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Query: UMLS:C0036341 (
schizophrenia
)
60,220
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A patient with gout and
schizophrenia
is described who during a schizophrenic paroxysm with paranoid-hypochondriac-hallucinatory syndrome attempted to commit suicide and took 200 tablets milurit (20 g). He developed the picture of acute intoxication with nausea, vomiting, profuse diarrhea, abdominal pain, flushing, temperature, collapse manifestations, hepatomegaly, direct
hyperbilirubinemia
, elevated transaminase, leukopenia, accelerated ESR. After reanimation and infusion therapy, the patient recovered within 4 days and 2 weeks later all blood indices reached the limits of the norm.
...
PMID:[Acute allopurinol (milurit) poisoning]. 402 4
Gilbert's syndrome is defined as a hereditary, mild, chronic, unconjugated
hyperbilirubinemia
occurring in the absence of overt hemolysis or any other evidence of liver disease. It is caused by a mutation of the specific UDP glucuronosyl transferase conjugating bilirubin with glucuronic acid resulting in a reduced activity of this enzyme. Gilbert's syndrome is considered as a rather benign disorder without necessity of any therapeutic intervention. It is therefore crucial to establish a correct diagnosis and differentiate this syndrome from serious disorders of the liver tissue. In recent years strong antioxidant effects of bilirubin were demonstrated in numerous studies and the protective role of
hyperbilirubinemia
in the pathogenesis of various oxidative stress-mediated diseases was suggested. Gilbert's syndrome and its relationship to associated disorders such as hemolysis, pigment cholelithiasis, neonatal jaundice,
schizophrenia
and drug interactions are also being discussed.
...
PMID:[Gilbert's syndrome--myths and reality]. 1530 63
Gilbert's syndrome (idiopathic unconjugated
hyperbilirubinemia
) is a benign
hyperbilirubinemia
found in the general population. We report one case in which the exacerbation and remission of
hyperbilirubinemia
closely correlated with the psychosis of
schizophrenia
. Some studies have reported that schizophrenic individuals had a significantly higher frequency of
hyperbilirubinemia
than patients suffering from other psychiatric disorders and the general healthy population. Stress and fasting are well-known contributors to elevated plasma bilirubin levels in patients with Gilbert's syndrome. A 38 year old woman inpatient with acute schizophrenic symptoms had a bilirubin plasma level of 2.7 mg/dl. She was treated with risperidone that produced no adverse effects on hepatic function. Schizophrenic symptoms improved and a decrease in bilirubin plasma concentration was observed.
...
PMID:[Gilbert's syndrome and schizophrenia]. 1673 95
Nerve cell injury induced by unconjugated bilirubin (UCB) has been implicated in brain damage during severe neonatal
hyperbilirubinemia
, although the molecular mechanisms underlying UCB neurotoxicity are still not clarified. It has been suggested recently that there is an association between
hyperbilirubinemia
and long-term neurologic dysfunctions. We incubated immature neurons with UCB to evaluate the short- and long-term effects of UCB on apoptotic death and on neuritic outgrowth and ramification. We also evaluated whether mature neurons, exposed previously to UCB in an early stage of differentiation, are more sensitive to apoptosis or to neuritic breakdown when treated with inflammatory agents, such as lipopolysaccharide and tumor necrosis factor-alpha. Results show that exposure of immature neurons to UCB increased apoptosis and provoked a reduction of both neurite extension and number of nodes. These injurious effects observed in immature cells treated with UCB were increasingly perpetuated along cell differentiation, as compared to neurons incubated in the absence of UCB. In addition, neurons that were exposed to UCB when immature showed an increased susceptibility to death by apoptosis, as well as an additional decrease in neurite outgrowth when incubated with an inflammatory agent afterward. This work shows, for the first time, that UCB induces neurite changes consistent with neurodevelopment abnormalities. Furthermore, pre-exposure to UCB followed by an inflammatory stimulus leads to an enhanced susceptibility to long-term apoptosis, as well as a greater neuritic breakdown. These data support the association between neonatal
hyperbilirubinemia
and the later development of mental illness, such as
schizophrenia
.
...
PMID:Apoptosis and impairment of neurite network by short exposure of immature rat cortical neurons to unconjugated bilirubin increase with cell differentiation and are additionally enhanced by an inflammatory stimulus. 1734 78
Idiopathic unconjugated
hyperbilirubinemia
(Gilbert's syndrome, GS) is a relatively common congenital hyperbilirubinemia occurring in 3-7% of the world's population. It has been recognized as a benign familial condition in which
hyperbilirubinemia
occurs in the absence of structural liver disease or hemolysis, and the plasma concentration of conjugated bilirubin is normal. Recently, it was reported that unconjugated bilirubin exhibited neurotoxicity in the developing nervous system. The 'neurodevelopmental hypothesis' of
schizophrenia
proposes that an as yet unidentified event occurs in utero or during early postnatal life. We have observed that patients suffering from
schizophrenia
frequently present an increased unconjugated bilirubin plasma concentration when admitted to the hospital. Therefore, we noticed a relation between unconjugated bilirubin and the etiology of and vulnerability to
schizophrenia
. Our reported findings suggest that there are significant biological and clinical character differences between schizophrenic patients with and without GS. From the viewpoint of the heterogeneity of
schizophrenia
, there may be a poor outcome for the subtype of
schizophrenia
with GS.
...
