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)

Rosiglitazone is a peroxisome proliferator active receptor. gamma agonist, which increases insulin sensitivity in adipose tissue, muscle, and liver. Rosiglitazone is a member of the thiazolidinedione group, and because of its significantly positive effect on glycemic control, it is especially preferred in type 2 diabetic patients with a high cardiovascular disease risk. This drug, because of its decreasing effect on insulin resistance, is used alone or combined with type 2 diabetic drugs. A 73-year-old female patient was admitted to the emergency department with dyspnea, pink frothing phlegm, cyanosis, and tiredness. She was lethargic, uncooperative, and had no orientation. In arterial blood gases, hypoxemia and hypercapnia were found. She was taken to the general intensive care unit, and oxygen was applied via mask. The patient had a history of 10 years of diabetes mellitus, hypertension, and atherosclerotic cardiac disease, and she was using rosiglitazone for the past 6 weeks. Her chest x-ray was taken, and acute pulmonary edema was diagnosed. In her last echocardiography, which was performed 1 year before, no signs indicating cardiac failure and pleural effusion could be found. Therefore, it was concluded that pulmonary edema occurred as a complication of rosiglitazone use. After stabilizing the patient's vital signs, blood glucose levels, and lactate levels, medical treatment of diabetes mellitus was rearranged, and she was discharged on the seventh day after her admittance. In a patient with diabetes mellitus who has been admitted to the intensive care unit because of acute pulmonary edema, for differential diagnosis, use of rosiglitazone should be kept in mind during the determination of treatment. Therefore, the authors aim to discuss the effect of rosiglitazone on creating acute pulmonary edema with a case report presentation.
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PMID:Acute pulmonary edema due to rosiglitazone use in a patient with diabetes mellitus. 1669 44

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

Metformin is a biguanide. Due to its effects in suppressing the hepatic production of endogenous glucose and in increasing insulin sensitivity in adipose tissue and skeletal muscle, the agent is used particularly in type 2 diabetes mellitus and metabolic syndrome, in which insulin resistance is especially pronounced. Lactic acidosis is one of the most important side effects of metformin. A male patient, born in 1923, was admitted to the emergency unit of our hospital for sudden vertigo, weakness, dyspnea, cyanosis, and lethargy. His history data showed that the patient had been suffering from type 2 diabetes mellitus for 10 years and taking Glargin (insulin), 12 U/kg, once daily and Glucophage (metformin), 850 mg thrice daily. The patient's general condition was fair; stupor, time and spatial orientation were absent. Analysis of arterial blood gases showed the presence of metabolic acidosis, hypokalemia, hypoxemia, and hypercapnia. Thereafter the patient was transferred to the intensive care unit of the hospital; intubated and connected to a T-bird ventilation apparatus. On the following day, an analysis of arterial blood gases indicated the proximity of the results to their physiological parameters. Ventilation was stopped; and monitoring of the patient continued by following the T-shape type of ventilation discontinuation. There were no X-ray signs of pneumonia or pulmonary edema. On the same day, the patient was extubated and oxygen inhalation in a dose of L/min was continued through a mask. On day 4 since therapy was initiated, the patient's vital signs, serum sugar and lactate levels became normal. By determining a new treatment regimen, the patient was discharged from the intensive care unit. Dyspnea, acidosis, and hypoxia developed in the patient resulted from lactic acidosis caused by the use of metformin. It should be remembered that dyspnea, acidosis, and hypoxia, which suddenly developed in metformin-treated patients with type 2 diabetes mellitus, may be caused by lactic acidosis.
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PMID:[A clinical case of development of lactic acid acidosis in a diabetic patient taking metformin]. 1675 49

The present study reports for the first time the incidence of congestive heart failure (CHF) in previously infarcted rats that died spontaneously. Previously, pulmonary (PWC) and hepatic (HWC) water contents were determined in normal rats: 14 control animals were evaluated immediately after sacrifice, 8 placed in a refrigerator for 24 h, and 10 left at room temperature for 24 h. In the infarcted group, 9 rats died before (acute) and 28 died 48 h after (chronic) myocardial infarction. Thirteen chronic animals were submitted only to autopsy (N = 13), whereas PWC and HWC were also determined in the others (N = 15). Seven rats survived 48 h and died during anesthesia. Notably, PWC differed in normal rats: ambient (75.7 +/- 1.3%) < control (77.5 +/- 0.7%) < refrigerator (79.1 +/- 1.4%) and there were no differences with respect to HWC. No clinical signs of CHF (dyspnea, lethargy or foot edema) were observed in infarcted rats before death. PWC was elevated in all chronic and anesthetized rats. HWC was increased in 48% of chronic and in all anesthetized rats. Our data showed that PWC needs to be evaluated before 24 h post mortem and that CHF is the rule in chronic infarcted rats suffering natural death. The congestive syndrome cannot be diagnosed correctly in rats by clinical signs alone, as previously proposed.
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PMID:Incidence of heart failure in infarcted rats that die spontaneously. 1694 Oct 55

