Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Basal serum amino acids (including central monoamine precursors), central monoamines, and hormones were studied in schizophrenic patients (drug-naive; n = 20; drug-withdrawn for 3 or more days, n = 67; neuroleptic-treated, n = 23) and healthy subjects (n = 90) to answer the following questions: (1) Do neuroleptic-withdrawn and neuroleptic-naive patients differ on these serum measures? (2) What are the effects of neuroleptic treatment on these measures? (3) On which variables do drug-free and neuroleptic-treated patients differ? Because serum amino acid, central monoamine, and hormone levels were similar in drug-naive and drug-withdrawn patients, data from these groups ("drug-free") were combined and compared to those of healthy subjects and neuroleptic-treated patients. Asparagine, citrulline, phenylalanine, and cysteine were higher, while tyrosine, tryptophan, and the ratio of tryptophan to competing amino acids were significantly lower in drug-free schizophrenic patients than in healthy subjects. Dopamine was increased, and melatonin and thyroid hormones were decreased in drug-free schizophrenic patients compared to healthy subjects. Norepinephrine, epinephrine, and prolactin were higher in neuroleptic-treated men compared to drug-free male patients or healthy men. These results are consistent with the hypothesis of dopaminergic overactivity in schizophrenia, which might be caused by altered amino acid precursor availability and could be related to the decrease in melatonin and reduction in thyroid hormone levels.
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PMID:Serum amino acids, central monoamines, and hormones in drug-naive, drug-free, and neuroleptic-treated schizophrenic patients and healthy subjects. 198 23

3,5,3'-Triiodothyroacetic Acid (Triac) is reputed to suppress pituitary secretion of TSH with minimal metabolic effects. Triac has been used successfully to treat eight patients with thyroid hormone resistance. We gave Triac to a woman with selective pituitary resistance for treatment of hyperthyroidism (patient 1) and to a man with generalized resistance and chronic schizophrenia to determine whether it would improve his schizophrenia (patient 2). Patient 1 was given 0.35-3.5 mg Triac/day; patient 2 was given 0.7-4.2 mg/day. Dosages were increased by 0.7 mg/day every 2 weeks. Serum T3, T4, free T4, TSH, TSH response to TRH, systolic time intervals (STI), angiotensin-converting enzyme (ACE), and lipids were monitored bimonthly. In both patients, there was no change in symptoms, weight, lipids, or STI. In patient 1, basal TSH suppressed from 16.3 to 1.5 mU/L; in patient 2, from 2.0 to 0.5 mU/L. The peak TSH response to TRH stimulation decreased from 144 to 12.5 mU/L in patient 1 and from 14.2 to 2.8 mU/L in patient 2. Serum T4 decreased from 160 to 109 nmol/L in patient 1 and from 270 to 192 nmol/L in patient 2. ACE levels were persistently elevated in both patients. Resting energy expenditure, measured by oxygen consumption, was increased by Triac in both patients (12% in patient 1 and 9% in patient 2). Although Triac suppressed TSH and T4 secretion in both patients, it did not reduce peripheral action of thyroid hormone as expressed in STI, resting energy expenditure, and ACE. We conclude that in these two patients with resistance to thyroid hormone, at the doses used to suppress TSH and T4 secretion, the intrinsic peripheral action of Triac offset whatever decrease in thyroid hormone secretion it produced.
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PMID:3,5,3'-triiodothyroacetic acid therapy for thyroid hormone resistance. 275 85

Increased dopaminergic activity has been postulated to be one of the main causes of schizophrenia. To evaluate this hypothesis further, the interrelation between dopamine, prolactin, thyrotropin (TSH) and L-thyroxine was studied by determining their concentrations in the serum of ten acutely ill schizophrenic patients exhibiting distinct stages of process activity and ten healthy subjects. The level of dopamine was elevated in the sera of schizophrenic patients, whereas the levels of prolactin, TSH and L-thyroxine were decreased. On the basis of these results we hypothesize that 1. increased dopaminergic activity affects pituitary secretory function, and 2. decreased beta-adrenergic activity may be a consequence of decreased thyroid hormone concentration in plasma.
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PMID:Altered interrelationship of dopamine, prolactin, thyrotropin and thyroid hormone in schizophrenic patients. 648 1

The case of a young woman is reported, who was treated one and a half years with psychopharmacologic agents and psychotherapy until hypothyroidism was diagnosed. Initially the psychopathology with prominent though disorders led to a tentative diagnosis of schizophrenia. Under administration of thyroid hormone the patient was free of psychiatric and somatic symptoms within 3 months. Problems of diagnosis, therapy and prognosis are discussed in relation of the literature.
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PMID:[Psychotic manifestation of hypothyroidism. A case report]. 832 43

