muscles. Nonhemolytic streptococci, Corynebacterium sp, Peptostreptococcus anaerobius, Fusobacterium nucleatum, and Bacteroides sp, were recovered from the exudate around one or both tusks. We postulated that the elephant died of hypoxia from prolonged ventral recumbency because of weakness and inability to rise secondary to toxemia from bilateral pulpitis and periodontitis.
A new generation of synthetic carbon adsorbents was used in production of deliganded human serum albumin preparation. Thermal effects of officinal and deliganded albumin interaction with specific chemical markers were analyzed by flow microcalorimetry. The results demonstrated a 2.5-fold increase of the complexing ability for the deliganded one. The detoxifying potentials of deliganded albumin were studied in comparison with officinal preparation in rats with burn toxemia after IIIB-IV degree thermal injury and in model experiments with blood serum of patients after severe thermal burn. The transfusion of a 5% officinal albumin solution in rats 1 h after burn trauma resulted in a decrease of serum and liver cytosols cytotoxicity 2.2 and 2.4 times, respectively, in comparison with those of burned rats. After deliganded albumin transfusion the cytotoxic activity of blood serum dropped 8.5 times and that of the liver cytosols 18.5 times. The incubation of blood serum of injured patients with equal amounts of a 5% solutions of officinal or deliganded albumin resulted in a fall of the cytotoxicity level and the growth of binding ability. A comparative analysis of detoxifying potentials of albumin preparations has unambiguously demonstrated deliganded albumin advantages.
Ocular fluorophotometry was performed in 24 patients with hypertension due to toxemia of pregnancy and in ten normal subjects. Patients showing features of accelerated hypertension in the fundus (eg, hemorrhage, cotton-wool spots, and disc edema) were excluded from the study. Fluorescein concentrations in the aqueous and posterior vitreous increased significantly in toxemic patients compared with those in normal subjects; the blood-aqueous barrier was disrupted earlier than the blood-retinal barrier. Nevertheless, these barriers were only disrupted when the arterial diameter was altered. Ocular fluorometric abnormalities disappeared after delivery in all but two cases.
The efficacy of three biochemical methods for the detection of fetal distress was assessed in a prospective study of 224 singleton pregnancies complicated by toxemia. Fetal distress was diagnosed in 65 cases (29 per cent). Abnormally low urinary estriol (E3) excretion pointed out 63 per cent, low serum levels of human placental lactogen (HPL) 27 per cent, and elevated maternal serum alpha fetoprotein (AFP) 10 per cent of distressed fetuses. The efficacy of each test increased with the severity of maternal disease. The frequencies of false pathologic levels were: E3 19 per cent, HPL 0 per cent, and AFP 1 per cent of the cases with a normal fetal outcome. Although E3 was by far the most effective marker, abnormal levels of HPL and AFP provided supportive evidence for fetal distress by pointing out those cases in which E3 reading was not a false positive.
The expanded toxemia syndrome or gestosis refers to polysymptomatic diseases that are associated with pregnancy. This report discusses those cases without initial hypertension or proteinuria that were "cured" by delivery and were associated with maternal and fetal morbidity (usually intrauterine growth retardation). A list of suggested tests is presented to document gestosis in pregnant women with medical illnesses. Unlike preeclampsia, gestosis may occur at almost any time in pregnancy.
The incidence of preeclamptic toxemia (PET) was investigated in 72 anovulatory, oligomenorrheic and previously nulliparous women who conceived after an induction of ovulation. One-thousand consecutive spontaneous pregnancies and 1,000 pregnancies of primiparae were used as control groups. The anovulatory group consisted of 33 consecutive well-documented cases of polycystic ovarian disease (PCO) and 39 anovulatory patients in whom PCO was excluded (A-NPCO). The results indicate that pregnancies after induction of ovulation are accompanied with a higher incidence of PET. The rate of this disorder was significantly higher in PCO groups than in A-NPCO women (28.5 vs. 4%), when calculated per number of all pregnancies. The difference between the incidence of PET in PCO, A-NPCO, control primiparae and normal control patients was even more pronounced when calculated on the basis of the number of patients (54.5, 12.5, 11 and 2.5%, respectively). Overproduction of steroid hormones, especially androgens, was suggested as the main factor for the appearance of PET in PCO patients.
