[Effect of the duration of late toxicosis on fetal and neonatal development taking into account late results].
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Acidosis↗
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Thyroxine toxicosis. A common variant of hyperthyroidism.
To determine the frequency of thyroxine (T4) toxicosis, we calculated a free triiodothyronine index (FT3I) on 124 patients who displayed elevations of the free T4 index (FT4I) on initial screening. If the clinical presentation was not characteristic of hyperthyroidism or if the FT3I was not elevated, a thyrotropin-releasing hormone (TRH) test was performed. Of 83 hyperthryoid patients, 70 displayed elevations of both the FT4 and FT3 indices. Thirteen patients, however, had elevations of the FT4I alone. This frequency of T4 toxicosis is higher than generally appreciated. Forty-one patients, most of whom were ill with nonthyroidal diseases, had normal TRH test results and were classified euthyroid. We conclude that FT4I elevations owing to T4 toxicosis and nonthyroidal illnesses are common and that the laboratory differentiation between the syndromes may be difficult.
Adolescent↗
Factors influencing neonatal morbidity in diabetic pregnancy.
The influence on neonatal morbidity of factors such as maternal duration of diabetes, third trimester blood glucose control, gestational age at delivery, mode of delivery, and hypertension in pregnancy was analyzed in 92 consecutive diabetic pregnancies (White B35, C22, D26, F9). In a subgroup of 52 diabetic pregnancies the analysis was extended to the influence of hemoglobin A1c at the start and end of pregnancy, blood glucose control during delivery, and fetal insulin secretion at birth. The infants were divided into 3 groups according to the degree of neonatal morbidity: either no (n = 37), minor (n = 27), or severe morbidity (n = 28). There were no significant differences between the groups with no and minor morbidity. Compared to the no-morbidity group, the group with severe morbidity had significantly longer duration of maternal diabetes (p less than 0.05), shorter gestational age at delivery (p less than 0.025), higher frequency of cesarean section (p less than 0.05), and higher frequency of toxicosis (p less than 0.01). The 3 groups did not differ significantly with regard to maternal blood glucose control during pregnancy and delivery. Discriminant analysis revealed that the most significant (p less than 0.001) influence on severe morbidity came from gestational age at delivery. After correction for this factor, there were no other factors with a significant influence on severe morbidity. Within the actual range (mean values 3.9-8.5 mmol/l), blood glucose control during the third trimester had no significant influence on morbidity.
Adult↗
[Pathobiochemistry of mineral and trace elements. II. Copper concentration in the whole blood and serum of pregnant women and newborn (author's transl)].
Following a description of the biochemical and pharmacodynamic significance of copper metabolism, we report on the kinetics of copper in the whole blood and in the serum using as subjects 158 gravid women during pregnancy and of 468 pregnant women and their neonates following birth. Be obtained the following findings: 1. The copper level increases slightly in the whole blood and significantly in the serum during the 20-40 weeks of pregnancy in both normal and pathological pregnancies. 2. Copper shows contrary kinetic behaviour during the entire pregnancy as compared with the corresponding zinc values. 3. The sequence of copper metabolism is identical in primiparas as well as multiparas. 4. Blood groups of pregnant women are without influence on the copper level. 5. The rhesus factor does not change the kinetics of copper in the whole blood and the serum of pregnant women. 6. It could not be ascertained with sufficient certainty whether the Apgar values correlate with copper concentrations. 7. In contrast to the mothers, a considerably lowered copper level could be ascertained in the whole blood of newborns; the extent of copper deficiency is considerably greater in male neonates than in female neonates. 8. Toxicosis of pregnancy does not correlate with the copper concentration in the whole blood or serum of mother and child.
Apgar Score↗
Copper metabolic defects and liver disease: environmental aspects.
