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)

Ten bitches with urinary incontinence due to incompetence of the urethral sphincter mechanism were treated with phenylpropanolamine hydrochloride at a dose of either 1 mg/kg orally three times daily or 2 mg/kg orally once daily in a prolonged release formulation. The signs of incontinence resolved in all the bitches, and improvements were maintained over periods ranging from one to more than two years, except in one bitch which became refractory to treatment after three months. One bitch which was inadvertently treated at a dose rate of 2.5 mg/kg showed signs of lethargy and inappetence but returned to normal when the dose rate was reduced.
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PMID:Phenylpropanolamine: an alpha-adrenergic agent for the management of urinary incontinence in the bitch associated with urethral sphincter mechanism incompetence. 259 66

Two elderly patients, who were chronically receiving aspirin, developed lethargy, incontinence, and confusion after dosing with acetazolamide. Unbound plasma acetazolamide concentrations were elevated and plasma protein binding was reduced, suggesting an interaction with aspirin. In vitro studies demonstrated a concentration-dependent effect of salicylate on acetazolamide binding to serum proteins. At a therapeutic serum acetazolamide level of 8.0 micrograms/ml, the unbound percentage of acetazolamide in serum was 3.3% and increased to 11.0% and 30.0%, with serum salicylate levels of 200 and 386 micrograms/ml, respectively. Furthermore, the apparent association constant of acetazolamide for binding to serum proteins was decreased by 58% and 86% of its control value at these respective salicylate concentrations. The maximal binding capacity of serum for acetazolamide was not affected by salicylate. Pharmacokinetic studies in four volunteers showed that the plasma protein binding and renal clearance of acetazolamide were significantly reduced during chronic salicylate dosing. Salicylate appears to competitively inhibit the plasma protein binding of acetazolamide and simultaneously to inhibit acetazolamide renal tubular secretion. Caution is advised when acetazolamide and salicylate are used concurrently.
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PMID:Toxic interaction between acetazolamide and salicylate: case reports and a pharmacokinetic explanation. 376 83

The value of the PCR for CMV in the CSF was evaluated. 23 samples from 20 patients were examined for CMV DNA, of which 11 were positive and 12 were negative for CMV. The clinical spectrum of the patients with positive samples included encephalitis, encephalitis, and polyradiculopathy, or isolated polyradiculopathy. The main symptoms were fever, confusion, lethargy, cognitive disturbance, cranial neuropathy, weakness of the legs, and incontinence. The laboratory evaluation showed a low CD4 lymphocyte count, a slightly increased blood sedimentation rate and a large variation of CSF patterns. The CMV early antigen tests were negative in all cases. In 4 cases the neuroradiological examination was compatible with CMV infection. 8 patients were treated with ganciclovir or foscarnet. Improvement of symptoms was observed in 2 cases and stabilization in 2 others. However, the CMV infection was rapidly progressive and 9 out of 10 patients died after a mean of 53 days after diagnosis.
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PMID:[Clinical value of a polymerase chain reaction on cytomegalovirus DNA in cerebrospinal fluid in HIV patients with neurological symptoms]. 774 Feb 95

A 74-year-old man became delirious 2 days after beginning oral therapy with methazolamide. The delirium was manifested by intermittent psychosis, incontinence of bowel and bladder, lethargy, and disorientation. These symptoms continued for 25 days despite many changes in his drug regimen, and complete laboratory, urologic, and neurologic work-ups. The symptoms resolved completely within 1 week of discontinuing methazolamide. This is the first case reported of delirium associated with methazolamide not accompanied by a metabolic imbalance.
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PMID:Methazolamide-induced delirium. 908 35