T-2 toxin is a trichothecene mycotoxin which is a member of a family of closely related sesquiterpenoids. It was recently shown that T-2 toxemia is associated with elevated plasma levels of eicosanoids. To study further the effect of T-2 on the cyclooxygenase pathway of arachidonate we examined the release of PGE2, TXB2 and 6-keto-FGF1 alpha from brain tissue exposed to T-2 toxin in vivo or in vitro. Administration of T-2 toxin (0.75 or 2 mg/kg) to conscious rats caused a transient increase in the rate of the release of 6-keto-PGF1 alpha and TXB2 from brain slices taken from the cortex (C); no effect was found in the hypothalamus (HT) or the nucleus tractus solitarius (NTS) region of the medulla oblogata. PGE2 showed time and dose related increments (over 5 folds) in both the C and HT but not in the NTS. Incubation of cortical or hypothalamic slices in oxygenated Krebs buffer with a wide range of T-2 toxin concentrations (10(-9)-10(-3) M) demonstrated a complex response: stimulation of PGE2 and TXB2 release from C slices at 10(-7) M (greater than 40%, p less than 0.01 and 20%, p less than 0.05, respectively) and inhibition at high concentrations (greater than 10(-4) M) of all PGs studied. Hypothalamic slices showed decrease in all PGs released by very low (10(-9)-10(-8)) or very high (10(-4) M) concentrations of T-2. These studies are consistent with the possibility that the arachidonate cascade in the central nervous system might have a role in the pathophysiology of trichothecene mycotoxicosis.
Pregnancy toxemia of ewes and does appears to occur when the animal cannot meet the glucose demands of the fetal-placental unit and hypoglycemia develops. There is individual variation in susceptibility, and there may be basic differences in glucose metabolism between susceptible animals and nonsusceptible animals. Increased serum NEFA and ketone body concentrations accompany the disease, but clinical signs do not appear to develop in the absence of hypoglycemia. The diagnosis is based on history, clinical signs, and the finding of ketone bodies in the urine. Numerous metabolic abnormalities develop subsequent to hypoglycemia and hyperketonemia, and these affect the prognosis. Important secondary abnormalities include acidosis, dehydration, and renal failure. Therapy is frequently unsuccessful, but frequent administration of small doses of glucose appears to be beneficial, if the other abnormalities, such as acidosis and dehydration, are controlled. Prevention can be readily achieved by nutritional means and is far more rewarding than therapy. Ewes and does must be fed in relation to their changing energy needs throughout the reproductive cycle.
The various phenomena of toxemia of pregnancy both in primiparous and multiparous women may be explained by postulating a defect in the calcium transport mechanism, both in the smooth muscle of the uterus and vascular smooth muscle as well as a similar defect in platelets. The involvement of prostaglandin E has not been proven to be a factor in human beings but could conceivably play an auxiliary role. Amelioration of the process by delivery would be due to dereased demand for the synthesis of the critical smooth muscle protein or proteins involved in calcium binding and transport because of uterine devolution. Eclampsia would be analogous to hypertensive encephalopathy and represent an acceleration of this process, particularly in the untreated woman.
A retrospective study investigated the epidemlologic characteristics of eclamptic patients seen at the University of Mississippi Medical Center. Between January 1955 and June 1973, 194 patients were discharged from our hospital with the diagnosis of eclampsia. Although our incidence of severe forms of toxemia of pregnancy has decreased from 6.8 per 1,000 deliveries from 1955 to 1960 to 4.8 per 1,000 deliveries from 1970 to 1973, it is still three times higher than for the United States overall. Our patients generally were young, unmarried, and without adequate prenatal care. Primary therapy for severe preeclampsia and eclampsia consists of bed rest and administration of magnesium sulfate until stable, and then delivery. Therapy for the eclamptic patient includes control of the convulsions, administration of magnesium sulfate, and delivery when the patient's condition has stabilized. Antihypertensives and diuretics are used for cardiovascular indications.
