Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An acute respiratory distress syndrome in 10 adult dogs was usually preceded by vomiting, anorexia and lethargy followed, after a short interval, by dyspnoea. The dyspnoea became increasingly severe, despite oxygen therapy, and cyanotic respiratory failure ensued. All 10 dogs died or were killed after illnesses lasting between one and eight days. Necropsies revealed pulmonary congestion, oedema, collapse and haemorrhage with loss of alveolar epithelial cells. Early alveolar fibrosis was also found. Paraquat was identified in post mortem samples from four of the 10 dogs.
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PMID:Acute respiratory distress in the dog associated with paraquat poisoning. 86 Mar 82

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

A total of 2248 infants born at All India Institute of Medical Sciences Hospital, New Delhi were selectively screened for hypoglycemia over a period of 15 months. Hypoglycemia (blood glucose less than 30 mg/dl) was diagnosed in 107 cases (4.8%). Preterm babies had three times increased risk (12.8%) as compared to term babies (3.6%). Small-for-dates (SFDs) and large-for-dates (LFDs) infants were at increased risk of manifesting hypoglycemia (7 and 10 times, respectively) as compared to the appropriate-for-dates (AFDs) babies (2.7%). Approximately two-thirds of the hypoglycemic babies (67.3%) had one or more risk factors including birth asphyxia (24.2%), diabetic mothers (23.8%), respiratory distress (13.9%) and septicemia (11.6%). A total of 59.8% cases were asmyptomatic while the rest had one or more symptoms. The most common symptom observed was lethargy (81.4%), followed by jitteriness (67.4%), respiratory abnormalities (41.9%), hypotonia (39.5%) and seizures (30.2%). The amount of glucose (mg/kg/min) needed to maintain a stable blood sugar in various categories of hypoglycemic babies was observed to be in the following decreasing order of amount; symptomatic babies with seizures (Gp IV), IGDM's/IDM's and symptomatic babies with other features (Gp III), SFDs and LFDs (Gp II) and AFDs (Gp I). Such a categorization of hypoglycemic babies will help to treat them more precisely.
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PMID:Neonatal hypoglycemia--clinical profile and glucose requirements. 159 96

The clinical features and haematologic indices of 100 young infants aged 3 months and below, admitted with suspected bacterial infections, were analysed. Fever, lethargy, hepatomegaly, poor feeding and irritability were the commonest features for suspecting a bacterial infection in these infants. However, the features significantly associated with bacterial infections were respiratory distress and cyanosis. Of the haematologic indices commonly associated with bacterial infections, only C-reactive protein and erythrocyte sedimentation rate were significantly predictive compared to leukocyte counts, absolute neutrophil counts and nitro-blue tetrazolium tests. When used in combination, a raised C-reactive protein with erythrocyte sedimentation rate, a raised erythrocyte sedimentation rate with abnormal leukocyte counts and a raised C-reactive protein with abnormal leukocyte counts were significantly associated with bacterial infections.
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PMID:Clinical features and haematological indices of bacterial infections in young infants. 162 Nov 14

Polycythemia (venous PCV greater than 65%) in neonates is not an infrequent occurrence. Over the last 2 years out of approximately 1500 admissions to the Neonatal Unit, polycythemia was detected in 46 babies (3.06%). Seventeen (36%) of these babies were preterm and 29 (63%) were term. Approximately one third were small for dates while 2 babies (4%) were large for dates. Four of them had been born to mothers with gestational diabetes and 7 were twin deliveries. Severe perinatal asphyxia (5 minute Apgar score less than or equal to 5) was present in 12 cases (26%). Symptoms suggestive of polycythemia included lethargy in 15%, refusal to feed in 13%, respiratory distress in 10%, vomiting in 8% and abdominal distension in 6%. Associated hypoglycemia was seen in 5 cases (10.8%) while twelve babies (26%) had significant jaundice (bilirubin greater than or equal to 12 mg/dl). Twenty eight babies (60.8%) were given a partial plasma exchange transfusion through the umbilical route. There was 6.5% mortality in these 46 babies with polycythemia. Blood letting through a peripheral vein along with a plasma infusion may be a safer alternative to partial plasma exchange transfusion through umbilical route in babies with polycythemia.
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PMID:Polycythemia in the newborn. 221 Aug 21

A total of 2288 infants were screened for hematocrit over a period of 15 months. Polycythemia was diagnosed in 27 cases (1.2%). Preterm and term babies had more or less equal risk to develop polycythemia (1.5% and 1.1% respectively) while postterm infants had at least three times increased risk (3.4%) when compared to their term counterparts. Large-for-dates (LFDs) and small-for-dates (SFDs) infants had increased risk of manifesting polycythemia which was nearly four times (2.2%) and twenty-five times (13.2%) respectively, as compared to appropriate-for-dates (AFDs) babies (0.5%). About one-third of polycythemic infants had one or more symptoms. The most common symptoms observed was jitteriness (25.9%) followed by respiratory distress (14.8%) and lethargy (11.1%). The mean (+/- SD) hematocrit of symptomatic newborns (76.0 +/- 4.04) was found to be significantly higher (p less than 0.001) as compared to asymptomatic babies (70.84 +/- 2.73). Partial exchange transfusion with plasma was performed in all the symptomatic cases within 8 hours of onset of symptoms. No such intervention was performed in asymptomatic cases. On neurodevelopment follow-up, the development indices (MDI and PDI) of both asymptomatic and symptomatic cases were found to be comparable.
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PMID:Polycythemia in the newborn: do asymptomatic babies need exchange transfusion? 236 43

