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)

102 children with acute gastroenteritis were thought by the admitting junior doctors to be 5% or more dehydrated. As judged by subsequent weight recovery in hospital, the main indicators of mild to moderate dehydration were decreased peripheral perfusion, deep breathing, decreased skin turgor, high urea, low pH, and a large base deficit; a history of increased thirst was just short of statistical significance. Dehydration was not indicated by a history of oliguria, by the presence of restlessness or lethargy, sunken eyes, dry mouth, or a sunken fontanelle or by the absence of tears. Clinical signs of dehydration became apparent at 3-4% rather than 5% dehydration. The degree of dehydration was overestimated by a mean of 3.2%; this caused unnecessary hospital admissions and overtreatment with intravenous fluid.
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PMID:Clinical signs of dehydration in children. 257 63

A retrospective study of nine sick premature infants with chronic lung disease who received captopril for control of systemic hypertension (systolic blood pressure (BP) greater than 113 mm Hg) was carried out to determine efficacy of therapy and associated complications. All nine infants had markedly elevated peripheral renin values, 134.3 +/- 128.1 ng/mL/hr (mean +/- SD). Five infants had abnormal renal sonographic and perfusion scans with evidence of renal artery thrombosis, parenchymal disease, or both. Captopril therapy (0.3 mg/kg) was instituted at a postnatal age of 123 +/- 108 days. After the initial dose, the systolic BP decreased significantly in all infants, the decrease ranging from 21% to 58% of the pretreatment value. Dosage was subsequently halved in all infants. Seventeen episodes of unpredictable decreases in BP more than 40% from baseline occurred during the reduced maintenance therapy. Four infants had a total of seven episodes during which the BP decreased by 57 +/- 10% from baseline; this decrease persisted for 17 +/- 6 hours and was unresponsive to volume reexpansion and inotropic therapy. All seven episodes were accompanied by oliguria (urine output less than 1 mL/kg/hr) that persisted for 18 +/- 12 hours. These episodes were accompanied by neurologic signs (subtle seizures, lethargy, and/or apnea) within 18 +/- 6 hours after the onset of oliguria. The remaining five infants had a total of 13 episodes of decreased BP of 50 +/- 8% of baseline, which were of significantly shorter duration and responded to volume reexpanders, inotropic therapy, or both and were unaccompanied by oliguria. These data suggest the need for close observation of BP in infants receiving maintenance captopril therapy.
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PMID:Renal failure in sick hypertensive premature infants receiving captopril therapy. 328 14

Myonecrosis is an unusual sequelae to carbon monoxide poisoning with only 16 cases having been reported in the English-language literature. At the University of Illinois Hospital, we encountered a 25-year-old fire academy student who presented to our Emergency Department with a carboxyhemoglobin level of 16% following a training exercise in a smoke-filled room. The patient was not wearing a self-contained breathing apparatus and his duration of exposure was 7-8 min, by which time he had blacked out for about 1 min. Upon arrival, the patient was lethargic, with a moderate inhalation burn. The patient was treated with hyperbaric oxygen at 2 1/2 ATA. Following 90 min of hyperbaric oxygen, slight flexor compartment weakness, along with tenderness of the proximal lower extremities was noted. CPK was elevated to 65,998 (100% mm) with urine dipstick being positive for blood and only occasional rbc's seen in the urine sediment. The patient did well with forced diuresis and alkalinization of the urine. No oliguria was noted and the CPK fell to 893 five days later. This is the only case in the English-language literature who developed myonecrosis from carbon monoxide, despite hyperbaric oxygen treatment. We believe that this case demonstrates that hyperbaric oxygen cannot prevent the development of myonecrosis induced by carbon monoxide.
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PMID:Myonecrosis in carbon monoxide poisoning. 335 79