Copper (Cu) is an essential trace element for many biological processes. Cu homeostasis is generally well maintained by inbuilt controls in intestinal absorption, biliary excretion and intrahepatic storage. Copper deficiency disorders are rare. Acute Cu toxicity occurs occasionally in accidental poisoning with Cu sulfate. Chronic Cu toxicity in the form of liver cirrhosis and damage to other organs is seen classically in Wilson's Disease (genetic abnormality of Cu metabolism) and in the presumed environmental disorder Indian Childhood Cirrhosis (ICC). The clinical, epidemiological and treatment aspects of ICC are described. The evidence linking ICC to environmental Cu is (i) greatly increased hepatic Cu; (ii) early introduction of Cu contaminated milk boiled or stored in brass vessels; (iii) dramatic decline in ICC throughout the country coincident with change in feeding vessels; and (iv) continued long-term remission in d-penicillamine-treated patients after withdrawal of the drug. The nature and role of a second factor in the causation of ICC remains unclear, although a genetic predisposition is strongly suspected. Scattered reports of an ICC-like illness from the West (Idiopathic Cu Toxicosis, Endemic Tyrolean Infantile Cirrhosis), suggest that different mechanisms (environmental, genetic or both) can lead to the same end stage liver disease-'ecogenetic' disorders.
Child, Preschool↗
[New methods of assessing intoxication and blood cell response in patients with infectious toxicoses].
The microviscosity indexes of cell membranes of erythrocytes, neutrophils, and lymphocytes were estimated in children with acute respiratory diseases with and without infectious toxicosis. The erythrocyte microviscosity most completely reflects the degree of toxicosis. The ratio of membrane microviscosity indexes of neutrophils to that of lymphocytes demonstrates the specific response of blood cells to infectious toxic exposure.
Acute Disease↗
[The iron overload syndrome in patients with severe bacterial inflammatory diseases and convalescents].
In convalescents after and in patients with sepsis, purulent meningoencephalitis, severe pneumonia the study of iron metabolism provided biochemical criteria of iron excess: low serum transferrin against high transferrin iron, elevated ferritin. The risk of hyperferremia rises considerably after blood or erythrocyte transfusions. The liver got affected in the presence of infectious toxicosis. The authors believe it risky to practice uncontrolled administration of iron preparations in subjects recovering from severe bacterial and inflammatory diseases in view of threatening hemochromatosis.
Acute Disease↗
Copper toxicosis in an Australian child.
A 20 month old Caucasian child living in rural Australia presented with liver failure after exposure from birth to milk formula made from acidic bore water containing excess copper leached from the copper piping. The liver pathology was identical to that seen in Indian childhood cirrhosis and similar disease in non-Indian children now termed idiopathic copper toxicosis (ICT). The only other Australian case, reported more than 20 years previously, had identical presentation, pathology and circumstances of occurrence. The rarity of ICT in Australia, despite a significant population at risk, and the implications of these cases are discussed.
Australia↗
Aversion learning in 5-day-old rats: taste-toxicosis and texture-shock associations.
Five-day-old rats that received a single pairing of a novel saccharin flavor with lithium treatment learned to suppress ingestion of saccharin on subsequent occasions (Experiment 1). This flavor aversion learning was inversely related to the interval between the novel flavor experience and drug administraton, wit h significant aversions being learned with intervals of 0 and 30 min but not with intervals of 60 and 90 min (experiment 2). The conditioning was observed when hypertonic lithium served as the unconditioned stimulus but did not occur with isotonic lithium or hypertonic saline injections (Experiment 3). These results indicate that flavor aversion learning in infant rats is a result of the joint action of two factors--pure drug effects and the somatic pain and irritation produced by the tonicity of the injected agent. The taste aversion learning was specific to the drug-paired flavor, and evidence was presented suggesting that 5-day-old rats display a natural hesitancy to consume novel edibles (neophobia) (Experiment 4). Experiment 5 demonstrated that 5-day-old rats selectively associate tactile stimuli with shock but not with the gastrointestinal consequences of lithium. Implications of the mechanisms involved in flavor aversion learning in infant rats are discussed as they relate to adaptation and food selection in adult animals.
