Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parkinson's disease dementia (PDD) ultimately develops in about 80% of patients with Parkinson's disease (PD), and cross-sectional studies have found that some 30% of these patients will experience neuropsychiatric symptoms, such as visual hallucinations and psychosis. The most consistently reported risk factors for dementia in PD are age, severe parkinsonism and mild cognitive impairment. In PDD, both subcortical cognitive and cortical cognitive profiles are described. Specific disorders of sleep, such as rapid eye movement sleep behaviour disorder, excessive daytime sleepiness and sleep attacks, occur frequently. Alzheimer and Lewy body pathology coexist, but the Lewy body pathology in limbic and cortical areas seems to be the main cause of dementia. Neurochemical changes in the biogenic amines and acetylcholine are common, and magnetic resonance imaging studies have shown cortical atrophy in wide cortical areas, including the hippocampus. All PD patients should be screened for mild cognitive impairment and dementia. A large randomised clinical trial showed that the cholinesterase inhibitor rivastigmine has desirable effects on cognition and neuropsychiatric symptoms in PDD patients. Atypical antipsychotic agents may improve psychosis in PDD, but the evidence for this is poor and adverse effects from such therapy are common and may be severe. Non-pharmacological interventions can also be effective but require further study.
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PMID:Management of Parkinson's disease dementia : practical considerations. 1706 84

Impairment in different cognitive domains such as executive functions, language, memory, and visuospatial skills occurs frequently in Parkinson disease (PD) even in the early stages of the disease. Although frank dementia (Parkinson disease dementia, PDD) is less frequent, risk for developing dementia is two to six times greater than the prevalence rate in general population and it increases in relation to disease duration. Clinically, dementia in PD is characterized by uninsidious onset and slowly progressive cognitive decline, with a predominant dysexecutive syndrome accompanied frequently by a variety of behavioral symptoms such as hallucinations, depression, anxiety, and excessive daytime sleepiness. Although the exact pathophysiology and neurobiological basis of PDD is not known, dementia in PD probably develops as a result of progressive involvement of subcortical and cortical structures by Lewy-type pathology and associated Alzheimer-like histological changes. Dysfunction of different monoamine transmitter has also been implicated in the cognitive deterioration of PD but reduced cholinergic activity in the cortex is thought to account for the strongest mechanism in the development of dementia. Recent evidence suggests that cholinesterase inhibitors are effective in the treatment of dementia and accompanying behavioral symptoms in PD.
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PMID:Cognitive dysfunction and dementia in Parkinson disease. 1817 97

Alzheimer's disease (AD) is the most common cause of dementias. Mild cognitive impairment (MCI) indicates the situation that a person has memory complaints and mild objective cognitive impairment but no evidence of dementia. Sleep disturbance, one of the behavioral and psychological symptoms of dementia (BPSD), frequently occurs in patients with AD or MCI. The alteration of sleep architectures in AD patients remains inconclusive. In this study, we conducted the polysomnography. (PSG) examination among patients with mild AD with cholinesterase inhibitors (N=10) or MCI (N=12) and age-matched nondemented controls (N=13). The results showed sleep efficiency, which was one of the important parameters for sleep quality was significantly lower in patients with MCI and AD (N=22), 79.14 +/- 11.06 % vs. 67.07 +/- 19.10 %, p=0.046. There were no statistic differences of sleep architecture but a trend of REM insufficiency in patients with MCI or AD. The mean scores of geriatric depression score (GDS) and Epworth sleepiness scale (ESS) did not differ among the three groups. Our study implicated maintenance of sleep was impaired in patients with cognitive impairment and it was independent with depressive symptoms.
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PMID:Low sleep efficiency in patients with cognitive impairment. 1967 60

Despite improvements to intensive care management and specific pharmacological treatments (atropine, oxime, diazepam), the mortality associated with organophosphate (OP) poisoning has not substantially decreased. The objective of this examination was to describe the role of fresh frozen plasma (FFP) in acute OP poisoning. After a deliberate ingestion of malathion, a 55-year-old male suffering from miosis, somnolence, bradycardia, muscular fasciculations, rales on auscultation, respiratory insufficiency, as well as from an inhibition of red blood cell acetylcholinesterase (AChE) and plasma butyrylcholinesterase (BuChE), was admitted to hospital. Malathion was confirmed in a concentration of 18.01 mg L(-1). Apart from supportive measures (including mechanical ventilation for four days), antidotal treatment with atropine, oxime-pralidoxime methylsulphate (Contrathion(R)), and diazepam was administered, along with FFP. The potentially beneficial effects of FFP therapy included a prompt increase of BuChE activity (from 926 IU L(-1) to 3277 IU L(-1); reference range from 7000 IU L(-1) to 19000 IU L(-1)) and a reduction in the malathion concentration, followed by clinical recovery. Due to BuChE replacement, albumin content, and volume restitution, FFP treatment may be used as an alternative approach in patients with acute OP poisoning, especially when oximes are not available.
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PMID:Fresh frozen plasma as a successful antidotal supplement in acute organophosphate poisoning. 2381 36