We have developed a rabbit model of toxic shock syndrome that uses a subcutaneous infusion pump to administer toxic shock syndrome toxin 1 (TSST-1). A dose of 150 micrograms, infused at a constant rate over a period of 7 days, resulted in a characteristic illness highlighted by fever, conjunctival hyperemia, cachexia, and lethargy. The illness was uniformly fatal, with a mean interval until death of 3.2 +/- 0.4 days. Serial determinations of serum chemistries confirmed the multisystem nature of this illness. Rabbits developed profound hypocalcemia, with levels falling from 15.5 +/- 0.2 to 7.6 +/- 0.4 mg/dl under the influence of TSST-1. Blood urea nitrogen and creatinine rose dramatically, in the setting of oliguria or anuria. Serum glutamicpyruvic transaminase was the most reliable indicator of hepatic dysfunction, with the mean rising from 48 U/liter before administration of TSST-1 to 546 U/liter among rabbits surviving 2 days of the infusion. Creatine phosphokinase also rose dramatically in 10 of 16 rabbits. Rabbits demonstrated relative neutrophilia and lymphopenia as well as an increase in the partial thromboplastin time. Histopathologic examination demonstrated disease of multiple organs, particularly the liver, spleen, and lymph nodes, all of which demonstrated inflammation, thrombosis, hemorrhage, and erythrophagocytosis. The concurrent administration of prednisolone with TSST-1 prevented death in four of four rabbits and greatly lessened the morbidity. Rabbits were not protected from morbidity or mortality by the concurrent administration of polymyxin B. We believe that a constant, subcutaneous infusion of TSST-1 in rabbits provides a reproducible model for studying the pathogenesis of TSS.
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PMID:A rabbit model of toxic shock syndrome that uses a constant, subcutaneous infusion of toxic shock syndrome toxin 1. 357 Apr 55

A review of records from the AnTox database of the American Society for the Prevention of Cruelty to Animals Animal Poison Control Center identified 43 dogs that developed increased blood urea nitrogen concentration, serum creatinine concentration, or both as well as clinical signs after ingesting grapes, raisins, or both. Clinical findings, laboratory findings, histopathological findings, treatments performed, and outcome were evaluated. All dogs vomited, and lethargy, anorexia, and diarrhea were other common clinical signs. Decreased urine output, ataxia, or weakness were associated with a negative outcome. High calcium x phosphorus product (Ca x P), hyperphosphatemia, and hypercalcemia were present in 95%, 90%, and 62% of the dogs in which these variables were evaluated. Extremely high initial total calcium concentration, peak total calcium concentration, initial Ca x P, and peak Ca x P were negative prognostic indicators. Proximal renal tubular necrosis was the most consistent finding in dogs for which histopathology was evaluated. Fifty-three percent of the 43 dogs survived, with 15 of these 23 having a complete resolution of clinical signs and azotemia. Although the mechanism of renal injury from grapes and raisins remains unclear, the findings of this study contribute to an understanding of the clinical course of acute renal failure that can occur after ingestion of grapes or raisins in dogs.
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PMID:Acute renal failure in dogs after the ingestion of grapes or raisins: a retrospective evaluation of 43 dogs (1992-2002). 1623 10

A case of Red-bellied Black snake envenomation resulting in intravascular haemolytic anaemia, rhabdomyolysis and anuric renal failure is described in the dog. A 12-year-old female desexed Golden Retriever was presented with a 15 hour history of profuse salivation, progressive lethargy, obtundence, inappetence and collapse. Significant findings on clinical examination were pallor, icterus, tachypnoea and dyspnoea with increased respiratory sounds and crackles in all lung fields. Generalised abdominal and muscular pain was apparent and dark red-brown urine was present around the perineal region. A diagnosis of Red-bellied Black snake (Pseudechis porphyriacus) envenomation was made and the dog was treated with intravenous fluid therapy, Tiger/Brown snake antivenom, packed red cell transfusions and Intermittent Positive Pressure Ventilation. Continued clinical deterioration occurred and a diagnosis of acute renal failure secondary to myohaemoglobinuric pigmenturia was made 12 hours after admission. Intensive treatment was attempted with diuresis and volume expansion. Oliguria and subsequent anuria ensued and the dog was euthanased due to a grave prognosis and lack of clinical response to treatment. Necropsy examination revealed muscular necrosis, accumulation of fluid in the thoracic and peritoneal cavities, and marked renal tubular necrosis with intraluminal occlusion secondary to pigmentary casts.
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PMID:Anuric renal failure in a dog after red-bellied black snake (Pseudechis porphyriacus) envenomation. 1673 24

