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)

Many studies in developed countries show a high frequency of psychological distress among women attending gynecology clinics. The aim of this study is to assess the prevalence of psychiatric morbidity among 239 women attending a gynecology clinic at Ilorin Maternity Hospital in Nigeria. The aim also was to test the validity of using the 30-item version of the General Health Questionnaire (GHQ-30) as a screening tool. Clinical diagnoses were recorded according to the International Classification of Diseases-Ninth Edition (ICD-9). Psychiatric morbidity was determined according to the method of Deshpande. Literate respondents used a self-administered GHQ-30 and illiterate respondents were interviewed with the GHQ-30. The psychiatric interview was conducted by a research psychiatrist. Patients were grouped into 1) patients with symptoms diagnoses according to ICD-9, 2) cases with subdiagnostic syndromes, and 3) patients without significant psychiatric symptoms. A basic demographic profile of patients is given. Obstetrics and gynecologic data reveal that 31.3% were nulliparous, 44.5% had between 1 and 4 children, and 24.5% had 5-8 children. 64.4% reported regular menses, 21.9% reported scanty menstrual flow, and 64.4% had a normal flow. 17/6% reported a history of induced abortion, and 43.4% reported previous spontaneous abortion. 23.6% had primary infertility and 28.3% had secondary infertility; infertility was the most common complaint. A score of 5 or higher on the GHQ-30 indicated a psychiatric case. 35/2% were found to suffer from definite psychiatric morbidity. An additional 6.4% had severe psychiatric symptoms. Of the psychiatric diagnoses, 34.1% were for neurotic depression, 24.4% for anxiety, 25.7% for adjustment reaction, 12.2% manic depressive psychosis (depressed type), 2.4% phobic state, and 1.2% schizophrenia. Psychiatric morbidity was found to be unrelated to age, marital status, religion, education, occupational group, or duration of marriage. Symptoms such as irregular menses, pelvic pain, ad having no children were factors significantly associated with psychiatric morbidity; this pattern is supported in the developed country literature. Policy should be directed to a preventive and biopsychosocial model of health care.
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PMID:Psychiatric morbidity in a gynaecology clinic in Nigeria. 161 88

Autoimmune disease occurs when the immune system attacks self-molecules as a result of a breakdown of immunologic tolerance to autoreactive immune cells. Many autoimmune disorders have been strongly associated with genetic, infectious, and/or environmental predisposing factors. Comprising multiple disorders and symptoms ranging from organ-specific to systemic, autoimmune diseases include insulin-dependent diabetes mellitus, rheumatoid arthritis, systemic lupus erythematosus, scleroderma, thyroiditis, and multiple sclerosis. There are also implications of autoimmune pathology in such common health problems as arteriosclerosis, inflammatory bowel disease, schizophrenia, and certain types of infertility. Largely of unknown etiology, autoimmune disorders affect approximately 3% of the North American and European populations, > 75% of those affected being women. This discussion provides a brief introduction to the immune system and tolerance maintenance, an overview of selected autoimmune diseases and possible mechanisms of immune autoreactivity, and a review of experimental autoimmune models.
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PMID:Introduction to immunology and autoimmunity. 1050 28