Invasion of the air passage, especially with intraluminal involvement of well-differentiated thyroid carcinoma, is rare. Establishing a patent airway before surgery is necessary, but difficult and risky. We report a case of thyroid cancer with intraluminal invasion of the trachea. A 62-year-old schizophrenic woman presented with blood-tinged sputum and dyspnea. She had undergone a thyroid lobectomy 8 years previously. Computed tomography and bronchoscopy showed a protruding mass in the upper trachea and limited movement of the bilateral vocal folds. Emergency tracheostomy was performed to relieve impending apnea. Fine-needle aspiration of the left protruding thyroid gland showed papillary carcinoma. Because the tumor diffusely infiltrated the thyroid gland and intermingled with fibrosis due to the previous thyroid operation, and because there was limited movement of bilateral vocal folds, the patient underwent total laryngectomy, total thyroidectomy, total parathyroidectomy, and tracheal resection. Neither radioactive iodine nor external irradiation were given because of anticipated poor compliance due to schizophrenia. The postoperative course was smooth and thyroid hormone and calcium were supplemented regularly. The patient has lived well and without local recurrence for more than 3 years since the operation. She can speak with an artificial larynx.
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PMID:Intraluminal involvement of thyroid cancer in the trachea. 958 83

Quetiapine has recently been approved for treatment of psychotic disorders. In short term (6 weeks) trials this atypical antipsychotic was shown to be as efficacious as the standard antipsychotics for the treatment of the positive symptoms of schizophrenia without causing any extrapyramidal symptoms or increase in the prolactin levels. Its efficacy for treating the negative symptoms was variable. Preliminary observations suggest its potential to improve the cognitive deficits of schizophrenia. It is metabolized by the p450 CYP 3A4 system with an estimated elimination half life of 6 hours. The optimal treatment is 300 mg to 400 mg/day in two to three divided oral doses. The most common side effects include dizziness, hypotension, somnolence and weight gain. Changes in the ECG, the thyroid hormone and hepatic enzymes levels appear to be clinically insignificant. Quetiapine interacts with phenytoin, carbamazepine, barbiturates, rifampin and glucocorticoids; and coadministration with these drugs may require dosage adjustment. Doses need not be adjusted when fluoxetine, imipramine, haloperidol and resperidone are coadministered. Quetiapine may enhance the effects of antihypertensive agents and may antagonize those of levodopa and dopamine. Long term efficacy of quetiapine has not been determined. Also undetermined are its effectiveness for treating the first episode and treatment-refractory schizophrenia. Data suggest that quetiapine may be used for the management of psychotic disorders in patients who may not tolerate the side effects of the typical antipsychotics and clozapine. It may also be helpful in patients whose psychotic manifestations did not adequately respond to risperidone and olanzapine.
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PMID:Quetiapine: a new atypical antipsychotic. 964 17

Recent reports have revealed that Nurr1 (also known as NOT/TINUR/RNR-1/HZF-3), a member of the steroid/thyroid hormone nuclear receptor superfamily, is predominantly expressed in the midbrain; substantia nigra (SN) and ventral tegmental area (VTA). Nurr1 null mice are born lethal, lacking the midbrain dopamine (DA) neurons, suggesting that Nurr1 is essential for the development and differentiation of midbrain DA neurons. Human Nurr1 gene has been mapped on chromosome 2q22-23, which is reported to associate weakly with schizophrenia. We cloned and sequenced the human Nurr1 gene, which is approximately 8.3kb long, consisting of eight exons and seven introns. Comparisons of the human Nurr1 with the mouse Nurr1, mouse Nur77 and human NOR-1 revealed that their genomic structures were highly conserved. The 5'-flanking region of the human Nurr1 included three transcriptional regulatory elements, cAMP-response element (CRE), CArG-like element and Sp-1 site, which were surrounded by CpG island, and showed a strong homology with the mouse Nurr1. We performed a primer extension analysis using mRNA from HeLa S3 cells stimulated with phorbol 12-myristate 13-acetate (PMA), Ca2+ ionophore A23187 and cycloheximide (CHX) in order to induce the Nurr1 mRNA expression, and determined one transcription initiation site within CRE. The transient transfection assay indicates that the regulatory elements in the 5'-flanking region are robust for mitogen-induced expression of the human Nurr1. Further analysis of the polymorphism of the human Nurr1 gene may reveal the association with diseases characterized by changes of the DA system, such as Parkinson's disease and schizophrenia.
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PMID:Organization of the human orphan nuclear receptor Nurr1 gene. 1021 61

