Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033377 (prolapse)
11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The adenosine A2a receptor (A2aAR) is thought to be implicated in the pathogenesis of panic disorder because caffeine, a potent antagonist for A2aAR, can precipitate panic attacks, and because disruption of the A2aAR gene increased anxiety-behaviors in mice. Recent studies demonstrated that the A2aAR 1976T > C genetic variant confers susceptibility to panic disorder though not by all studies. The present study tested the hypothesis that the A2aAR 1976T > C genetic variant confers susceptibility to panic disorder using a Chinese population of 104 panic disorder patients and 192 normal controls. We also tested whether the A2aAR 1976T > C polymorphism relates to the age of onset or subtype of panic disorders. Neither the distribution of the A2aAR 1976T > C genotypes (P = 0.296) or alleles (P = 0.864), nor the age of onset (P = 0.719) were significantly different among genotype groups. Furthermore, no association was demonstrated between this A2aAR polymorphism and either mitral-valve prolapse or agoraphobia in panic-disorder patients. These findings suggested that it is unlikely that the A2aAR 1976T > C polymorphism plays a major role in panic disorder pathogenesis in the Chinese population. The positive association between this polymorphism and panic disorder found in western population but not in Asian population suggests that this association could be ethnicity-dependent. The 1976C > T polymorphism may be in linkage disequilibrium with a functional variant that affects panic disorder, and the extent of this linkage disequilibrium is not similar for all ethnic populations.
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PMID:Association study of A2a adenosine receptor genetic polymorphism in panic disorder. 1577 65

Myasthenia gravis (MG) is a chronic, autoimmune disease involving neuromuscular junctions. It is frequently associated with symptoms such as loss of muscle strength, difficulty in respiration and swallowing, diplopia and ptosis. All chronic diseases, including MG, may have psychiatric consequences in terms of coping and adaptation. Psychiatric morbidity usually appears as anxiety disorders, such as panic disorder and generalised anxiety disorder, and as depressive disorders. However, there are very few data on the prevalence and aetiology of such psychiatric symptoms in patients with MG, and those available in the literature are generally from old studies with poor methodology. The interaction between MG and psychiatric disorders needs to be appreciated, especially in the primary care setting, since the symptoms may overlap. MG may be under-recognised initially because the psychiatric symptoms may coincide with those of the actual disease, such as fatigue, lack of energy and shortness of breath. On the other hand, co-morbid psychiatric symptoms that appear during the course of the illness may be misdiagnosed as true myasthenic symptoms; thus, leading to unnecessary drug treatment. Differentiation of the aetiology of these symptoms might alter the treatment choice and, therefore, affect the treatment success rate and patients' well-being. Psychiatric treatments must be carefully planned because of the risk of aggravating the underlying neurological disease. Even though there appears to be an intricate relationship between MG and psychiatric symptoms, there is very limited information on this subject. As such, prospective, randomised, controlled pharmaco/psychotherapy studies are needed to better direct the management of patients and, thus, improve quality of life during the course of the illness.
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PMID:Mood and anxiety disorders in patients with myasthenia gravis: aetiology, diagnosis and treatment. 1752 Dec 27


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