Animals↗
Idiopathic copper toxicosis.
Liver diseases of infancy and childhood are generally rare and within the spectrum of these disorders, only a few subtypes are related to abnormal hepatic copper accumulation. Idiopathic copper toxicosis has been defined as such a subtype; although this disease is characterized by distinct clinical and pathologic features, its exact etiology is still controversial. On the basis of a review of the literature, supplemented by our own observations of 138 cases endemic to western Austria, we hypothesize that idiopathic copper toxicosis is caused by a synergy of an autosomal-recessive inherited defect in copper metabolism and excess dietary copper. Increased awareness of the disease should enable early diagnosis and lead to successful treatment, thereby improving the overall poor prognosis of affected patients.
Child, Preschool↗
[Phosphorus-potassium metabolism in puerperae with late toxicosis and its correlation with the status of the maxillodental system].
A deficiency of mineral components in the breast milk and saliva and shifts in the protein, carbohydrate, and lipid metabolism are observed in puerperae with a history of late gestosis; this fact tells negatively on the maxillodental system of the mother and her baby.
Adult↗
The canine copper toxicosis gene MURR1 does not cause non-Wilsonian hepatic copper toxicosis.
BACKGROUND: Non-Wilsonian hepatic copper toxicosis includes Indian childhood cirrhosis (ICC), endemic Tyrolean infantile cirrhosis (ETIC) and the non-Indian disease known as idiopathic copper toxicosis (ICT). These entities resemble the hepatic copper overload observed in livers of Bedlington terriers with respect to their clinical presentation and biochemical and histological findings. We recently cloned the gene causing copper toxicosis in Bedlington terriers, MURR1, as well as the orthologous human gene on chromosome 2p13-p16. AIM: To study the human orthologue of the canine copper toxicosis gene as a candidate gene for ICC, ETIC, and ICT. METHODS: We sequenced the exons and the intron-exon boundaries of the human MURR1 gene in 12 patients with classical ICC, one patient with ETIC, and 10 patients with ICT to see whether these patients display any mutations in the human orthologue of the canine copper toxicosis gene. RESULTS: No mutations in the MURR1 gene, including the intron-exon boundaries, were identified in a total of 23 patients with non-Wilsonian hepatic copper toxicosis. CONCLUSIONS: Our results demonstrate that copper toxicosis in Bedlington terriers is not an animal model for the non-Wilsonian hepatic copper toxicosis described in this study.
Adaptor Proteins, Signal Transducing↗
[Preventive use of intermittent normobaric hypoxic hypoxia in pregnant women at high risk of developing late toxicosis].
The authors studied the efficiency of preventive usage of intermittent normobaric hypoxic hypoxia (INHH) in 44 pregnant females at high risk for late gestosis in presence of essential hypertension, stages I-II, and hypertensive type of neurocirculatory asthenia. The authors paid attention to a decrease in the incidence of late gestosis, its severe patterns especially, and perinatal mortality.
Adult↗
[The clinicoimmunological evaluation of the use of timogeksin in different forms of measles].
Materials are submitted concerning the use of thymohexine in the treatment of measles. Efficacy of thymohexine in 133 children with grave and complicated forms of measles was assessed. Thymohexine was found out to reduce the duration of the infectious toxicosis and local inflammatory events. Under the influence of the above drug the total counts of T- and B-lymphocytes (CD11, CD8, CD4, CD22) returned to normal as did the immunoregulatory index (D4/CD8), levels of circulating immune complexes, their molecular composition.
Acute Disease↗
Wilson disease and idiopathic copper toxicosis.