Serum concentrations of thyroxine (T(4)), triiodothyronine (T(3)), reverse triiodothyronine (rT(3)) and thyrotropine (TSH) were measured in 31 acutely ill in-patients with schizophrenia before and after four weeks of treatment with the phenothiazine derivative perazine. The serum levels of all the above hormones were also determined in 19 schizophrenic patients in remission who were receiving no medication, 20 schizophrenic patients in remission taking neuroleptic drugs, and 24 patients with residual-type schizophrenia. The serum levels of T(4) of acutely ill schizophrenic patients were elevated, while those of T(3), rT(3) and TSH were normal. Their T(4) levels showed a positive correlation with the severity of illness and the degree of clinical response to neuroleptic treatment. There was a significant fall in serum concentrations of T(4) and rT(3) during four weeks of drug treatment and the decrease was significantly correlated to clinical response. No abnormalities in the serum concentrations of any of the hormones measured were found in schizophrenic patients in remission or in residual-type schizophrenia. In conclusion, our results indicate that the elevated serum levels of T(4) may be specific for acutely ill schizophrenic patients and that neuroleptic medication may affect thyroid hormone metabolism, this interaction being involved in the mechanism of action of these drugs.
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PMID:The hypothalamic-pituitary-thyroid axis in patients with schizophrenia. 1096 25

We describe the first reported case of symptomatic psychosis with the 'hallucination of soliloquy.' A 48[correction of 40]-year-old woman with Hashimoto disease exhibited of compulsive checking, mysophobia, and excessive hand washing. When these obsessive-compulsive symptoms diminished, she began to suffer from the 'hallucination of soliloquy', the automatic flow of meaningless words inside her mind. As the 'soliloquy' increased, her mood became unstable and she attempted suicide by analgesic ingestion. After this, she was admitted to the psychiatric ward of a general hospital. The administration of clomipramine (150 mg daily) decreased the 'soliloquy' symptoms, but they did not resolve. When hypothyroidism became available, thyroid hormone treatment (levothyroxine at 50 mg daily) was started. Four weeks later, her 'soliloquy' symptoms had almost resolved and after three months in a stable state, thyroid hormone treatment was stopped and her 'soliloquy' symptoms soon reappeared. After thyroid hormone treatment was resumed, her 'soliloquy' symptoms disappeared immediately. Typical auditory hallucinations and delusions of reference were not observed throughout the clinical course. We speculate that the symptoms were symptomatic psychosis induced by hypothyroidism secondary to Hashimoto disease, because the changes of her hallucinations were related to free T3 values and the symptoms disappeared soon after starting thyroid hormone treatment. The main features of this case were 'soliloquy' alternating with obsessive-compulsive symptoms, but her 'soliloquy' symptoms were thought to be autochthonous ideas rather than obsessive thoughts. Furthermore, the symptoms in this case were different from schizophrenia, since there was no disturbance of communication, and she had the sensation of both speaking and hearing her own voice. The psychopathology of this 'hallucination of soliloquy' may be related to the theory of 'vocalization of background thinking' (N. Nakayasu). Detailed observation of patients with symptomatic psychosis and a psychopathological description of their symptoms may help to contribute to the etiologic elucidation and treatment of psychosis.
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PMID:[A case of 'hallucination of soliloquy' with hypothyroidism induced Hashimoto disease. Meaning of psychopathological research about symptomatic psychosis]. 1132 41

Recent studies have revealed that an orphan receptor gene of the steroid/thyroid hormone nuclear receptor superfamily, the Nurr1 gene, is essential for the neurogenesis and differentiation of dopaminergic neurons in the midbrain of mice. Transgenic mice lacking the Nurr1 gene soon die after birth and are devoid of dopaminergic neurons in the midbrain. Heterozygous mice survive postnatally without obvious locomotor deficits; however, they have increased vulnerability to dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). In view of the importance of dopamine neurotransmission in brain function, we were interested to know if the human homologous gene of murine Nurr1, the NR4A2 gene, may play a role in the pathogenesis of schizophrenia. We systematically sequenced all the exons of the human NR4A2 gene to search for molecular variants in a cohort of Chinese schizophrenic patients from Taiwan. Two molecular variants were identified: a G-insertion in intron 6 (designated IVS6 + 17 [see text] + 18insG), and a G-deletion in the untranslated exon 1 (designated c.-469delG). The IVS6 + 17 [see text] + 18insG is a polymorphic one; further case control study, however, did not reveal association of this polymorphism with schizophrenia. The c.-469delG is a rare variant found in two unrelated patients among 177 schizophrenic patients, but not in 130 nonpsychotic controls. The result suggests that the c.-469delG and possibly other variants of the NR4A2 gene may be of relevance to the complex factors involved in the pathogenesis of schizophrenia.
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PMID:Mutation analysis of the human NR4A2 gene, an essential gene for midbrain dopaminergic neurogenesis, in schizophrenic patients. 1180 25


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