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)

This report describes the clinical, roentgenologic, pathologic, and virologic findings in a 2 years and ten months old girl who died from a severe pneumonia. Initially, the patient presented with fever and cough for 2 days. Physically, the patient appeared lethargic, and breathing sounds revealed diffuse rales and wheezing. Hemogram showed mild leukocytosis and lymphocyte predominant. Chest X ray revealed diffuse interstitial infiltration of the right upper lung, left upper and left lower lung field. Bacteria infection was first impressed. Although treated with several antibiotics (ampicillin, cefuroxime, amikacin, penicillin, cephazolin, imipenem and vancomycin) in three different hospitals, the patient's condition went downhill and the patient died 2 weeks later. Finally, adenoviurs type 3 was isolated from sputum specimen taken before death and necropsy lung tissue. The lung pathology showed diffuse necrotizing inflammation with fibrinopurulent exudate, and eosinophilic intranuclear inclusion bodies were also noted in the alveolar cells. These data proved the diagnosis of adenovirus pneumonia. This case adds to the evidence that adenovirus type 3 infection during childhood may cause fatal disease.
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PMID:A fatal case of viral pneumonia in a child infected with adenovirus type 3. 227 28

We studied the relation between the amount of textile and other soft fiber wall materials used in the office and the symptoms related to sick building syndrome in two identical, mechanically ventilated, eight-story office buildings. The study population consisted of 400 workers (85% of the source population): 264 males (66%) and 136 females (34%). A self-administered questionnaire inquired about the occurrence of symptoms and related personal and environmental determinants. The office environment was assessed concurrently. Exposure was defined as the surface area of textile or other soft wall material (SWM) in the office. The outcomes were formed using the 7-d prevalences of individual symptoms, including mucosal irritation score (eye irritation, nasal dryness, nasal congestion, pharyngeal irritation); allergic reaction score (eye irritation, nasal congestion, nasal excretion, sneezing); asthma reaction score (wheezing, breathlessness, cough); skin reaction score (dryness, itch, or irritation, rash); and general symptom score (headache, lethargy). In the logistic regression controlling for potential confounders, the adjusted odds ratio for the symptoms of mucosal irritation was 1.82 (95% confidence interval [95% CI] = 1.14, 2.90) in the low-exposure group, compared with the unexposed reference group; and 2.46 (95% CI = 1.15, 5.28) in the high-exposure group, compared with the reference group. Corresponding odds ratios for the symptoms of allergic reaction were 1.82 (95% CI = 1.14, 2.90) and 3.16 (95% CI = 1.41, 7.09). No difference was found in the risk for asthmatic or skin reactions or general symptoms. The results support a hypothesis that textile and other soft-fiber wall materials used in the office environment are possible determinants of sick building syndrome.
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PMID:Textile wall materials and sick building syndrome. 818 88

The developmental toxicity of glycolic acid was assessed in rats by orally administering solutions of the test material in water over days 7-21 of gestation (the day of copulation plug detection was defined as day 1 of gestation). Groups of 25 mated female Crl: CD BR rats were gavaged at daily dose levels of 0, 75, 150, 300 or 600 mg/kg. The dams were euthanized on day 22 and the offspring were weighed, sexed, and examined for external, visceral, and skeletal alterations. Clear evidence of maternal toxicity was demonstrated at 600 mg/kg; adverse clinical observations were statistically significantly increased (wheezing/lung noise, abnormal gait/staggering, lethargy). In addition, maternal body weights, weight changes, and food consumption were statistically significantly reduced at this dose level. Marginal evidence of maternal toxicity was demonstrated at 300 mg/kg; wheezing/lung noise similar to that seen at 600 mg/kg was observed in 2 of 25 dams. This increase approached statistical significance (p = 0.0553). There was marked evidence of developmental toxicity at 600 mg/kg. Mean fetal weight was statistically significantly reduced while the incidences of skeletal (ribs, vertebra, and sternebra) malformations and variations were statistically significantly increased. At 300 mg/kg/day, there was a slight (2 affected fetuses from 2 litters) increase in the incidence of two skeletal malformations: fused ribs and fused vertebra. Although these increases were not statistically significant (p = 0.0555), they were consistent with findings seen at 600 mg/kg/day and thus were considered relevant. There was no other evidence of developmental toxicity at 300 mg/kg/day nor was any developmental toxicity seen at 150 or 75 mg/kg/day. Thus, the maternal and developmental no-observed-effect level (NOEL) was considered 150 mg/kg.
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PMID:Developmental toxicity study of glycolic acid in rats. 1053 49

