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)

Recombinant preparations of the cytokine interferon (IFN)-alpha are increasingly used to treat a number of medical conditions, including chronic viral hepatitis and several malignancies. Although frequently effective, IFN alpha induces a variety of neuropsychiatric adverse effects, including an acute confusional state that develops rapidly after initiation of high-dose IFN alpha, a depressive syndrome that develops more slowly over weeks to months of treatment, and manic conditions most often characterised by extreme irritability and agitation, but also occasionally by euphoria. Acute IFN alpha-induced confusional states are typically characterised by disorientation, lethargy, somnolence, psychomotor retardation, difficulties with speaking and writing, parkinsonism and psychotic symptoms. Strategies for managing delirium should be employed, including treatment of contributing medical conditions, use of either typical or atypical antipsychotic agents and avoidance of medications likely to worsen mental status. Significant depressive symptoms occur in 21-58% of patients receiving IFN alpha, with symptoms typically manifesting over the first several months of treatment. The most replicated risk factor for developing depression is the presence of mood and anxiety symptoms prior to treatment. Other potential, but less frequently replicated, risk factors include a past history of major depression, being female and increasing IFN alpha dosage and treatment duration. The available data support two approaches to the pharmacological management of IFN alpha-induced depression: antidepressant pretreatment or symptomatic treatment once IFN alpha has been initiated. Pretreatment might be best reserved for patients already receiving antidepressants or for patients who endorse depression or anxiety symptoms of mild or greater severity prior to therapy. Several recent studies demonstrate that antidepressants effectively treat IFN alpha-induced depression once it has developed, allowing the vast majority of subjects to complete treatment successfully. Recent data suggest that IFN alpha-induced depression may be composed of two overlapping syndromes: a depression-specific syndrome characterised by mood, anxiety and cognitive complaints, and a neurovegetative syndrome characterised by fatigue, anorexia, pain and psychomotor slowing. Depression-specific symptoms are highly responsive to serotonergic antidepressants, whereas neurovegetative symptoms are significantly less responsive to these agents. These symptoms may be more effectively treated by agents that modulate catecholaminergic functioning, such as combined serotonin-noradrenaline (norepinephrine) antidepressants, bupropion, psychostimulants or modafinil. Additional factors to consider in selecting an antidepressant include potential drug-drug interactions and adverse effect profile. Finally, IFN alpha appears capable of inducing manic symptoms. Mania, especially when severe, is a clinical emergency. When this occurs, IFN alpha and antidepressants should be stopped, an emergency psychiatric consultation should be obtained, and treatment with a mood stabilizer should be initiated.
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PMID:Neuropsychiatric adverse effects of interferon-alpha: recognition and management. 1569 25

The differential diagnoses for mental status alteration is broad. Endocrine or metabolic causes for emergency department patients who present with lethargy, anxiety, psychosis, and seizures should be considered. Using the complaint-based approach, this article discusses some of the often less obvious etiologies for these presentations related to endocrine and metabolic disease states.
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PMID:Altered mental status due to metabolic or endocrine disorders. 1598 51

Pellagra is a systemic disturbance caused by a cellular deficiency of niacin, resulting from inadequate dietary nicotinic acid and/or its precursors, the essential amino-acid tryptophan. In Europe and North America cases of pellagra are rarely encountered, but in some developing countries this disease is frequent, and is the most frequent clinical feature of nutritional deficiency of adult. The principal causes of pellagra are: nutritional niacin deficiency; chronic alcoholism; gastro-intestinal malabsorption; some medications (5-fluoro-uracil, isoniazid, pyrazinamide ehtionamide, 6-mercaptopurine, hydantoins, phenobarbital and chloramphenicol). The diagnosis of pellagra is based on the patient's history and the presence of "3 D syndrome": dermatitis, diarrhea, and dementia. The dermatitis caused by pellagra is a bilaterally symmetrical erythema at the sites of solar exposure. The dermatitis begins in the form of an erythema with acute or intermittent onset gradually changing to an exsudative eruption on the dorsa of the hand, face, neck, and chest with pruritus and burning. Acute dermatitis of pellagra resembles sunburn in the first stages, sometimes with vesicles and bullae. The gastro-intestinal disturbances are: anorexia, nausea, epigastric discomfort and chronic or recurrent diarrhea. Anorexia and malabsorbative diarrhea lead to a state of malnutrition and cachexia. Stools are typically watery, but occasionally can be bloody and mucoid. Neuropsychologic manifestation included photophobia, asthenia, depression, hallucinations, confusions, memory loss and psychosis. As pellagra advances, patient become disoriented, confused and delirious; then stuporous and finally die. Pathological changes in the skin is non-specific, there are no chemical tests available to definitively diagnose pellagra. However low levels of urinary excretion of N-methylnicotinamide and pyridone indicates niacin deficiency. The treatment of pellagra consisted to exogenous administration of niacin or nicotinamide cures. Topical management of skin lesions with emollients may reduce discomfort. The therapy should also include other B vitamins, zinc and magnesium as well as a diet rich in calories. The prevention is based in the nutritional education (food sources of niacin: eggs, bran, peanuts, meat, poultry, fish, red meat, legumes and seeds), and the eviction of alcohol.
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PMID:[Pellagra]. 1620 85