The hypercoagulable state in patients with toxemia of pregnancy was investigated in comparison with normal pregnant women using new coagulation parameters, mainly thrombin-antithrombin III (TAT) complexes, alpha 2-antiplasmin-plasmin complexes (PIP), and D-dimer FDP. When the patients were categorized by the classification of the WHO Study Group (1985), significant increases of TAT complexes and alpha 2-PIP complexes with decreases of the ATIII level were observed in the groups with preeclampsia and severe gestational hypertensive disease as compared to normal pregnant women. A significant increase of D-dimer FDP was observed in a group with severe gestational hypertensive disease. Additionally, the relationship between clinical signs and the hypercoagulable state in the patients was analyzed using canonical correlation analysis as a multivariate analysis. The clinical signs and coagulation parameters had a significantly high correlation of lambda 1 = 0.7219, p less than 0.01. The results showed that clinical signs were associated with simultaneous coagulation abnormalities. The indices obtained from the results of canonical correlation analysis, which were called the clinical index and the coagulation index, should be useful in evaluating the efficacy of anticoagulation therapy.
The role of the renin-angiotensin system in the development of hypertension was studied by infusing an angiotensin II analog, 1-Sar, 8-Ile angiotensin II, in women with toxemia and women on estrogen-containing oral contraceptives or estrogen treatment. In 3 of 4 women who developed hypertension on oral contraceptives or estrogen treatment, the blood pressure was reduced with the infusion of 1-Sar, 8-Ile angiotensin II. In 3 women who remained normotensive on oral contraceptives or estrogen treatment, the blood pressure was not reduced, although there was no significant difference in plasma renin activity (PRA) between the women who developed hypertension and those who remained normotensive on oral contraceptives. In 6 pregnant women who developed hypertension, the blood pressure increased remarkably with the infusion of 1-Sar, 8-Ile angiotensin II, although PRA was increased significantly in all of them. In these women, however, sodium excretion was less than that in normal pregnant women. In 4 normal pregnant women, the blood pressure remained unchanged or increased slightly, and PRA was almost similar to that of women who developed hypertension. The above results suggest that increased PRA in women who developed hypertension whilst on estrogen-containing oral contraceptives or estrogen treatment is more closely related to the development or maintenance of hypertension than that in pregnant women who develop hypertension, although there remains a possibility that the response of blood pressure to 1-Sar, 8-Ile angiotensin II in pregnant women who develop hypertension is influenced by sodium retention.
A murine monoclonal antibody (15H6) against the trichothecene mycotoxin T-2 was capable of neutralizing the in vitro protein synthesis inhibitory effect of T-2 toxin in human B lymphoblastoid cultures. It was further shown that 15H6 given to rats (250 mg/kg) 30 min before or 15 min after a lethal dose (1 mg/kg) of T-2 toxin conferred 100% survival. A lower dose of 15H6 (125 mg/kg), given 15 min after the lethal dose of T-2 toxin, protected 25% of the rats. An increased time to death and 45% survival was seen in rats given the full dose of 15H6 antibody 60 min after lethal toxin. These data are the first demonstration of effective prophylaxis and therapy for T-2 toxemia.
The neuropathology and biochemical features of 17 sheep with clinical signs and gross necropsy features of naturally occurring pregnancy toxemia were retrospectively evaluated. The sheep ranged in age from 3 to 6 years and were of seven different breeds and three breed crosses. Thirteen sheep (case Nos. 1-4, 6-9, 11-14, 16) showed astrocytic nuclear swelling, hypertrophy and proliferation, and cerebrocortical neuronal necrosis. Seven of these sheep had Purkinje cell necrosis (case Nos. 2, 3, 6, 11, 12, 14, 16), and seven had vacuolation of cerebral and cerebellar sub-cortical white matter (case Nos. 1-4, 9, 12, 13). The neuropathologic features were similar to those of naturally occurring hypoglycemia of human beings and experimentally induced hypoglycemia of primates and the rat. The lesions seen in the sheep studied may have been caused by cerebral hypoglycemia, but data for blood or cerebral glucose concentrations were not available.
Three women presenting with toxemia of pregnancy revealed reversible increased signal intensity on T2-weighted images by MRI. Overall, neuroradiologic techniques, with MRI the most sensitive, help elucidate the pathophysiology and facilitate the diagnosis in this condition.