The Helsinki Office Environment Study, a population-based cross-sectional study was carried out in Finland in 1991 among 2,678 workers in 41 randomly selected office buildings. The aim was to evaluate the relations between work with office equipment and supplies and the occurrence of eye, nasopharyngeal, skin, and general symptoms (often denoted as sick building syndrome (SBS)), chronic respiratory symptoms, and respiratory infections. Work with self-copying paper was significantly related to weekly work-related eye, nasopharyngeal, and skin symptoms, headache and lethargy, as well as to the occurrence of wheezing, cough, mucus production, sinusitis, and acute bronchitis. Photocopying was related to nasal irritation, and video display terminal work to eye symptoms, headache, and lethargy.
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PMID:Office equipment and supplies: a modern occupational health concern? 1099 50

RSV is the most important respiratory pathogen in infants and young children. About 1% of primary RSV infections result in hospitalization. The virus is spread by large droplets of secretions or contact with contaminated secretions. Infants infected with RSV may demonstrate poor feeding, rhinorrhea, apnea, lethargy, wheezing, and respiratory distress. Diagnosis may be made by clinical signs and symptoms (especially those observed during epidemics), by chest radiographs showing hyperinflation, or by rapid antigen detection with immunofluorescence of nasopharyngeal aspirates. Risk factors for severe disease accompanied by complications include chronic heart disease, chronic lung disease, immunodeficiency, HIV, and prematurity. Immunity is incomplete and of short duration, and reinfection is common. Treatment remains supportive and consists of oxygen administration, hydration, and diligent monitoring. Use of corticosteroids, bronchodilators, antibiotics, and ribavirin is controversial and is dependent largely on physician preference. Use of ribavirin should be reserved for patients who have severe underlying conditions associated with increased mortality rates. Intravenous RSV Ig has been replaced by palivizumab, which is generally recommended for infants at high risk for severe RSV, including those with a history of prematurity and those with chronic lung disease.
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PMID:RSV infection in infants and young children. What's new in diagnosis, treatment, and prevention? 1060 68

Biotinidase deficiency is a treatable cause of severe neurological disorders and skin problems. Spinal cord impairment is a rare complication of this disease and is commonly unrecognized. The authors encountered 3 Chinese patients with progressive spinal cord demyelination associated with biotinidase deficiency. Case 1 exhibited fatigue, proximal muscular weakness, and hypotonic paraplegia from the age of 7 years 4 months. Demyelination of cervical and thoracic cord was evident on magnetic resonance imaging (MRI). Case 2 developed visual impairment, blepharoconjunctivitis, and optic nerve atrophy from 5 years of age, which combined with progressive hypertonic paralysis, ataxia, and alopecia from the age of 7 years. His spinal MRI T2-weighted sequence revealed an extensive hyperintense lesion involving the cervical spinal cord C(2) to C(4). Bilateral optic nerves were significantly thick. In case 3, intercurrent wheezing, tachypnea, dyspnea, and lethargy occurred from the age of 1 year. Medulla and upper cervical spine edema and demyelination were found on MRI. Markedly elevated urine organic acids and decreased blood biotinidase activities were observed in the 3 patients. Biotin supplementation led to a dramatic improvement of clinical symptoms in 3 patients. The findings indicate that biotinidase deficiency should be considered in the differential diagnosis of unexplained spinal cord demyelination because prompt diagnosis and treatment with biotin may enable an excellent recovery.
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PMID:Spinal cord demyelination associated with biotinidase deficiency in 3 Chinese patients. 1762 76