Although drug-drug interactions constitute only a small proportion of adverse drug reactions, they are important because they are often predictable and therefore avoidable or manageable. Their frequency is related to the age of the patient, the number of drugs prescribed, the number of physicians involved in the patient's care and the presence of increasing frailty. The most important mechanisms for drug-drug interactions are the inhibition or induction of drug metabolism, and pharmacodynamic potentiation or antagonism. Interactions involving a loss of action of one of the drugs are at least as frequent as those involving an increased effect. It is likely that only about 10% of potential interactions result in clinically significant events and, while death or serious clinical consequences are rare, low-grade, clinically unspectacular morbidity in the elderly may be much more common. Nonspecific complaints (e.g. confusion, lethargy, weakness, dizziness, incontinence, depression, falling) should all prompt a closer look at the patient's drug list. There are a number of strategies that can be adopted to decrease the risk of potential clinical problems. The number of drugs prescribed for each individual should be limited to as few as is necessary. The use of drugs should be reviewed regularly and unnecessary agents withdrawn if possible, with subsequent monitoring. Patients should be encouraged to engage in a 'prescribing partnership' by alerting physicians, pharmacists and other healthcare professionals to symptoms that occur when new drugs are introduced. Physicians with a responsibility for elderly people in an institutional setting should develop a strategy for monitoring their drug treatment. For those interactions that have come to clinical attention, it is important to review why they happened and to plan for future prevention. Clinicians should also report, via the appropriate postmarketing surveillance scheme, any drug-drug interactions they have encountered. Finally, multidisciplinary education about the nature of physiological aging and its effect on drug handling, and the possible presentations of drug-related disease in older patients, is an important element in reducing interactions in the elderly.
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PMID:Important drug-drug interactions in the elderly. 963 96

Here, we report the case of a five-year-old boy with carbonic monoxide (CO) poisoning. The patient initially recovered after the initiation of hyperbaric oxygen (HBO) therapy, but lethargy as well as visual and gait disturbances appeared two days later. Left hemiparesis and mood lability also subsequently appeared. Slow frontal activity was noted on electroencephalography, while fluid-attenuation inversion recovery and diffusion-weighted magnetic resonance imaging (MRI) revealed high signal-intensity lesions in the hippocampus and deeper layers of the occipital and frontal cerebral cortex. The neurological symptoms subsided gradually during the 10-day course of HBO therapy, but the left-hand paresis and quadrantic hemianopsia persisted, in association with impaired attention, slow mental processing, and incontinence. Lesions in the globus pallidum were noted on follow-up MRI at 14 days, and cortical lesions became evident as linear, low signal-intensity areas on T1-weighted imaging 4 months after presentation. Delayed neuropsychiatric syndrome in CO poisoning is rare in childhood, although children should be carefully monitored after CO exposure. The finding of cortical laminar necrosis in this patient is quite atypical in CO poisoning, and suggests a broader and previously nonpredicted pathomechanism in this condition.
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PMID:Delayed neuropsychiatric syndrome in a child following carbon monoxide poisoning. 1700 41

An 18-year-old male neutered domestic shorthair cat was presented for investigation of haematuria and lethargy. The cat had sustained a traumatic T3-L3 lesion 5 years prior resulting in upper motor neuron incontinence. On further investigation the cat was found to be hyperkalaemic, hypothermic and dehydrated. Ultrasonography of the bladder revealed a markedly hypoechoic, thickened bladder wall with an irregular, hyperechoic mucosal layer. The patient responded to symptomatic and supportive care and was discharged. Despite initial improvement, the patient returned 10 days after discharge with recurrence of haematuria and lethargy. Ultrasound-guided aspiration and culture of the material on the mucosal surface of the bladder confirmed diagnosis of UTI caused by Corynebacterium urealyticum. On post-mortem examination, gross and histopathological features were consistent with encrusting cystitis. This is the first case report of encrusting cystitis in a cat. C urealyticum, an uncommon urinary tract pathogen in small animals, should be considered in patients with predisposing conditions.
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PMID:Encrusting cystitis in a cat secondary to Corynebacterium urealyticum infection. 2104 Nov 6

We report a case of a patient with newly diagnosed, locally extensive and cystic, suprasellar papillary craniopharyngioma successfully treated with single-agent Dabrafenib. The patient was symptomatic with gait imbalance with falls, lethargic episodes, fatigue and incontinence. Diagnostic imaging demonstrated a cystic suprasellar tumor extending into the third ventricle causing obstructive hydrocephalus. The tumor was partially debulked, and bilateral shunts were placed. NGS sequencing demonstrated BRAF V600E mutation, and the patient was prescribed dual agent Dabrafenib and Trametinib. However, due to insurance denial for Trametinib, he only received single-agent Dabrafenib (150mg BID). The treatment resulted in a major response (over two years), including reduction of the tumor cyst, and improvement of the clinical symptoms. No adverse events have been reported. The patient continues on Dabrafenib (150 mg BID) with a steady reduction in tumor size, and improvement in cognitive function leading to independent living.
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PMID:Newly diagnosed papillary craniopharyngioma with BRAF V600E mutation treated with single-agent selective BRAF inhibitor dabrafenib: a case report. 3166 33