The pathogenic agent of both Wilson disease (WD) and non-Indian childhood cirrhosis (which we term idiopathic copper toxicosis, or ICT) is copper accumulating to excess in the liver. Inheritance of a pair of alleles of an autosomal recessive gene on chromosome 13 is necessary and sufficient to cause such copper accumulation in WD; reducing the dietary intake of copper cannot prevent the development of WD. In contrast, the lethal accumulations of copper in children with ICT have been attributed primarily to an increased dietary intake of copper. However, 64 124 child-year exposures of children under the age of 6 y to drinking water containing a copper concentration of approximately 125.9 micromol/L (8 mg/L) produced no deaths from any form of liver disease. Moreover, the ICT of seven infants was attributed primarily to drinking water containing < 110.2 micromol Cu/L (7 mg/L) despite evidence of the presence of a genetic defect in three of the patients, one of whom was exclusively breast-fed. These data suggest that ICT cannot be caused solely by increased dietary intake of copper and occurs only in children with an identified genetic defect.
Alleles↗
[Measuring volume and density of human organs and its significance in medicine and forensic medicine: lung].
OBJECT: To obtain values of normal human lung and diffuse pathological changes, in order to provide a simple and convenient diagnostic method for measuring human visceral organs in the autopsy of pathology and forensic pathology. METHODS: The exact mass, volume and density of normal and pathological lung were synchronously measured with the intelligentized volume-densimeter made by authors. RESULTS: The date-base about the volume and density of human lung with different races were established for anatomy, anthropology and biodynamics. In two cases of over-load in circulation and water toxicosis, the severe lung edema was proved with the scale of lung density, which was atypical edema in the lung tissue. CONCLUSION: Measurement of visceral organs in the autopsy can assist to an integrative pathological diagnosis.
Adolescent↗
Value of simultaneous T3, T4, and TSH measurements for management of graves' disease in children.
One hundred simultaneous determinations of serum T4 and T3 were performed during the course of treatment of 23 children and adolescents with Graves' disease. Five patients were previously untreated and six were experiencing relapse after treatment was discontinued. During relapse, increased T3 concentration is frequently present when serum T4 concentration is normal and T3 measurement is therefore more reliable for early detection of relapse. During therapy with thionamides, T4 measurement alone is often misleading in assessing adequacy of control achieved by therapy. Commonly, patients who clinically have hyperthyroidism have serum T4 concentrations within the normal range but continue to have elevated T3 concentrations (T3 toxicosis). Similarly, T4 can be suppressed into the hypothyroid range in the clinically euthyroid patient with either a normal or high T3 concentration. In these patients, determination of serum T3 often prevents premature reduction of thionamide dosage. When T4 and T3 concentrations do not clearly demonstrate presence or absence of hypothyroidism, measurement of serum thyroid stimulating hormone can be of value.
Graves Disease↗
[Angiogenesis in gynecology and obstetrics].
In current scientific discussion, increasing importance is being given to the clinical significance of the new formation of vessels (angiogenesis) in the course of physiological, inflammatory and neoplastic processes. Angiogenesis is best studied in the growth of malignant tumors, since cancer may be regarded as the most important angiogenesis-dependent disease in terms of social and economic aspects. The significance of angiogenesis in gynecological oncology is as follows: 1) Intratumoral vessel density is an indicator for the emergence and growth of malignant tumours and their precursor lesions, 2) intratumoral vessel density is an independent prognostic factor for solid malignancies and 3) the inhibition of tumor angiogenesis by means of anti-angiogenetic substances causes tumor growth to be suppressed. Angiogenesis also plays an important role in the regulation of the female menstrual cycle. Proliferation of the endometrium and the formation of the corpus luteum in the second half of the menstrual cycle are examples of angiogenesis in the physiological field. The function of angiogenetic factors in the emergence of endometriosis and in female and male infertility are currently under study. In obstetrics, the new formation of blood vessels is significant for the implantation of impregnated blastocysts and for the development and growth of the placenta. Preeclempsia (gestational toxicosis), for instance, is a typical pregnancy-related disease whose pathophysiological mechanism is attributed to a disturbed development and function of small placental vessels. The present paper is an overview of current knowledge and current approaches of research concerning angiogenesis in the field of gynecology and obstetrics. The paper is focused on the clinical significance of angiogenesis.
Angiogenesis Inducing Agents↗