Hyperprolactinaemia is an important but neglected adverse effect of antipsychotic medication. It occurs frequently with conventional antipsychotics and some atypical antipsychotics (risperidone and amisulpride) but is rare with other atypical antipsychotics (aripiprazole, clozapine, olanzapine, quetiapine, ziprasidone). For this reason the terms 'prolactin-sparing' and 'prolactin-raising' are more useful than 'atypical' and 'conventional' when considering the effect of antipsychotic drugs on serum prolactin. During antipsychotic treatment prolactin levels can rise 10-fold or more above pretreatment values. In a recent study approximately 60% of women and 40% of men treated with a prolactin-raising antipsychotic had a prolactin level above the upper limit of the normal range. The distinction between asymptomatic and symptomatic hyperprolactinaemia is important but is often not made in the literature. Some symptoms of hyperprolactinaemia result from a direct effect of prolactin on target tissues but others result from hypogonadism caused by prolactin disrupting the normal functioning of the hypothalamic-pituitary-gonadal axis. Symptoms of hyperprolactinaemia include gynaecomastia, galactorrhoea, sexual dysfunction, infertility, oligomenorrhoea and amenorrhoea. These symptoms are little researched in psychiatric patients. Existing data suggest that they are common but that clinicians underestimate their prevalence. For example, well conducted studies of women treated with conventional antipsychotics have reported prevalence rates of approximately 45% for oligomenorrhoea/amenorrhoea and 19% for galactorrhoea. An illness-related under-function of the hypothalamic-pituitary-gonadal axis in female patients with schizophrenia may also contribute to menstrual irregularities. Long-term consequences of antipsychotic-related hypogonadism require further research but are likely and include premature bone loss in men and women. There are conflicting data on whether hyperprolactinaemia is associated with an increased risk of breast cancer in women. In patients prescribed antipsychotics who have biochemically confirmed hyperprolactinaemia it is important to exclude other causes of prolactin elevation, in particular tumours in the hypothalamic-pituitary area. If a patient has been amenorrhoeic for 1 year or more, investigations should include bone mineral density measurements. Management should be tailored to the individual patient. Options include reducing the dose of the antipsychotic, switching to a prolactin-sparing agent, prescribing a dopamine receptor agonist and prescribing estrogen replacement in hypoestrogenic female patients. The efficacy and risks of the last two treatment options have not been systematically examined. Antipsychotic-induced hyperprolactinaemia should become a focus of interest in the drug treatment of psychiatric patients, particularly given the recent introduction of prolactin-sparing antipsychotics. Appropriate investigations and effective management should reduce the burden of adverse effects and prevent long-term consequences.
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PMID:Antipsychotic-induced hyperprolactinaemia: mechanisms, clinical features and management. 1545 28

Leuproreline acetate is a gonadotropin-releasing hormone (GnRH) analog which is used for in vitro fertilization (IVF) treatment. This compound suppresses gonadal estrogen secretion prior to hormonal stimulation. We report a 37-year-old woman who suffered from a schizoaffective psychosis for several years. She received IVF treatment with leuproreline acetate (Uno-Enantone) because of primary infertility. Under this treatment she developed acute schizoaffective symptoms. Suppression of gonadal secretion can result in exacerbation of schizophrenic psychosis, which is in line with the hypothesis of protective effects of estrogen in schizophrenia. We recommend that IVF treatment with leuproreline acetate in patients with psychiatric disorders be initiated only with special attention to their mental condition. In addition, patients should be informed about the possible mental effects of the treatment.
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PMID:[Exacerbation of a schizoaffective psychosis after in vitro fertilization with leuproreline acetate]. 1748 67

Gene duplications alter the genetic constitution of organisms and can be a driving force of molecular evolution in humans and the great apes. In this context, the study of genomic disorders has uncovered the essential role played by the genomic architecture, especially low copy repeats (LCRs) or segmental duplications (SDs). In fact, regardless of the mechanism, LCRs can mediate or stimulate rearrangements, inciting genomic instability and generating dynamic and unstable regions prone to rapid molecular evolution. In humans, copy-number variation (CNV) has been implicated in common traits such as neuropathy, hypertension, color blindness, infertility, and behavioral traits including autism and schizophrenia, as well as disease susceptibility to HIV, lupus nephritis, and psoriasis among many other clinical phenotypes. The same mechanisms implicated in the origin of genomic disorders may also play a role in the emergence of segmental duplications and the evolution of new genes by means of genomic and gene duplication and triplication, exon shuffling, exon accretion, and fusion/fission events.
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PMID:Evolution in health and medicine Sackler colloquium: Genomic disorders: a window into human gene and genome evolution. 2008 Jun 65

