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At least 199 records · Page 11Linked to original sources
PubMed1975

[Infusion treatment in severe dehydration (infantile toxicosis)].

Severe dehydration in infants is a common life threatening condition. The therapy of different forms of dehydration has been described. Many practical suggestions for diagnostic procedures have been added. Clinical and pathophysiological peculiarities typical of the treatment of severe infantile dehydration have been stressed.

Alkalosis↗
PubMedDate not supplied

The greater susceptibility of North Ronaldsay sheep compared with Cambridge sheep to copper-induced oxidative stress, mitochondrial damage and hepatic stellate cell activation.

Sheep of the semi-feral North Ronaldsay (copper-sensitive) and domesticated Cambridge (copper-tolerant) breeds were compared in respect of pathological changes and protein expression in the liver as a result of excessive dietary copper. Acute mitochondrial damage and hepatic stellate cell (HSC) activation with collagen synthesis occurred in response to moderate copper overload in North Ronaldsay but not in Cambridge sheep. Mitochondrial degradative changes occurred either as ballooning degeneration and rupture with subsequent autophagic degradation or as mitochondrial matrical condensation (pyknosis). In North Ronaldsay sheep prolonged exposure to copper produced mitochondrial hyperplasia and hypertrophy, and nuclear damage with necrosis. Cytosolic isocitrate dehydrogenase (IDH), an enzyme responsive to oxidative stress, was induced in the liver of Cambridge sheep receiving a Cu-supplemented diet but was undetectable in the non-supplemented control sheep. Conversely, IDH was detected at similar levels in both control and copper-supplemented North Ronaldsay sheep, indicating a lower threshold response, and an enhanced susceptibility, to oxidative stress. "Upregulation" of mitochondrial thioredoxin-dependent peroxidase reductase (antioxidant protein-1) in the hepatic cytosol of the North Ronaldsay (but not Cambridge) sheep affirmed the increased susceptibility of the mitochondria to Cu-induced oxidative stress in this breed. Likewise the upregulation of cathepsin-D indicated increased lysosomal activity and HSC activation. The findings may be relevant to copper toxicosis in human infants.

Animals↗
PubMed1979

[Lesions of the nervous system in premature children with "conjugated" jaundices].

Results of many-year observation of 110 prematurely born children who had had nuclear jaundice in the precence of hyperbilirubinemia showed that this pathology not only had distinct temporal parameters, but in most cases also a characteristic clinical picture. The principal symptoms are: an abrupt tossing of the head back, general tonic convulsions, tonic stretching of the arms with pronation of the hands, monotonous constrained cry, amimic face, paroxysms of apnoe, and gross impairments on the part of the brain stem. The most important for the diagnosis and prognosis was the "setting sun" symptom. The diagnosing is difficult when the nuclear jaundice joins pre- or intranatal damage to the nervous system or is combined with an infectious toxicosis. Observation of infants during the first six months makes it possible to confirm the diagnosis. The gravity of the sequelae makes it necessary to transfer infants from the maternity home to pediatric hospitals even if the jaundice is only suspected.

Apnea↗
PubMed2004

White monkey syndrome in infant baboons (Papio species).

Over 23 months, zinc toxicosis was diagnosed in 35 baboons aged 5-12 months in one galvanized metal and concrete cage complex with conditions that led to excessive exposure to environmental zinc. Clinical signs included reduced pigmentation of hair, skin, and mucous membranes (whiteness), alopecia, dehydration, emaciation, cachexia, dermatitis, diarrhea and, in six cases, severe gangrenous dermatitis of extremities. The syndrome was characterized by pancytopenia, elevated zinc and low copper serum concentrations, low vitamin D and bone-specific alkaline phosphatase levels, and atypical myelomonocytic proliferation of bone marrow. This syndrome emphasizes the importance of proper husbandry and cage design and indicates the potential of infant baboons as a model to study the effects of excessive zinc on development. This is the first report describing the epidemiologic and clinical presentation of zinc toxicosis in infant baboons in captivity.

Alopecia↗
PubMedDate not supplied

[Functional study of the hypophyseal-thyroid and adrenal systems in physiological pregnancy and late toxicosis].