We report a case of 30 year old alcoholic male admitted with vomiting, drowsiness, limb weakness and fasciculations after alleged history of consumption of 30 ml of chlorpyriphos insecticide. He had low serum cholinesterase levels. With standard treatment for organophosphorus poisoning (OPP), he improved gradually until day 5, when he developed neck and limb weakness and respiratory distress. This intermediate syndrome was treated with oximes, atropine and artificial ventilation. During treatment, his ECG showed fresh changes of ST elevation. High CPK & CPK-MB levels, septal hypokinesia on 2D echo suggested acute coronary syndrome. Coronary angiography was postponed due to his bedridden and obtunded status. The patient finally recovered fully by day 15 and was discharged. Acute coronary syndrome is a rare occurrence in OP poisoning. The present case thus emphasises the need for careful electrocardiographic and enzymatic monitoring of all patients of organophosphorus poisoning to prevent potential cardiac complication which can prove fatal.
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PMID:Acute organophosphorus poisoning complicated by acute coronary syndrome. 2567 37

Amitraz is used as an ectoparasiticide for dogs and cattle. Human poisoning due to amitraz may be misdiagnosed as organophosphate/carbamate (OPC) toxicity, since amitraz poisoning shares several clinical features (miosis, bradycardia and hypotension) encountered with OPC poisoning. A 19-year-old man with an alleged history of suicidal ingestion of a pesticide presented with drowsiness and was found to have constricted pupils, hypotension and bradycardia. He was diagnosed as a case of OPC poisoning and was treated with atropine and pralidoxime prior to presentation to our centre. Absence of a hypersecretory state, and the presence of hyperglycaemia and hypothermia along with a normal serum cholinesterase level suggested an alternate possibility. Retrieval of the poison container confirmed the diagnosis of amitraz poisoning. The patient made a rapid recovery with supportive management. Clinician awareness is key to successful management of this poisoning, which carries a good prognosis.
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PMID:Amitraz: a mimicker of organophosphate poisoning. 2643 Feb 28

Rivastigmine is a non-competitive reversible inhibitor of acetylcholinesterase which is approved as one of the fi rst-line treatment options for Alzheimer's disease. We present the case of a 33-year-old woman with acute cholinergic syndrome secondary to deliberate rivastigmine poisoning. The patient presented at the emergency department (ED) with drowsy consciousness, dizziness, vomiting, diarrhea, sweating, and hypertension (171/103 mmHg). At the scene, an empty bottle of Rivast 120 mL/Bot, containing rivastigmine 2 mg/mL, was found beside the patient. Two hours later, we noted bronchorrhea and persistent salivation along with drowsiness, agitation, fatigue, incontinence, and limbs paralysis. A notably low serum cholinesterase level (651 U/l) was identified. Acute cholinergic syndrome secondary to rivastigmine intoxication was diagnosed. Endotracheal intubation with ventilator support was required due to respiratory failure. Atropine (0.5 mg intravenous injection) was administered. She was subsequently admitted to the intensive care unit for further care. Extubation was performed on the third day. The patient insisted on being discharged on the second day after extubation, and after administration of a total of 11 mg of atropine, no signs of either intermediate syndrome or delayed polyneuropathywere noted. rivastigmine, an acetylcholinesterase inhibitor, can precipitate an acute cholinergic crisis in cases of intoxication. Typical clinical features of cholinergic excess include increased secretions in the airway and oral cavity, miosis, diarrhea, anxiety, twitching, bronchoconstriction, convulsions, confusion, and gastrointestinal and muscular cramps. The treatment for acute cholinergic crisis is administration of atropine alone or in combination with an antidote to the cholinesterase inhibitor (such as pralidoxime). Patients often recover well with atropine supplements and optimal supportive care.
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PMID:Successful Resuscitation of a Young Girl Who Drank Rivastigmine With Respiratory Failure. 3299 49


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