Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have used an antihuman tumor necrosis factor monoclonal antibody, CB006 (murine IgG1), to prevent the OKT3-induced acute clinical syndrome. This syndrome is due to the massive, although transient release in the circulation of various cytokines (TNF, interferon gamma, interleukin 2, interleukin 6) and represents one important side effect linked to in vivo use of OKT3. Fourteen kidney allograft recipients undergoing prophylactic OKT3 therapy were treated with CB006 in a single i.v. injection of either 0.4 mg/kg (group I, 7 patients) or 2 mg/kg (group II, 7 patients), 1 hr before the first OKT3 administration. Nineteen consecutive patients formed a historical control group. None of the CB006-pretreated patients showed any of the common, severe OKT3-associated symptoms (hypotension, respiratory distress, or neurotoxicity), which were observed in 10% of the historical controls. In addition, CB006-treated patients showed a lower frequency of pyrexia (> or = 39 degrees C) and gastrointestinal symptoms. None of the CB006-treated patients presented severe vomiting or diarrhea, defined as repeated episodes inducing significant fluid and electrolyte loss. Two out of the 7 patients in group I and group II had mild transitory diarrhea. Mild single vomiting episodes occurred in 2 group I patients and 3 group II patients. At variance in all controls, gastrointestinal symptoms were long lasting and associated with major prostration due to electrolyte and fluid loss. Importantly, CB006-treated patients who presented mild symptoms had detectable bioactive circulating TNF, showing incomplete inactivation of OKT3-induced TNF by CB006. CB006 was perfectly well tolerated, did not induce xenosensitization, and did not affect the biological or clinical effectiveness of OKT3.
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PMID:Evidence that antihuman tumor necrosis factor monoclonal antibody prevents OKT3-induced acute syndrome. 146 94

This study analyzed the capacity of an anti-human tumour necrosis factor (TNF) monoclonal antibody, CB006 (murine IgG1, Celltech), to prevent the OKT3-induced acute clinical syndrome. Fourteen renal allograft recipients undergoing prophylactic OKT3 therapy were included. CB006 was administered as a single i.v. injection, 0.4 mg/kg (Group I, 7 patients) and 2 mg/kg (Group II, 7 patients), one hour prior to the first OKT3 administration. Nineteen consecutive patients that were part of a randomized multicenter trial constituted the historical control group. In all patients CB006 was perfectly well tolerated and significantly decreased the frequency of the common OKT3-associated acute symptoms. None of the CB006 pretreated patients showed severe life threatening symptoms (hypotension, respiratory distress or neurotoxicity), observed in 10 per cent of historical controls. At variance with controls, in CB006 treated patients gastrointestinal symptoms (vomiting, diarrhea) and pyrexia (body temperature greater than or equal to 39 degrees C) appeared in low frequency, were mild and short lasting, never promoting major prostration of the patients due to electrolytes and fluid loss. Importantly, the presence in some patients of these mild symptoms, correlated with detectable bioactive TNF in the circulation thus reflecting incomplete blockade by CB006 of OKT3-induced TNF. CB006 pharmacokinetics data further stressed the need for adequate dosage adaptation. CB006 did not affect the biological or clinical effectiveness of OKT3. None of the patients showed evidence of anti-CB006 xeno-sensitization.
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PMID:[Acute clinical syndrome associated with OKT3 administration. Prevention by single injection of an anti-human TNF monoclonal antibody]. 183 13

The response of the neurolipomastocytoid cells (NLMs) and elements in their vicinity within the central nervous system of various animal species was studied following injection of the animals with the specific mast cell (MC)-discharger compound 48/80. The observed alterations were grouped into those occurring early (0--21 days) and later (up to 18 months). In the present report, only the acute changes are described, light and electron microscopically. Most experimental animals developed prostration, scratching, acral-type reaction, signs of respiratory distress and salivation, and, in the monkey, uncontrollable somnolence. Within about 2 weeks after the injection some animals (especially guinea pigs) manifested various degrees of limb paralysis. The NLMs, like MCs outside the CNS, responded to injection by various degrees of degranulation, vacuolation, marked variation in granule size, apparent cell loss and sometimes an increase in number. Electron microscopically, particulate breakdown products of the granules of the NLMs appeared in the cytoplasm; occasionally there was suggestive evidence that they had passed inward across the vessel wall to reach the lumen, and also outward through the outermost basal lamina. Perivascular astrocytic feet showed swelling and vacuolation shortly after the injection, which was followed by evidence of gliosis and later scarring; occasionally, alterations in the mitochondria were observed. In the spinal cord of the guinea pig, capillary neoformation was observed with endothelial cells and adjacent NLMs taking up tritiated thymidine. The discussion centers on the partial similarity of response to compound 48/80 of the NLMs to that of MCs outside the CNS, and the probable involvement of NLM-damage in the parenchymal changes.
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PMID:The mast cells of the mammalian central nervous system. V. The effect of compound 48/80 on the neurolipomastocytoid cells and related areas of the CNS: early changes. 743 98