PMID:[Schizophrenia and idiopathic unconjugated hyperbilirubinemia (Gilbert's syndrome)]. 1756 69
Idiopathic unconjugated
hyperbilirubinemia
(Gilbert's syndrome, or GS) is a relatively common congenital hyperbilirubinemia occurring in 3-7% of the world's population. It has been recognized as a benign familial condition in which
hyperbilirubinemia
occurs in the absence of structural liver disease or hemolysis, and the plasma concentration of conjugated bilirubin is normal. Recently, it has been reported that unconjugated bilirubin exhibited neurotoxicity in the developing nervous system. The 'neurodevelopmental hypothesis' of
schizophrenia
proposes that an as-yet-unidentified event occurs in utero or during early postnatal life. We have observed that patients suffering from
schizophrenia
frequently present with an increased unconjugated bilirubin plasma concentration when admitted to the hospital. As a result, we noticed a relationship between unconjugated bilirubin and the etiology of, and vulnerability to,
schizophrenia
. Our reported findings suggest that there are significant biological and clinical character differences between schizophrenic patients with and without GS. From the viewpoint of the heterogeneity of
schizophrenia
, there may be a poor outcome for the subtype of
schizophrenia
with GS.
...
PMID:[Schizophrenia and idiopathic unconjugated hyperbilirubinemia (Gilbert's syndrome)]. 2170 27
Abstract Objective. Alteration of serum bilirubin level in acute episodes of psychosis in patients with
schizophrenia
has been reported but the pattern of this alteration is controversial. Methods. Patients diagnosed as
schizophrenia
(162, group S) or bipolar disorder (155, group B) entered the study. The control group consisted of 95 patients admitted to cardiac care unit who had no personal or family history of major psychiatric disorders. Pre- and post-admission levels of bilirubin were measured and compared within and between the groups. Patients were examined to exclude all other causes of
hyperbilirubinemia
. Group S and B participants were also evaluated using positive and negative syndrome subscale (PANSS) both at admission and discharge. Results. The mean admission bilirubin levels of all the groups were in the normal range (significantly higher in group S than groups B and C) and were affected by the score of general psychopathology subscale rather than the scores of positive symptoms subscale. Conclusions. Although bilirubin decreased in all three groups at discharge, the rate of decrease was significantly higher in group S. The reason for this is not clear and needs further study.
...
PMID:Alteration of serum bilirubin level in schizophrenia. 2491 37
Idiopathic unconjugated
hyperbilirubinemia
(Gilbert's syndrome) is a common genetic enzyme deficiency found in 3-10% of the general population. It occurs with greater frequency in patients with
schizophrenia
. We report the case of a young man with mainly negative symptoms of
schizophrenia
in whom there has been little improvement in mental state with prolonged treatment despite an improvement in total bilirubin, contrary to other published cases. We examine the literature related to Gilbert's syndrome and symptom severity and we discuss the research into the pathophysiology of
schizophrenia
in Gilbert's syndrome and negative symptom
schizophrenia
.
...
PMID:Gilbert's syndrome in a patient with predominantly negative symptoms of schizophrenia. 2494 64
Oligodendrocytes are the myelinating cells of the central nervous system that constitute about 5 to 10% of the total glial population. These cells are responsible for myelin sheath production, which is essential not only for the rapid and efficient conduction of the electrical impulses along the axons, but also for preserving axonal integrity. Oligodendrocytes arise from oligodendrocyte progenitor cells that proliferate and differentiate just before and after birth, under a highly-regulated program. Both oligodendrocytes and their precursors are very susceptible to injury by several mechanisms, including excitotoxic damage, oxidative stress and inflammatory events. In this review, we will cover not only several important aspects of oligodendrocyte development and regulatory mechanisms involved in this process, but also some of the most important pathways of injury associated to oligodendrogenesis. Moreover, we will also address some neurological disorders along life journey that present impairment in oligodendrocyte function and in myelination during neurodevelopment, such as periventricular leukomalacia, hypoxia/ischemia and
hyperbilirubinemia
that in turn can potentiate the emergence of neurological and neurodegenerative diseases like
schizophrenia
, multiple sclerosis and Alzheimer's disease.
...
PMID:Oligodendrocyte Development and Myelination in Neurodevelopment: Molecular Mechanisms in Health and Disease. 2663 71
Gilbert's syndrome (often abbreviated as GS) is most common hereditary cause of mild unconjugated (indirect)
hyperbilirubinemia
. Various studies have been published depicting clinical and pharmacological effects of Gilbert's syndrome (GS). However GS as a sign of precaution for physician and surgeons has not been clearly established. A systematic study of the available literature was done. Key words of Gilbert's syndrome,
hyperbilirubinemia
and clinical and pharmacological aspects of GS were searched using PubMed as search engine. Considering the study done in last 40 years, 375 articles were obtained and their abstracts were studied. The criterion for selecting the articles for through study was based on their close relevance with the topic. Thus 40 articles and 2 case reports were thoroughly studied. It was concluded that Gilbert's syndrome has immense clinical importance because the mild
hyperbilirubinemia
can be mistaken for a sign of occult, chronic, or progressive liver disease. GS is associated with lack of detoxification of few drugs. It is related with spherocytosis, cholithiasis, haemolytic anaemia, intra-operative toxicity, irinotecan toxicity,
schizophrenia
and problems in morphine metabolism. It also has profound phenotypic effect as well. The bilirubin level of a GS individual can rise abnormally high in various conditions in a person having Gilbert's syndrome. This can mislead the physicians and surgeons towards false diagnosis. Therefore proper diagnosis of GS should be ascertained in order to avoid the concealed adversities of this syndrome.
...
PMID:GILBERT'S SYNDROME - A CONCEALED ADVERSITY FOR PHYSICIANS AND SURGEONS. 2672 Oct 45
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