Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0232487 (abdominal discomfort)
 1,724 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Idiopathic environmental intolerance (IEI), also known as multiple chemical sensitivity, is a clinical description for a cluster of symptoms of unknown etiology that have been attributed by patients to multiple environmental exposures when other medical explanations have been excluded. Because allergy has not been clearly demonstrated and current toxicological paradigms for exposure-symptom relationships do not readily accommodate IEI, psychogenic theories have been the focus of a number of investigations. A significantly higher lifetime prevalence of major depression, mood disorders, anxiety disorders, and somatization disorder has been reported among patients with environmental illness compared with that in controls. Symptoms often include anxiety, lightheadedness, impaired mentation, poor coordination, breathlessness (without wheezing), tremor, and abdominal discomfort. Responses to intravenous sodium lactate challenge or single-breath inhalation of 35% carbon dioxide versus a similar breath inhalation of clean air have shown a greater frequency of panic responses in subjects with IEI than in control subjects, although such responses did not occur in all subjects. Preliminary genetic findings suggest an increased frequency of a common genotype with panic disorder patients. The panic responses in a significant proportion of IEI patients opens a therapeutic window of opportunity. Patients in whom panic responses may at least be a contributing factor to their symptoms might be responsive to intervention with psychotherapy to enable their desensitization or deconditioning of responses to odors and other triggers, and/or may be helped by anxiolytic medications, relaxation training, and counseling for stress management.
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PMID:Responses to panic induction procedures in subjects with multiple chemical sensitivity/idiopathic environmental intolerance: understanding the relationship with panic disorder. 1219 4

Irritable bowel syndrome (IBS), a functional gastrointestinal disorder, is present in 10% to 20% of the U.S. adult population. The syndrome is best defined as chronic abdominal discomfort with changes in stool frequency, consistency, and passage, with associated symptoms such as abdominal bloating or presence of mucus in stools. Several studies have shown that up to 70% to 90% of patients with IBS who seek treatment have psychiatric comorbidity, most notably mood and anxiety disorders. Recent studies have shown a high prevalence of IBS in psychiatric patients who seek treatment, with a prevalence of 19% in schizophrenia, 29% in major depression, and 46% in panic disorder among other disorders. Our article reviews the comorbidity of IBS in psychiatric patients and discusses implications for treatment.
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PMID:Comorbidity of irritable bowel syndrome in psychiatric patients: a review. 1252 23

Pain or sensory symptoms are a frequent complaint in Parkinson disease (PD), which reduce health-related quality of life (QOL) and interfere with patient's ability to participate in activities of daily living, thus contributing to sleep disturbance or major depression. The frequency of pain is thought to have a bimodal distribution. The initial peak seems to occur before, or at the onset of PD and a second peak occurs later in the disease course in conjunction with the development of motor fluctuations or dyskinesia. The spectrum of sensory symptoms is wide, and the most common sites that experience pain are the back, legs, and shoulders. In cases, pain occurs on the side that is more affected by parkinsonism; however unusual distributions, such as oral or genital pain syndrome, chest pain, and upper or lower abdominal discomfort may be observed. The etiological basis of PD-related pain is multifactorial, with varying degrees of contribution from peripheral and central sources. Central mechanisms include derangement of the intrinsic pain-modulating monoaminergic mechanism in addition to plastic central nervous system changes induced by chronic anti-parkinsonian medication. The importance of dopaminergic deficits as a causal factor in PD-related pain is supported by the normalization of these abnormalities after L-dopa administration, which suggests that the human striatum plays a central role in processing nociceptive information. Nevertheless, the lack of response to dopaminergic agents in some patients suggests the involvement of non-dopaminergic structures in PD. Abnormalities of noradrenergic and serotonergic pathways descending to the spinal cord are assumed to play a role in pain perception in PD. Some reports have highlighted the problem of delayed diagnosis in PD patients with an initial presentation of pain. Greater awareness of this possibility among physicians is important. Physicians also should bear in mind that psychological factors are major components of pain and that patient education and support are critical to successful treatment.
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PMID:[Pain and sensory disturbance in Parkinson disease]. 2248 9