The aim of this paper was to present basic data about gender identity disorders and psychotic transsexual desires. From time to time in scientific literature there are descriptions of a diagnosis of psychotic disorders in persons previously diagnosed and treated as transsexuals, in whom the transsexual thinking disappears after using antipsychotic agents. Coexistence of transsexualism and schizophrenia causes a lot of doubt--it is observed in scientists opinions but also in the diagnostic criteria of DSM-IV and ICD-10. Moreover, delusions of sex change are probably more frequent than it is thought. It causes, that in some cases the differential diagnosis of psychosis and gender identity disorders may be very difficult. Transsexuals treatment is on one hand connected with expected effects but on the other hand with many serious, often irreversible health consequences (e.g. cardiovascular disease, risk of neoplasma development, infertility, consequences of surgical sex reassignment). That is why the differential diagnosis of transsexualism and schizophrenia should be made carefully and thoughtfully.
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PMID:[Transsexualism or delusions of sex change? Avoiding misdiagnosis]. 2020 83

It is hard to imagine that all the cells of the human organism (about 10(14)) share identical genome. Moreover, the number of mitoses (about 10(16)) required for the organism's development and maturation during ontogeny suggests that at least a proportion of them could be abnormal leading, thereby, to large-scale genomic alterations in somatic cells. Experimental data do demonstrate such genomic variations to exist and to be involved in human development and interindividual genetic variability in health and disease. However, since current genomic technologies are mainly based on methods, which analyze genomes from a large pool of cells, intercellular or somatic genome variations are significantly less appreciated in modern bioscience. Here, a review of somatic genome variations occurring at all levels of genome organization (i.e. DNA sequence, subchromosomal and chromosomal) in health and disease is presented. Looking through the available literature, it was possible to show that the somatic cell genome is extremely variable. Additionally, being mainly associated with chromosome or genome instability (most commonly manifesting as aneuploidy), somatic genome variations are involved in pathogenesis of numerous human diseases. The latter mainly concerns diseases of the brain (i.e. autism, schizophrenia, Alzheimer's disease) and immune system (autoimmune diseases), chromosomal and some monogenic syndromes, cancers, infertility and prenatal mortality. Taking into account data on somatic genome variations and chromosome instability, it becomes possible to show that related processes can underlie non-malignant pathology such as (neuro)degeneration or other local tissue dysfunctions. Together, we suggest that detection and characterization of somatic genome behavior and variations can provide new opportunities for human genome research and genetics.
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PMID:Somatic genome variations in health and disease. 2135 82

Hyperprolactinemia is a common, but neglected, adverse effect of conventional antipschycotics and of some of the atypical antipshycotics. It occurs in almost 42% of men and in 75% of women with schizophrenia who are treated with prolactin-raising antipshycotics, even though it has aroused minimal interest within the scientific community when compared with extra-pyramidal effects. Conventional antipsychotics and some of the atypical antipsychotics, such as risperidone, paliperidone, amisulpride and zotepine, are frequently associated with the raise in prolactin plasma levels. Because of this increment in prolactin secretion, they are usually known as prolactin-raising antipshycotics. On the contrary, some of the atypical antipsychotics, such as clozapine, quetiapine, olanzapine, aripiprazole and ziprazidone, have a minimal or no significant effect in prolactin levels, being known as prolactin-sparing antipsychotics. Hyperprolactinemia clinical symptoms include gynaecomastia, galactorrhoea, menstrual irregularities, infertility, sexual dysfunction, acne and hirsutism. Some of these symptoms are due to the prolactin direct action in body tissues, while a couple of them can be due to a hypothalamic-pituitary-gonadal axis dysregulation mediated by the elevation of prolactin. Some studies seem to point the evidence of an association between hyperprolactinemia and long-term consequences, such as bone mineral density decrement and breast cancer. However, these results must be confirmed through further studies. Antipsychotic treatment is the most common cause of hyperprolactinemia in psychiatric patients. However, the evidence of a prolactin increased plasma level demands the differential diagnosis with other pathologies, such as hyphotalamic and pituitary neoplasic disease. The management of a patient with antipsychotic-induced hyperprolactinemia must be adapted to each patient and it may include a reduction in the dosage of the offending antipsychotic, switching to a prolactin-sparing antipsychotic or the use of a dopamine receptor agonist, such as bromocriptine, cabergoline and amantadine. Given the osteopenic and osteoporosis risk, combined oral contraceptives must be considered in female patients in fertile age which have amenorrhoea for at least a one year period. With the exception of the Maudsley Prescribing Guidelines and the National Collaborating Centre for Mental Health, none of the current international psychiatric guidelines recommend a routine baseline prolactin determination, neither periodic prolactin levels without the presence of any hyperprolactinemia symptoms.
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PMID:[Hyperprolactinemia in mentally ill patients]. 2271 95