A 6-year-old male, Belgian shepherd dog was presented with lethargy, oliguria, hematuria, and reluctance to move. The dog developed hypertrophic osteopathy secondary to renal pelvis transitional cell carcinoma. A nephrectomy was performed and after a year, the dog was completely asymptomatic, and no evidence of metastatic disease was present.
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PMID:Hypertrophic osteopathy associated with renal pelvis transitional cell carcinoma in a dog. 1782 62

A postpartum mare and foal were presented for evaluation of fever and lethargy in the mare. The mare was diagnosed with endometritis and initially responded well to treatment. On the second day of hospitalization, the mare developed renal insufficiency characterized by oliguria, azotemia, hemolysis, and thrombocytopenia. Concurrently, the foal developed rapidly progressive central nervous system signs culminating in refractory seizures. Both animals failed to respond to treatment and were euthanized. Thrombotic microangiopathy involving glomeruli was evident on microscopic examination of the mare's kidneys. Microscopic evidence of brain edema was the principal postmortem finding in the foal. No specific etiology was confirmed in either case. Notably, Escherichia coli 0103:H2 was isolated from the mare's uterus and the gastrointestinal tracts of both animals. To the authors' knowledge, this is the first report in which an organism implicated as a cause of hemolytic-uremic syndrome was isolated from an animal with clinical signs and postmortem findings consistent with the disease.
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PMID:Hemolytic-uremic syndrome in a postpartum mare concurrent with encephalopathy in the neonatal foal. 1831 42

A 3.5-year-old male neutered cat was presented for investigation of renomegaly appreciated during a routine physical examination. Marked renomegaly due to bilateral hydronephrosis was detected and further testing identified International Renal Interest Society stage 2, non-hypertensive, non-proteinuric chronic kidney disease. Ten months later the cat was evaluated for acute lethargy; severe azotemia with oliguria was documented. Medical therapy failed to result in clinical improvement and the cat was euthanased. Necropsy revealed bilateral marked hydronephrosis secondary to a tortuous proximal ureter consistent with proximal ureteropelvic junction stenosis. This is the first report of this disorder leading to progressive renal failure in a cat.
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PMID:Bilateral ureteropelvic junction stenosis causing hydronephrosis and renal failure in an adult cat. 2291 71

Mycoplasma pneumoniae (M. pneumoniae) primarily causes respiratory tract infections in persons aged 5-20 years. Tracheobronchitis and bronchopneumonia are the most commonly recognized clinical symptoms associated with M. pneumoniae infection. Complications of this infection are unusual; in particular, cardiac involvement is very rare and is generally accompanied by pneumonia. Nonrespiratory illness can therefore involve direct invasion by M. pneumoniae or autoimmune mechanisms, as suggested by the frequency of cross reaction between human antigens and M. pneumoniae. Herein, we report a case of severe acute myopericarditis with pneumonia caused by M. pneumoniae in a healthy young child who presented with fever, lethargy, oliguria and dyspnea. She survived with aggressive therapy including clarithromycin, intravenous immunoglobulin, inotropics, and diuretics. The patient was discharged on the 19th day after admission and followed up 1 month thereafter at the outpatient clinic without sequelae.
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PMID:A case of acute myopericarditis associated with Mycoplasma pneumoniae infection in a child. 2317 Jan 1


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