Presence of nocturnal symptoms is related to asthma severity. Clinically stable asthmatic children, too, report frequent nocturnal symptoms and sleep disturbances. The study determined these parameters in stable, asthmatic children, in their home environment. This case-control, questionnaire-based study in 70 school-going children comprised 40 asthmatics (Group 1) and 30, age/gender matched, healthy children (Group 2). Parents maintained peak expiratory flow (PEF) and sleep diaries for one week. Group 1 had significantly lower mean morning (250.3 vs. 289.1 I/minute) and mean evening PEF values (261.7 vs. 291.3 I/minute). Group 1 (38.95%), reported frequent nocturnal symptoms like cough (36.90%), breathlessness (32.80%), wheeze (27.68%) and chest tightness (14.35%). Sleep disturbances, significant in Group 1 (38, 95% vs. 14.35%), included daytime sleepiness (24.60%), daytime tiredness (20.50%), difficulty in maintaining sleep (15.38%), early morning awakening (14.35%), struggle against sleep during daytime (12.30%), and involuntarily falling asleep (17.43%). On a scale of 1-6, Group 1 scored significant sleep disturbances/patient (3 vs. 0.8); lethargy/tiredness in morning (2.9 vs. 2.2), poorer sleep quality (4.7 vs. 5.4), less parents' satisfaction with child's sleep (4.5 vs. 5.5) and daytime fitness (4.1 vs. 5.3). Group 1, when exposed to environmental tobacco smoke (22, 55%), reported significant nocturnal symptoms (18/22, 81%) and reduced mean morning and evening PEF values (17/22, 77%). It is concluded that clinically stable, asthmatic children reported increased nocturnal symptoms, sleep disturbances and poorer sleep quality. Lack of awareness of asthma-sleep association and its clinical implications could lead to poor asthma control and impaired daytime activity.
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PMID:Nocturnal symptoms and sleep disturbances in clinically stable asthmatic children. 1713 79

A review of U.S. poison center data for 2004 showed over 40,000 exposures to salicylate-containing products. A guideline that determines the conditions for emergency department referral and pre-hospital care could potentially optimize patient outcome, avoid unnecessary emergency department visits, reduce health care costs, and reduce life disruption for patients and caregivers. An evidence-based expert consensus process was used to create the guideline. Relevant articles were abstracted by a trained physician researcher. The first draft of the guideline was created by the lead author. The entire panel discussed and refined the guideline before distribution to secondary reviewers for comment. The panel then made changes based on the secondary review comments. The objective of this guideline is to assist poison center personnel in the appropriate out-of-hospital triage and initial out-of-hospital management of patients with a suspected exposure to salicylates by 1) describing the process by which a specialist in poison information should evaluate an exposure to salicylates, 2) identifying the key decision elements in managing cases of salicylate exposure, 3) providing clear and practical recommendations that reflect the current state of knowledge, and 4) identifying needs for research. This guideline is based on an assessment of current scientific and clinical information. The expert consensus panel recognizes that specific patient care decisions may be at variance with this guideline and are the prerogative of the patient and the health professionals providing care, considering all of the circumstances involved. This guideline does not substitute for clinical judgment. Recommendations are in chronological order of likely clinical use. The grade of recommendation is in parentheses: 1) Patients with stated or suspected self-harm or who are the victims of a potentially malicious administration of a salicylate, should be referred to an emergency department immediately. This referral should be guided by local poison center procedures. In general, this should occur regardless of the dose reported (Grade D). 2) The presence of typical symptoms of salicylate toxicity such as hematemesis, tachypnea, hyperpnea, dyspnea, tinnitus, deafness, lethargy, seizures, unexplained lethargy, or confusion warrants referral to an emergency department for evaluation (Grade C). 3) Patients who exhibit typical symptoms of salicylate toxicity or nonspecific symptoms such as unexplained lethargy, confusion, or dyspnea, which could indicate the development of chronic salicylate toxicity, should be referred to an emergency department (Grade C). 4) Patients without evidence of self-harm should have further evaluation, including determination of the dose, time of ingestion, presence of symptoms, history of other medical conditions, and the presence of co-ingestants. The acute ingestion of more than 150 mg/kg or 6.5 g of aspirin equivalent, whichever is less, warrants referral to an emergency department. Ingestion of greater than a lick or taste of oil of wintergreen (98% methyl salicylate) by children under 6 years of age and more than 4 mL of oil of wintergreen by patients 6 years of age and older could cause systemic salicylate toxicity and warrants referral to an emergency department (Grade C). 5) Do not induce emesis for ingestions of salicylates (Grade D). 6) Consider the out-of-hospital administration of activated charcoal for acute ingestions of a toxic dose if it is immediately available, no contraindications are present, the patient is not vomiting, and local guidelines for its out-of-hospital use are observed. However, do not delay transportation in order to administer activated charcoal (Grade D). 7) Women in the last trimester of pregnancy who ingest below the dose for emergency department referral and do not have other referral conditions should be directed to their primary care physician, obstetrician, or a non-emergent health care facility for evaluation of maternal and fetal risk. Routine referral to an emergency department for immediate care is not required (Grade C). 8) For asymptomatic patients with dermal exposures to methyl salicylate or salicylic acid, the skin should be thoroughly washed with soap and water and the patient can be observed at home for development of symptoms (Grade C). 9) For patients with an ocular exposure of methyl salicylate or salicylic acid, the eye(s) should be irrigated with room-temperature tap water for 15 minutes. If after irrigation the patient is having pain, decreased visual acuity, or persistent irritation, referral for an ophthalmological examination is indicated (Grade D). 10) Poison centers should monitor the onset of symptoms whenever possible by conducting follow-up calls at periodic intervals for approximately 12 hours after ingestion of non-enteric-coated salicylate products, and for approximately 24 hours after the ingestion of enteric-coated aspirin (Grade C).
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PMID:Salicylate poisoning: an evidence-based consensus guideline for out-of-hospital management. 1736 28