BACKGROUND Salicylates continue to be marketed and to be used in developing countries as over-the-counter (OTC) antipyretics in children, whereas in developed countries they are no longer used in children because of safety concerns. The presenting signs of salicylate poisoning, especially chronic (repeated administration of therapeutic or excessive doses for longer than 12 h), can include metabolic acidosis, hypoglycaemia, lethargy, and coma and fits. These signs are also common in severe malaria in African children. Admission of two probable cases of chronic salicylate poisoning prompted us to look for other cases among children presenting to our hospital in Kenya, apparently with severe malaria. METHODS All children admitted to Kilifi District Hospital between July and September, 1994, who had a positive blood film for Plasmodium falciparum, and one or more of coma, prostration, or respiratory distress were eligible. As well as routine tests for malaria and routine biochemistry, salicylate concentrations were measured. Management of children (aged 6 months to 10 years) in the community was assessed by a cross-sectional survey of 463 households and by interviews with mothers 2 days after they had bought OTC drugs for a child with fever. FINDINGS Data were available for 143 of 154 children with initial primary diagnoses of severe malaria. 129 (90 percent) had detectable (>l mg/dL) salicylate. Six of these had salicylate concentrations of 20 mg/dL or higher. All six had neurological impairment and metabolic acidosis and four were, or became, hypoglycaemic. OTC drugs were the first-line treatment in 188 (74 percent) of 254 fever episodes during the 2 weeks before the cross-sectional survey. Of 250 mothers who bought drugs for a febrile child, 236 (94 percent) bought a preparation containing salicylates and 50 (21 percent) gave a dose higher than the manufacturer's recommended maximum. INTERPRETATION These cases suggest that in some children salicylate poisoning may cause or contribute to the development of metabolic acidosis and hypoglycaemia, complications of severe malaria associated with high mortality.
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PMID:Chronic salicylate poisoning and severe malaria. 865 7

During the period of transmission of malaria, from August to November of 1993 and 1994, we conducted a study to determine the frequency of the clinical forms of severe and complicated malaria. The study involved children, from 6 months through 15 years old, admitted to the pediatric ward of the hospital in Ouagadougou, Burkina Faso. The criteria for inclusion followed the definition of severe malaria stated by the World Health Organization. We carefully noted the symptoms and signs on admission. Of the total of 719 children enrolled in the study, there was a prevalence of children under 5 years old. The most frequent clinical forms were those of coma (377 cases, 52.4%), prostration (268 cases, 37.3%), convulsion (152 cases, 21.4%), anemia (115 cases, 15.9%), and hypoglycemia (55 cases, 10.3%). No renal failure form was observed. We also observed the respiratory distress form (35 cases, 4.9%) and the hemorrhagic form (11 cases, 1.5%). Malaria remains a major cause of childhood morbidity and mortality in the developing world. Early therapeutic management of febrile attacks with chloroquine would reduce the incidence of severe and complicated malaria.
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PMID:[Clinical signs of severe malaria in a pediatric hospital in Ouagadougou]. 917 71

Severe falciparum malaria is responsible for 2 million annual deaths, mostly among children under five years living in sub-Saharian Africa. In France, about 1500 paediatric malaria cases are diagnosed each year, among which 1% are severe and 1-2 deaths occur. Children are at high risk for severe forms, since malarial immunity is not yet acquired and symptoms are rapidly progressive. The definition of severe malaria relies upon WHO criteria revised in 2000. In children living in endemic areas, the most frequent criteria are impaired consciousness, severe anaemia, respiratory distress or acidosis, multiple convulsions and hypoglycaemia. Some of them have a high prognostic value, e.g., coma, hypoglycaemia or respiratory distress. The pertinence of WHO criteria was not assessed in travelling children, since severe cases are rare. Other severity criteria found in recent surveys from endemic zones, such as thrombocytopenia or, in infants, dehydration or bacteraemia, should also be investigated in childhood imported malaria. However, any fever associated with a convulsion, prostration, or impaired consciousness, in a child returning from the tropics, should be consider severe malaria and indicate an emergency admission to hospital. In France, intravenous quinine is recommended for the treatment of severe forms, without loading dose in children.
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PMID:[Criteria of severity in childhood falciparum malaria]. 1502 77