Cryptorchidism represents a risk factor for infertility and germ cell testicular neoplasia. An increased rate of cryptorchidism has been reported in subjects with Down's syndrome. Cyclic nucleotide phosphodiesterases (PDEs) are important messengers that regulate and mediate a number of cellular responses to extracellular signals, such as neurotransmitters and hormones. PDE4B, cAMP-specific (PDE4B) gene which maps to chromosome 1p31.3 appears to be involved in schizophrenia, chronic psychiatric illness, learning, memory, and mood disturbances. Expression of PDE4 enzymes have been studied in testes of cryptorchid rats. Expression of PDE4B protein examination showed marked degenerative changes in the epithelial lining of the seminiferous tubules. These findings led us to evaluate PDE4 mRNA expression in leukocytes of peripheral blood of five men with DS and cryptorchidism and eleven subjects with DS without cryptorchidism compared with healthy men (controls) by quantitative Real Time PCR (qRT-PCR). This study showed that the PDE4B gene was downexpressed in men with DS and cryptorchidism compared to normal controls and DS without cryptorchidism. A lower expression of the PDE4B gene may be involved in the neurological abnormalities in subjects with Down's syndrome. Moreover, PDE4B gene may be involved in the testicular abnormalities of men with DS and cryptorchidism.
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PMID:Expression of Phosphodiesterase 4B cAMP-Specific Gene in Subjects With Cryptorchidism and Down's Syndrome. 2554 71

Over the last decade, there has been a significant increase in average paternal age when the first child is conceived, either due to increased life expectancy, widespread use of contraception, late marriages and other factors. While the effect of maternal ageing on fertilization and reproduction is well known and several studies have shown that women over 35 years have a higher risk of infertility, pregnancy complications, spontaneous abortion, congenital anomalies, and perinatal complications. The effect of paternal age on semen quality and reproductive function is controversial for several reasons. First, there is no universal definition for advanced paternal ageing. Secondly, the literature is full of studies with conflicting results, especially for the most common parameters tested. Advancing paternal age also has been associated with increased risk of genetic disease. Our exhaustive literature review has demonstrated negative effects on sperm quality and testicular functions with increasing paternal age. Epigenetics changes, DNA mutations along with chromosomal aneuploidies have been associated with increasing paternal age. In addition to increased risk of male infertility, paternal age has also been demonstrated to impact reproductive and fertility outcomes including a decrease in IVF/ICSI success rate and increasing rate of preterm birth. Increasing paternal age has shown to increase the incidence of different types of disorders like autism, schizophrenia, bipolar disorders, and childhood leukemia in the progeny. It is thereby essential to educate the infertile couples on the disturbing links between increased paternal age and rising disorders in their offspring, to better counsel them during their reproductive years.
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PMID:Effects of increased paternal age on sperm quality, reproductive outcome and associated epigenetic risks to offspring. 2592 23


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