One may have only minutes to change the trajectory of a child who is deteriorating from either congenital or acquired cardiac disease. However, these children may present with rather cryptic patterns of symptoms (e.g. failure to thrive, lethargy, colic, neonatal shock, respiratory distress, wheezing and syncope with exercise). Thus, it is essential that any health care practitioner who cares for children be familiar with key clinical presentations that require consideration of underlying cardiac disease and time sensitive diagnoses that require rapid recognition and therapy in order to optimize the chances of saving the child's life. The objectives of this manuscript are: 1) to review the initial identification and management of cardiac emergencies in children; and 2) to present a brief summary of key cardiac diagnoses that may need to be considered when caring for children in an acute care setting.
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PMID:Recognition and initial management of cardiac emergencies in children. 1932 20

A 3-y-old male rhesus macaque (Macaca mulatta) was noticed to be lethargic in the compound. Physical exam revealed cyanotic mucous membranes, dyspnea, bilateral harsh lung sounds, wheezing on expiration, and a firm mass possibly associated with the liver. Radiographs revealed bilateral soft tissue opacities in the thorax. Due to poor prognosis, the rhesus was euthanized, and a necropsy was performed. Both right and left lung lobes were consolidated and had multifocal white-tan masses. On cut section, the masses were firm, had areas of necrosis, hemorrhage, and often contained a tenacious exudate. Masses were identified in the liver and both kidneys. Given the morphologic features of the neoplasm, a diagnosis of squamous cell carcinoma was made. Immunohistochemistry staining for thyroid transcription factor, a nuclear transcription factor normally found in lung, thyroid, and tumors arising from either of those tissues, confirmed that the masses originated from the lung. Malignant primary lung tumors are divided into 8 main histologic subtypes: squamous cell carcinoma, small-cell carcinoma, large-cell carcinoma, adenocarcinoma, adenosquamous carcinoma, sarcomatoid carcinoma, carcinoid tumor, and salivary gland tumors. Clinical signs associated with lung tumors include, but are not limited to, dyspnea, coughing, hemoptysis, lethargy, anorexia, and weight loss. Although squamous cell carcinoma will be low on the differential list for these clinical signs, we encourage clinicians and researchers to not rule it out solely based on incidence and age of the animal.
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PMID:Spontaneous primary squamous cell carcinoma of the lung in a rhesus macaque (Macaca mulatta). 2164 39

Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-, cell-mediated food allergy of unknown prevalence and pathophysiology. Onset is typically during the first year of life; seafood-induced FPIES may start in adulthood. Acute FPIES manifests within 1-4 hours after ingestion with repetitive emesis, pallor, and lethargy progressing to dehydration and hypovolemic shock in 15% of cases. Chronic FPIES manifests with intermittent emesis, watery diarrhea, and poor growth progressing to dehydration and hypovolemic shock over a period of days to weeks. Chronic FPIES has been only reported in infants aged less than 3 months fed with cow milk (CM) or soy formula. The most common triggers are CM, soy, rice, and oat. Diagnosis of FPIES relies on recognition of a pattern of clinical symptoms and may be missed owing to the absence of typical allergic symptoms (eg, urticaria, wheezing) and delayed onset in relation to food ingestion. Physician-supervised food challenge is recommended if diagnosis or the trigger food is not clear and to evaluate for resolution. Testing for food-specific IgE is usually negative, although a subset of patients, usually with CM-induced FPIES may develop sensitization to foods. Such atypical FPIES tends to have a more prolonged course. Despite the potential severity of the reactions, no fatalities have been reported, and FPIES has a favorable prognosis. In most cases, FPIES resolves by age 3-5 years, although persistence of CM-induced FPIES and soy FPIES into adulthood has been reported. The first international consensus guidelines on diagnosis and management of FPIES were published in 2017. Given that the pathophysiology of FPIES is poorly understood, there are no diagnostic biomarkers and no therapies to accelerate resolution. These unmet needs warrant future investigations to improve the care of patients with FPIES.
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PMID:Food Protein-Induced Enterocolitis Syndrome. 2821 41