This study determined the effects of acute cypermethrin toxicity in the rat and its dose-response characteristics The intraperitoneal LD50 of cypermethrin from the study was 44.0 mg/kg body weight. The symptoms of toxicity were muscular weakness, swaying gait and respiratory distress; pallor and prostration occurred at higher doses and convulsions preceded death, apparently due to respiratory failure.
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PMID:The acute intraperitoneal toxicity of cypermethrin. 1508 Feb 14

The symptoms of severe malaria and their contribution to mortality were assessed in 290 children in northern Ghana. Common symptoms were severe anemia (55%), prostration (33%), respiratory distress (23%), convulsions (20%), and impaired consciousness (19%). Age influenced this pattern. The fatality rate was 11.2%. In multivariate analysis, circulatory collapse, impaired consciousness, hypoglycemia, and malnutrition independently predicted death. Children with severe malaria by the current World Health Organization (WHO) classification, but not by the previous one (1990), showed relatively mild clinical manifestations and a low case fatality rate (3.2%). In hospitalized children with severe malaria in northern Ghana, severe anemia is the leading manifestation, but itself does not contribute to mortality. In this region, malnutrition and circulatory collapse were important predictors of fatal malaria. The current WHO criteria serve well in identifying life-threatening disease, but also include rather mild cases that may complicate the allocation of immediate care in settings with limited resources.
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PMID:Manifestation and outcome of severe malaria in children in northern Ghana. 1530 5

Epidemics of malaria have occurred in highland areas of East Africa since the 1980s, but the clinical spectrum of severe malaria in these areas has not been described. Over a 17-month period from 2001 to 2002, we assessed 117 consecutive patients admitted to Kabale Hospital in highland Uganda who met the World Health Organization 2000 criteria for severe malaria. Sixty-six persons (56.4%) were age 5 years or older, and 51 (43.6%) were under 5 years of age. Fever, vomiting, and cough were the most frequent symptoms. Hepatomegaly and splenomegaly were infrequent. Prostration was the most frequent manifestation of severe malaria in children under 5 years of age (45.1%) and persons 5 years or older (65.2%), followed by respiratory distress (29.4%) and severe anemia (19.6%) in children under 5 years, and respiratory distress (15.2%) and impaired consciousness (13.6%) in persons 5 years or older. Strictly defined cerebral malaria was uncommon (3.4%). In a multivariate regression model, children under 5 years were more likely than persons 5 years or older to present with severe anemia (OR 5.2, 95% confidence interval [CI] 1.2-21.9) and respiratory distress (OR 3.5, 95% CI 1.3-11.1) and less likely to present with prostration (OR 0.3, 95% CI 0.1-0.7) and impaired consciousness (OR 0.2, 95% CI 0.0-0.9). In highland Uganda, severe malaria often occurs in persons older than 5 years of age. "Typical" signs like splenomegaly are frequently absent, prostration is the major manifestation, and other manifestations vary in frequency according to age.
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PMID:Clinical manifestations of severe malaria in the highlands of southwestern Uganda. 1589 Nov 30

The objectives of this retrospective study were to describe initial clinical profiles and subsequent outcome of adult patients in France who were diagnosed with severe imported malaria, as defined by the World Health Organization (WHO). Forty-two patients diagnosed from 1996 to 2002 were included (median age: 30 years, men: 78%, non-immune persons: 74%, return from Africa: 100%, inappropriate antimalarial chemoprophylaxis: 95%). At the time of hospital admission, jaundice (62%), hyperparasitemia (56%), and prostration (52%) were the most frequent findings, followed by acute renal failure (31%). Other findings, as described by the WHO criteria, were less common. Twenty-three patients presented only with jaundice, hyperparasitemia, or prostration in isolation, or in combination. Of these 23, five non-immune persons subsequently developed coma, shock, acute respiratory distress syndrome or acute renal failure; this led to death in 2 of these cases. This suggests that non-immune persons with imported malaria who present with jaundice, hyperparasitemia, or prostration should be admitted to the intensive care unit for close monitoring.
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PMID:Severe imported malaria: clinical presentation at the time of hospital admission and outcome in 42 cases diagnosed from 1996 to 2002. 1624 92


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