The case of a 63-year-old woman who presented with status epilepticus, coma and hypoventilation is reported. A primary neurological cause was considered. Hypothermia led to further investigations and a diagnosis of severe hypothyroidism. The neurological complications of hyperthyriodism include alteration in mental status with slowness, decreased concentration and lethargy, headache, cranial nerve palsies, dysarthria, hoarseness, myopathy, neuropathy, reflex changes, ataxia, and psychotic episodes. Our patient suffered from a rare consequence of severe hypothyroidism presenting with status epilepticus and she died despite treatment. To our knowledge this is the second patient to be reported with myxoedema coma with this kind of presentation. Despite therapeutic options, there is a high mortality rate.
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PMID:Status epilepticus caused by a myxoedema coma. 1712 58

Psychogenic polydipsia (PPD), a clinical disorder characterized by polyuria and polydipsia, is a common occurrence in inpatients with psychiatric disorders. The underlying pathophysiology of this syndrome is unclear, and multiple factors have been implicated, including a hypothalamic defect and adverse medication effects. Hyponatremia in PPD can progress to water intoxication and is characterized by symptoms of confusion, lethargy, and psychosis, and seizures or death. Evaluation of psychiatric patients with polydipsia warrants a comprehensive evaluation for other medical causes of polydipsia, polyuria, hyponatremia, and the syndrome of inappropriate secretion of antidiuretic hormone. The management strategy in psychiatric patients should include fluid restriction and behavioral and pharmacologic modalities.
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PMID:Psychogenic polydipsia review: etiology, differential, and treatment. 1752 21

We report two cases of serotonin syndrome in elderly patients during treatment of psychotic depression with atypical antipsychotics and antidepressants. The first case is a 69-year-old man who was admitted for depression with psychosis and treated with trazodone, risperidone, and sertraline. Subsequently, he developed myoclonus, tremor, cogwheel rigidity, and diaphoresis. The second case is a 72-year-old female initially admitted to a medical inpatient unit for a change in mental status that presented as increased confusion, lethargy, slurred speech, and a fever of 101.5 degrees. She had been on phenelzine and quetiapine. In both cases, all symptoms resolved within 24 hours of the psychotropics being stopped. In both cases, we believe that serotonin syndrome was produced by a combination of an antidepressant and an atypical antipsychotic. There have been several case reports of serotonin syndrome from similar combinations of antidepressant and atypical antipsychotic treatment. Clinicians treating elderly patients with a combination of serotonergic antidepressants and atypical antipsychotics for psychotic depression should be aware of the potential for serotonin syndrome.
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PMID:Serotonin syndrome in elderly patients treated for psychotic depression with atypical antipsychotics and antidepressants: two case reports. 1766 87

We report 10 children (7 male, 3 female), 3 homozygous for c.319C>T mutation and 7 heterozygous for c.319C>T on one allele and c.625G>A variant on the other in the short-chain acyl-CoA dehydrogenase (SCAD) gene (ACADS). All were of Ashkenazi Jewish origin in which group we found a c.319C>T heterozygote frequency of 1:15 suggesting the presence of a founder mutation or selective advantage. Phenotype was variable with onset from birth to early childhood. Features included hypotonia (8/10), developmental delay (8/10), myopathy (4/10) with multicore changes in two and lipid storage in one, facial weakness (3/10), lethargy (5/10), feeding difficulties (4/10) and congenital abnormalities (3/7). One female with multiminicore myopathy had progressive external ophthalmoplegia, ptosis and cardiomyopathy with pneumonia and respiratory failure. Two brothers presented with psychosis, pyramidal signs, and multifocal white matter abnormalities on MRI brain suggesting additional genetic factors. Two other infants also had white matter changes. Elevated butyrylcarnitine (4/8), ethylmalonic aciduria (9/9), methylsuccinic aciduria (6/7), decreased butyrate oxidation in lymphoblasts (2/4) and decreased SCAD activity in fibroblasts or muscle (3/3) were shown. Expression studies of c.319C>T in mouse liver mitochondria showed it to be inactivating. c.625G>A is a common variant in ACADS that may confer disease susceptibility. Five healthy parents were heterozygous for c.319C>T and c.625G>A, suggesting reduced penetrance or broad clinical spectrum. We conclude that the c.319C>T mutation can lead to wide clinical and biochemical phenotypic variability, suggesting a complex multifactorial/polygenic condition. This should be screened for in individuals with multicore myopathy, particularly among the Ashkenazim.
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PMID:Short-chain acyl-CoA dehydrogenase gene mutation (c.319C>T) presents with clinical heterogeneity and is candidate founder mutation in individuals of Ashkenazi Jewish origin. 1805 10

