Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

BACKGROUND Depression and insomnia in chronic hepatitis B (CHB) patients affect the quality of life, disease diagnosis, and mortality. CHB patients are more likely to have psychological disorders, but the underlying mechanisms have not been elucidated. This study investigated the incidence of depression in patients with CHB and sought to identify risk factors for depression and insomnia in these patients, focusing on changes in liver function and thyroid hormone levels. MATERIAL AND METHODS This cross-sectional cohort study used the Hamilton Depression Scale and Athens Insomnia Scale to assess the depressive and insomnia states, respectively, of 209 CHB patients. Liver function, thyroid hormone levels, hepatitis B surface antigen, hepatitis B e-antigen, and hepatitis B virus-deoxyribonucleic acid load were evaluated. Liver cirrhosis was assessed by imaging (color Doppler ultrasound and computed tomography). A multivariate logistic regression model was used to analyze the correlation among various factors and depression and insomnia. RESULTS Subclinical and clinical depressive states were found in 23.9% and 5.3% and subclinical and clinical insomnia in 11% and 35.4% of patients, respectively. Depression and insomnia severity were significantly correlated with low FT3 (<3.5 mol/L). The odds ratios of low FT3 for subclinical and clinical depression and clinical insomnia were 3.07 (95% confidence interval (CI), 1.248-7.568), 7.85 (95% CI, 1.839-33.547), and 3.91 (95% CI, 1.417-10.789), respectively. CONCLUSIONS CHB patients are prone to depression and insomnia. FT3 reduction may be a risk factor for depression and insomnia. In clinical settings, more attention needs to be paid to the mental state of patients with FT3 reduction.
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PMID:Depression and Insomnia Are Closely Associated with Thyroid Hormone Levels in Chronic Hepatitis B. 3097 43

Research in the last few years has indicated that most voltage-gated potassium channel- (VGKC-) complex antibodies without leucine-rich glioma-inactivated protein 1 or contactin-associated protein-like 2 antibody specificity lack pathogenic potential and are not clear markers for autoimmune inflammation. Here we report on a patient with double-negative VGKC who developed severe peripheral nerve hyperexcitability, central nervous system symptoms with agitation and insomnia, dysautonomia, and systemic symptoms with weight loss, itch, and skin lesions. The disease started acutely one month after an episode of enteroviral pericarditis and responded well to immunotherapy. The patient is presumed to have developed a postinfectious immunotherapy-responsive autoimmune disease. In the setting of anti-VGKC positivity, it seems likely that anti-VGKC contributed to the pathogenesis of the patient's symptoms of nerve hyperexcitability and that the disease was caused by an acquired autoimmune effect on the neuronal kinetics of VGKC. It is still unknown whether or not there are unidentified extracellular molecular targets within the VGKC-complex, i.e., a novel surface antigen and a pathogenic antibody that can cause affected individuals to develop a peripheral nerve hyperexcitability syndrome. This case highlights the fact that less well-characterized autoimmune central and peripheral nervous system syndromes may have infectious triggers.
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PMID:A Patient with Double-Negative VGKC, Peripheral Nerve Hyperexcitability, and Central Nervous System Symptoms: A Postinfectious Autoimmune Disease. 3312 94