3-methylindole (3-MI) dissolved in the lipophilic carrier Cremophore EL was administered intraperitoneally to male, twelve-week-old Sprague-Dawley rats. Gross and histopathologic changes in the lungs were studied using light microscopy at three time-periods following administration: 16, 24, and 46 hours. Both 3-MI and Cremophore caused changes in bronchiolar epithelium at 16 hours. By 46 hours, Cremophore-injected rats showed no effects of the carrier; whereas, 3-MI rats showed severe lung changes characterized by airway epithelial and pulmonary vascular endothelial necrosis and sloughing, cellular infiltration by lymphocytes and macrophages, perivascular edema, alveolar edema, and lymph stasis. Grossly, the controls showed no effect of the carrier and none died during the studies. In contrast, 3-MI injected rats quickly became lethargic and displayed tachypnea, anorexia, and progressive respiratory distress. Two of five 3-MI rats in the final group died just prior to 46 hours. All of this group had grossly congested lungs and marked pleural effusion. The lesions and time course showed similarities to those observed in ruminants and mice. We conclude that 3-MI in Cremophore causes an acute progressive pneumonitis in rats and suggest that the rats may be a suitable model for 3-MI-induced and similar toxic lung diseases in domestic animals and people.
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PMID:Pulmonary changes in rats following administration of 3-methylindole in cremophore EL. 298 Feb 17

The case of a 3-week-old male infant is described. After receiving an iatrogenic overdose of metoclopramide (1.0 mg/kg every six hours) throughout a 36-hour period for the treatment of suspected gastroesophageal reflux, he became cyanotic, lethargic, and irritable, he fed poorly, and he had diarrhea and respiratory distress. Methemoglobinemia (20.5%) and reduced oxyhemoglobin saturation (79%) were identified. The patient had an excellent clinical response following a single IV dose of methylene blue. Subsequently, methemoglobin reductase activity was normal and there was no measurable hemoglobin M. The diagnosis of methemoglobinemia should be considered in any infant receiving large doses of metoclopramide who has clinical findings of cyanosis, ashen color, or a history of lethargy and/or motor restlessness.
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PMID:Metoclopramide-induced methemoglobinemia. 340 65

We report the broad spectrum of clinical manifestations in 23 infants with positive cultures for Listeria monocytogenes who were treated in our hospital during a recent epidemic. The majority of infants (70%) were preterm and none was small for gestational age. Thirteen (56%) had respiratory distress at birth with evidence of congenital pneumonia. Four of the 5 deaths occurred among these infants. Four infants considered healthy after resuscitation developed fever and lethargy within 36 hours after birth. Only one of these infants had evidence of pneumonia. We conclude that congenital pneumonia with respiratory distress at birth is the major cause of mortality and morbidity from L. monocytogenes infection in the neonate.
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PMID:Clinical manifestations of epidemic neonatal listeriosis. 367 Sep 48

We report the results of a two-part study examining the frequency of symptoms and other findings associated with neonatal polycythemia. In the first part of the investigation, we evaluated the occurrence and features of the disorder in a cohort of 3,768 infants born at our institution that had been screened for the disorder during a 4-year period. Fifty-five infants (1.46%) had neonatal polycythemia. Of these infants, 85% had features associated with the disorder. Frequent signs and symptoms included "feeding problems" (21.8%), plethora (20.0%), lethargy (14.5%), cyanosis (14.5%), respiratory distress (9.1%), jitteriness (7.3%), and hypotonia (7.3%). Other findings included hypoglycemia (40.0%) and hyperbilirubinemia (21.8%). Of the polycythemic infants, 14.5% had no clinical symptoms or associated laboratory abnormalities. In the second portion of the study, we reviewed the features of polycythemia in all infants so diagnosed who were born in United States Army hospitals, worldwide, during a 5-year period. There were 220,050 infants born during this period; 932 (0.42%) were diagnosed as having neonatal polycythemia. Frequent findings were hyperbilirubinemia (33.5%), hypoglycemia (13.0%), and respiratory distress (6.6%). In this large group, only 13 (1.4%) had necrotizing enterocolitis, and nine (1.0%) were thrombocytopenic. Several findings among the 932 infants were unexpected. Six of the infants (only one premature) had intracranial hemorrhages. Additionally, three of the 932 had gonadal dysgenesis and three had cystic fibrosis. We found that premature infants were not less prone to having polycythemia and that the overall frequency of the disorder was less than that which has been previously reported.
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PMID:Neonatal polycythemia: frequency of clinical manifestations and other associated findings. 372 98


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