To provide a rational basis for reconceptualizing catatonia in Diagnostic and Statistical Manual of Mental Disorders (Fifth Edition), we briefly review historical sources, the psychopathology of catatonia, and the relevance of catatonic schizophrenia in contemporary practice and research. In contrast to Kahlbaum, Kraepelin and others (Jaspers, Kleist, and Schneider) recognized the prevalence of motor symptoms in diverse psychiatric disorders but concluded that the unique pattern and persistence of certain psychomotor phenomena defined a "catatonic" subtype of schizophrenia, based on intensive long-term studies. The enduring controversy and confusion that ensued underscores the fact that the main problem with catatonia is not just its place in Diagnostic and Statistical Manual of Mental Disorders but rather its lack of conceptual clarity. There still are no accepted principles on what makes a symptom catatonic and no consensus on which signs and symptoms constitute a catatonic syndrome. The resulting heterogeneity is reflected in treatment studies that show that stuporous catatonia in any acute disorder responds to benzodiazepines or electroconvulsive therapy, whereas catatonia in the context of chronic schizophrenia is phenomenologically different and less responsive to either modality. Although psychomotor phenomena are an intrinsic feature of acute and especially chronic schizophrenia, they are insufficiently recognized in practice and research but may have significant implications for treatment outcome and neurobiological studies. While devising a separate category of catatonia as a nonspecific syndrome has heuristic value, it may be equally if not more important to re-examine the psychopathological basis for defining psychomotor symptoms as catatonic and to re-establish psychomotor phenomena as a fundamental symptom dimension or criterion for both psychotic and mood disorders.
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PMID:The catatonia conundrum: evidence of psychomotor phenomena as a symptom dimension in psychotic disorders. 1977 8

Delirium may present with hyperactive, hypoactive or mixed clinical pictures. The signs of hypoactive delirium are lethargy, confusion, apathy, hypersomnia, muttering, difficulty in maintaining attention, and difficulty in understanding and performing commands. Valproate is commonly used for the treatment of epilepsy and bipolar disorders. It is also used for the management of alcohol withdrawal delirium and agitative-aggressive deliriums. However, few reports are available about the valproate-induced delirium. In this report, we present a 46 years-old woman with bipolar disorder for 14 years. During her last two hospital admissions, she had been diagnosed with manic episode with psychotic features and she had received valproate. She experienced three hypoactive delirium episodes lasting 2-3 days throughout the treatment period of first week. The patient predominantly had the following signs; vomiting, hypersalivation, confusion, drowsiness, dysphasia, and hypoactivity. At the first day of delirium episode, serum valproate level was found to be within the therapeutic range (98.4, 117.1, and 65.6 mug/ml; respectively). In addition, she had normal results of cranial MRI, complete blood count, urine analysis, electrocardiogram, ALT, AST, albumin, bilirubin, BUN, creatinine and electrolytes. The serum ammonia level of the patient could not been measured due to limitations of laboratory facilities. The patient's consciousness improved dramatically 2-3 days after cessation of valproate. In conclusion, valproate can induce delirium at therapeutic blood levels in some patients via various mechanisms and this side effect has to be considered during valproate use.
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PMID:[Valproate induced hypoactive delirium in a bipolar disorder patient with psychotic features]. 2020 7

Of the 37 patients enrolled for this treatment, 13 have been lost to follow up and 4 have died. Of the remaining 20, 8 are already in remission (40%), while 12 are still having active disease. Of the 8 patients who are now in remission, 1 is in phase II and taking monthly dexamethasone cyclophosphamide pulse and 50 mg cyclophosphamide daily while in 3 patients all the treatment has already been withdrawn (phase IV). All these patients are being followed up for any recurrence. The duration of remission has been more than 6 months in 7 patients (maximum 2 years). The chief side-effect observed was increased susceptibility to pyogenic and candidal infections of the skin and oral mucosa respectively. The other side-effects noted were generalized weakness and lethargy following DCP (1), irregular menstrual periods (1), amenorrhoea (1), general darkening of complexion (1), steroid psychosis (1), transient eosinophilia (1) and marked transient oligospermia.
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PMID:Dexamethasone - Cyclophosphamide pulse (DCP) therapy in Pemphigus. 2094 77


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