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

A 3-year-old neutered male British shorthair cat was presented to the Clinic for Small Animal Medicine, Internal Medicine and Clinical Pathology, at the Justus-Liebig-University Giessen with a short history of lethargy, severe dyspnoea, fever, anaemia, thrombocytopenia and hyperbilirubinaemia. In blood smears and lymph node aspirates, large pleomorphic lymphatic blasts were detected. On necropsy splenic infarcts and moderate hydrothorax as well as moderate ascites could be observed. Histological examination revealed large numbers of lymphoid blasts within the lumen of the vessels of the lung, lymph nodes, the liver, the chorioid coat of the eyes, in meningeal vessels, arteries and veins of the brain, and within the larger splenic vessels. Neoplastic cells immunohistochemically stained positive for CD45R and CD3. Based on these findings, an intravascular lymphoma was diagnosed.
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PMID:A case of intravascular lymphoma with mixed lineage antigen expression in a cat. 1804 42

Over the course of 4 weeks, two female aged bonnet macaque (Macaca radiata) group-housed females died after the dominant male was removed from the group and the newly dominant male persistently chased, caught and bred all females in the pen. The two aged affected females were observed exhibiting lethargy, dyspnea, with widespread necroulcerative lesions in and around the mouth, muzzle and bridge of their noses. Extensive ulcerative glossitis, necrotic bronchopneumonia with intra-nuclear inclusions and the absence of other evidence is highly suggestive that death was caused by an alphaherpes virus commonly known as herpes B virus. Herpes B virus is a potentially zoonotic disease periodically shed by macaques, which is structurally related to herpes simplex viruses I and II of humans. The emergence of fatal B virus to primates in this pen may have been associated with the combination of age and stress in the affected individuals.
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PMID:Lethargy, ulcers, bronchopneumonia and death in two aged female bonnet macaques presumed to be caused by Cercopithicine herpes virus I. 1826 31

It remains unclear whether advances in the understanding of the pathophysiology and improvements in cardiovascular imaging over the years have impacted the clinician's recognition of cardiac tamponade (CT). We sought to evaluate signs and symptoms of CT in a present-day population and compare it to a similar group from a decade prior. We performed a retrospective analysis of two cohorts of patients presenting to a tertiary hospital with CT, all of whom underwent pericardial drainage (PD). Group 1 (Gp1) included subjects presenting from 1988 to 1991 and Group 2 (Gp2) included subjects from 2002 to 2005. Fifty-five patients comprised each group, with an average age of 55 years. Seventy-one percent of patients in Gp1 had identifiable cardiovascular symptoms 1 week prior to presentation, compared to 33% in Gp2. Dyspnea was the most common symptom in both groups, and was less frequent in Gp2. Compared with Gp1, chest pain, cough, and lethargy were also less frequent in Gp2. One day prior to PD, tachypnea and pulsus paradoxus were detected more frequently in Gp1 compared to Gp2. Large, circumferential pericardial effusions were the most frequent echocardiographic findings in both groups and the most common etiology of CT was malignancy in Gp1and postoperative bleeding in Gp2. Thus, the recognition of symptoms and physical signs in patients presenting with CT has changed over the past decade, as has etiology of pericardial effusions. However, the diagnosis of CT still remains delayed, and the present data emphasize the need for a heightened index of suspicion for recognizing this hemodynamically-important process.
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PMID:Has the clinical presentation and clinician's index of suspicion of cardiac tamponade changed over the past decade? 1830 35


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