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)

Two patients with familial dysalbuminaemic hyperthyroxinaemia (FDH) are described in whom the albumin variant resulted in raised total T4 levels, and artefactually raised free T4 using a 'single-step' technique employing an analogue of T4 as tracer. The first patient was clinically euthyroid and presented with relapse of schizophrenia and abnormal thyroid function tests (total T4 336 nmol/L, total T3 4.2 nmol/L, TSH 1.8 mU/L, free T4 73 pmol/L). These results led to diagnostic confusion and the patient was treated with a short course of anti-thyroid drugs. The second patient had signs and symptoms of thyrotoxicosis at her first visit but was clinically euthyroid 5 months later when she was 10 weeks pregnant. Thyroid function tests were total T4 259 nmol/L, total T3 3.6 nmol/L, TSH 3.8 mU/L, free T4 46 pmol/L. Further studies showed both patients to be biochemically euthyroid. A variant albumin was confirmed in both patients by a screening test for FDH and by reverse-flow electrophoresis. Family studies on 10 relatives of the first patient identified eight with FDH. A simple screening procedure for the indentification of FDH is described and the use of laboratory tests in suspected cases is discussed.
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PMID:Thyroid function tests in patients with familial dysalbuminaemic hyperthyroxinaemia (FDH). 376 54

Psychiatric symptoms suggesting panic, affective, and even schizophrenic disorders have been described in thyrotoxic patients. However, this has not been previously described among Nigerians. We have therefore conducted a cross-sectional study of psychiatric symptoms among thyrotoxic Nigerians. The self-rated General Health Questionnaire (GHQ-30) and the Hospital Anxiety and Depression Scale (HADS) were administered on 8 previously untreated newly diagnosed thyrotoxics. Eight age and sex-matched diabetics and 8 apparently healthy controls were also recruited as controls. 1 subject was a male while 7 were females. Their ages ranged from 29 to 60 years, mean 44.5 +/- 11.4 years. Graves' disease was the cause of thyrotoxicosis in 7 subjects while the other had toxic multinodular goiter. Symptoms of thyroid disease had been present in them for a mean of 9.1 +/- 6.8 months. Based on GHQ-30 scores, 4 thyrotoxics, 4 diabetics and 2 healthy controls had significant psychiatric symptoms. The HADS identified symptoms of anxiety in 3 thyrotoxics, no diabetic and 2 healthy controls. Symptoms of depression was however present in 2 thyrotoxics, 1 diabetic and no healthy control. The mean GHQ-30, Anxiety and Depression scores were comparable across all subject groups: P = 0.489, 0.277, and 0.125 (ANOVA), respectively. None of the psychiatric symptom ratings significantly correlated with serum T3 levels. Our result does not show prominence of psychiatric symptoms in our thyrotoxic patients. Further, larger studies are required to validate this finding.
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PMID:A study of psychiatric symptoms in thyrotoxic Nigerians. 1503 63

Psychotic syndromes in the context of hyperthyroidism are seldom mentioned in medical textbooks and only a few cases have been published. Typically, such cases present as an affective psychosis. Schizophrenia-like psychosis is a rare occurrence in hyperthyroidism and the link between these two conditions is still poorly understood.We report the case of a female patient with a known history of chronic lymphocytic thyroiditis. The patient presented to our emergency department with an acute schizophrenia-like psychosis. Elevated levels of T4 and free T4 were found. These resulted from the patient's voluntary intake of excess levothyroxine as an attempt to lose weight (thyrotoxicosis factitia). Normalisation of thyroid hormone levels and antipsychotic treatment led to prompt remission of the psychosis. Even though the patient stopped the antipsychotics, she remained free of symptoms during the follow-up. Similar cases are briefly reviewed and some of the data from basic research is also considered.
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PMID:Acute psychotic episode in a patient with thyrotoxicosis factitia. 2168 86

Schizophrenia is of mysterious causation. It is not infectious, not congenital, but shows familial aggregation, the Mendelian genetics indicating involvement of multiple codominant genes with incomplete penetrance. This is the pattern for autoimmune diseases, such as Graves' disease of the thyroid, where forbidden clones of B lymphocytes develop, and cause thyrotoxicosis by secreting autoantibodies that react with the thyroid gland's receptor for thyroid-stimulating hormone from the pituitary gland. In 1982, Knight postulated that autoantibodies affecting the function of neurons in the limbic region of the brain are a possible cause of schizophrenia. Today, this is even more probable, with genes predisposing to schizophrenia having being found to be immune response genes, one in the MHC and two for antibody light chain V genes. Immune response genes govern the immune repertoire, dictating the genetic risk of autoimmune diseases. The simplest test for an autoimmune basis of schizophrenia would be trial of immunosuppression with prednisone in acute cases. The urgent research need is to find the microbial trigger, as done by Ebringer for rheumatoid arthritis and for ankylosing spondylitis. This could lead to prophylaxis of schizophrenia by vaccination against the triggering microbe.
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PMID:The autoimmune model of schizophrenia. 2373 11

Historically endocrinologists and psychiatrists are aware that disturbances in thyroid disease in beginning or even in clinically intensified states of thyrotoxicosis or hypothyroidism exhibit pathological mental manifestations, masking or potentiating the underlying disease. Immune system disorders cause thyroid organ-specific autoimmune process. This autoimmune thyroid disease binds with a number of disorders in both endocrine or non-endocrine organs. This appears in vascular, neurological, skin, connective tissue, gastrointestinal tract and mental pathology. These disorders are part of autoimmune polyglandular syndromes (APS) type I -III, especially the APS type III. Originally it was assumed that these mental disorders are caused by direct exposure to excess or deficiency of thyroid hormones. Recently, however, it appears that these psycho-immune-endocrine disorders have common etiologic mechanisms of formation and on cellular and molecular level they involve similar, if not in some cases, common mechanisms.Key words: antithyroid peroxidase antibody - autoimmune polyglandular syndrome type I., II., III. - autoimmune thyroid disease - bipolar disorder - depression - Hashimotos encephalopathy - postpartum psychosis - psycho-immuno-endocrinology - schizophrenia.
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PMID:[Psycho-immuno-endocrinology of the thyroid gland]. 2773 2