A comprehensive study was conducted in 30 healthy nonpregnant women, 115 healthy pregnant women and in 38 pregnant women with late toxicosis as well as in 25 healthy infants and 29 infants born to mothers with late toxicosis. A radioimmunoassay was used to measure serum thyrotropin (TSH), somatotropin (STH), adrenocorticotropin (ACTH), thyroxine (T4), triiodothyronine (T3), cortisol (CORT) and aldosterone (ALDO) levels. A catecholamine (CA) level was determined dy fluorimetry. Elevated ACTH, TSH, CORT and ALDO levels were noted in normal pregnancy. The above data indicated that the pituitary-thyroid and pituitary-adrenal systems of pregnant women formed adaptive reactions to the body demand for hormones. The reduction of ACTH and T3 levels and rise of CORT, ALDO, T4 levels and the serum protein thyroxine-binding capacity were noted in the pregnant women with late toxicosis. These hormonal differences may be indicative of a decrease in the reserves of women with late toxicosis. It is concluded that the pituitary-thyroid and pituitary-adrenal systems in newborns are capable of maintaining homeostasis by the moment of birth.

Adolescent↗
PubMed1992

[Immunologic correction with immunoglobulin of toxemia with exicosis in infants with acute intestinal infections].

The clinical course of acute intestinal infections complicated by toxicosis and exicosis was studied in 150 infants undergoing multimodality therapy, including natural human immunoglobulin for intravenous injections. The use of the new complex in the treatment of intestinal toxicoses was accompanied by increasing host immunological reactivity within short periods and decreasing of the treatment duration by 5.0 +/- 1.3 days; there were no persisting and chronic forms of the diseases and fatal outcomes. It was concluded that the use of the immunoglobulin for intravenous injections in the multimodality therapy of intestinal toxicoses in infants made it possible to prevent death in complicated intestinal infections and at the same time to accelerate their recovery.

Acute Disease↗
PubMed2001

Congenital thyrotoxicosis in premature infants.

OBJECTIVES: Graves' disease (GD) complicates 0.1% to 0.2% of pregnancies, but congenital thyrotoxicosis is rare occurring in one in 70 of these pregnancies independent of maternal disease status. Antenatal prediction of affected infants is imprecise; however, maternal history, coupled with a high maternal serum TSH receptor binding immunoglobulin index (TBII) predict adverse neonatal outcome. Mortality is reported to be as high as 25% in affected infants and would therefore be expected to be higher in premature infants. This study illustrates that in sick, premature, extreme low birth weight (ELBW) or intrauterine growth retarded (IUGR) infants, the diagnosis maybe overlooked especially in the absence of antenatal risk assessment and management of thyrotoxicosis in this setting is complex. DESIGN AND PATIENTS: The records of premature neonates born at the three main maternity units in Brisbane, between January 1996 and July 1998 diagnosed with congenital thyrotoxicosis were reviewed. Data were recorded on gestational age, birth weight (B Wt), maternal thyroid history and current status, and neonatal course. Thyroid function and TBII status was assessed using standard biochemical assays. RESULTS: Seven neonates from five pregnancies were identified (four female, three male). Mean gestational age was 30 week (25--36 week) and median B Wt was 1.96 kg (0.50--2.62 kg). Only one mother received formal antenatal counselling by a paediatric endocrine service and had a TBII (54%) measured prior to delivery. Three of five mothers had elevated TBII measured after diagnosis in their offspring (57%, 65%, 83%) and in one mother, a TBII was not performed. All mothers were biochemically euthyroid at delivery. Mean age at diagnosis was 9 days (1--16 days) and mean age at commencement of treatment was 12 days (7--26 days). Two infants received propylthiouracil and five received a combination of carbimazole and propranolol. Four became biochemically hypothyroid, in three this resolved with cessation of the antithyroid drug (ATD), and one required ongoing T4 supple-mentation. Only one infant required treatment for cardiac failure and there were no deaths in this cohort. CONCLUSIONS: This is a large series of extremely small and premature infants with neonatal thyro-toxicosis. Presentation was nonspecific. The diagnosis was delayed because of low birth weight, prematurity, multiple birth and/or an unrecognized maternal history of Graves' disease. The treatment of neonatal thyrotoxicosis was difficult in these extreme low birth weight infants yet no infant died and significant morbidity was confined to high output cardiac failure in one infant. With antenatal recognition of past or active Graves' disease, assessment of maternal TSH receptor binding immunoglobulin index prior to delivery and postnatal monitoring of cord TSH and venous fT4 and TSH on days 4 and 7 rapid treatment of affected infants may have further reduced neonatal morbidity.

Antithyroid Agents↗