Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As mentioned at the beginning of this article, many questions were raised in our one particular case including the problem of verifying true arsenic toxicity and in determining the source of the exposure. In our case, there was a markedly elevated concentration of arsenic in samples of pubic hair and in the sample of urine. While arsenic toxicity can present with GI symptoms, we felt that in this particular case the association of the abdominal pain with arsenic toxicity was unlikely. For one, the patient's symptoms persisted despite apparent adequate treatment for arsenic toxicity. Also, the usual symptom of chronic arsenic toxicity is peripheral neuropathy (which was not documented in our case) and not abdominal pain. After the exhaustive diagnostic workup, we felt that this patient had irritable bowel syndrome and that the discovery of arsenic toxicity was serendipitous. In regards to the etiology of the toxicity, the patient's occupation involved working in the construction industry for a number of years. He indicated a definite exposure to termite-treated wood throughout that period. Wood for building houses, etc. is commonly pressure-treated with an arsenic-based compound; therefore, this source of occupational exposure appears to be a likely one. Another remotely possible source was the ingestion of contaminated illicit drugs. Cases of the use of illicit drugs laced with various toxic agents such as cyanide and strychnine have been reported. Although our patient required analgesics not commensurate with his symptoms, he categorically denied any use of "street" drugs. The random urine drug screen for such was negative.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Arsenic toxicity in Hawaii: a case report and review. 827 Apr 14

The fibromyalgia syndrome (FM) seems an unlikely candidate for classification as a neuropathic pain. The disorder is diagnosed based on a compatible history and the presence of multiple areas of musculoskeletal tenderness. A consistent pathology in either the peripheral or central nervous system (CNS) has not been demonstrated in patients with FM, and they are not at higher risk for diseases of the CNS such as multiple sclerosis or of the peripheral nervous system such as peripheral neuropathy. A large proportion of FM sufferers have accompanying symptoms and signs of uncertain etiology, such as chronic fatigue, sleep disturbance, and bowel/bladder irritability. With the exception of migraine headaches and possibly irritable bowel syndrome, the accompanying disorders are clearly not neurological in origin. The impetus to classify the FM as a neuropathic pain comes from multiple lines of research suggesting widespread pain and tenderness are associated with chronic sensitization of the CNS. An examination of how the term neuropathic pain is defined reveals a conceptual split into 2 partially overlapping groups of disorders: those with demonstrable pathology in the nervous system and those characterized primarily by enduring dysfunction in the nervous system. Requiring demonstrable pathology in the nervous system in the definition of neuropathic pain is the traditional approach. The expansion of the definition to require only enduring nervous system dysfunction is less palatable because it opens the classification to many disorders of uncertain etiology, including complex regional pain syndrome. As it is uncertain which of the many different chronic pain syndromes include an enduring component of central sensitization, restricting the term "neuropathic pain" to those disorders with a primary etiology clearly related to the peripheral or CNS is prudent and consistent with clinical practice.
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PMID:Is fibromyalgia a neuropathic pain syndrome? 1607 59

The gastrointestinal tract is controlled by the independent enteric nervous system. It is also closely connected to the central nervous system, and bi-directional communication exists between them. The communication involves neural pathways as well as immune and endocrine mechanisms. The brain-gut axis plays a prominent role in the modulation of gut functions. Signals from different sources (e.g. sound, sight, smell, somatic and visceral sensations, pain) reach the brain. These inputs are modified by memory, cognition and affective mechanisms and integrated within the neural circuits of the central nervous system, spinal cord, autonomic and enteral nervous systems. These inputs can have physiologic effects, such as changes in motility, secretion, immune function, and blood flow to the gastrointestinal tract. One of the most important neurotransmitters is serotonin that plays a key role in the pathogenesis of the most common chronic functional gastrointestinal disorder: the irritable bowel syndrome. It is a biopsychosocial disease, resulting from the dysregulation of the brain-gut axis. Endogenous pain facilitation rather than inhibition, pathologic gradation of visceral perception and reduced threshold for pain are all evident in these patients. Abuse history is common in their anamnesis. Exaggerated conscientiousness, perfectionism, oversensitivity, feeling of deficiency in effectiveness, and higher demand for social parity, neuroticism and alexithymia have been detected among their constant personality features. Females are also characterized by gender role conflict and low assertiveness. Antidepressants and psychotherapy have important roles in their treatment. Also patients with inflammatory bowel disease are characterized by neuroticism and alexithymia and altered mother-child attachment is often described in their anamnesis. Autonomic neuropathy is a frequent and early neurological complication. Reflux disease and obstructive sleep apnea mutually generate each other and their severities significantly correlate. In the celiac disease the most common neurological manifestations are ataxia, peripheral neuropathy and myopathy. Up to 85% of patients with histologically proven coeliac disease have no gastrointestinal symptoms; consequently, measurement of antigliadin antibody titre is therefore vital in all cases of idiopathic ataxia. Complete resolution of neurological symptoms is the result of gluten-free diet.
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PMID:[Neurological and psychiatric aspects of some gastrointestinal diseases]. 1895 27

The balance between descending controls, both excitatory and inhibitory, can be altered in various pain states. There is good evidence for a prominent alpha(2)-adrenoceptor-mediated inhibitory system and 5-HT(3) (and likely also 5-HT(2)) serotonin receptor-mediated excitatory controls originating from brainstem and midbrain areas. The ability of cortical controls to influence spinal function allows for top-down processing through these monoamines. The links between pain and the comorbidities of sleep problems, anxiety, and depression may be due to the dual roles of noradrenaline and of 5-HT in these functions and also in pain. These controls appear, in the cases of peripheral neuropathy, spinal injury, and cancer-induced bone pain to be driven by altered peripheral and spinal neuronal processes; in opioid-induced hyperalgesia, however, the same changes occur without any pathophysiological peripheral process. Thus, in generalized pain states in which fatigue, mood changes, and diffuse pain occur, such as fibromyalgia and irritable bowel syndrome, one could suggest an abnormal engagement of descending facilitations with or without reduced inhibitions but with central origins. This would be an endogenous central malfunction of top-down processing, with the altered monoamine systems underlying the observed symptoms. A number of analgesic drugs can either interact with or have their actions modulated by these descending systems, reinforcing their importance in the establishment of pain but also in its control.
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PMID:Preclinical and early clinical investigations related to monoaminergic pain modulation. 1978 74

Non-celiac gluten sensitivity (NCGS) is a syndrome characterized by intestinal and extraintestinal symptoms related to the ingestion of gluten-containing food in subjects who are not affected by either celiac disease (CD) or wheat allergy (WA). The prevalence of NCGS is not clearly defined yet. Indirect evidence suggests that NCGS is slightly more common than CD, the latter affecting around 1% of the general population. NCGS has been mostly described in adults, particularly in females in the age group of 30-50 years; however, pediatric case series have also been reported. Since NCGS may be transient, gluten tolerance needs to be reassessed over time in patients with NCGS. NCGS is characterized by symptoms that usually occur soon after gluten ingestion, disappear with gluten withdrawal, and relapse following gluten challenge within hours/days. The 'classical' presentation of NCGS is a combination of irritable bowel syndrome-like symptoms, including abdominal pain, bloating, bowel habit abnormalities (either diarrhea or constipation), and systemic manifestations such as 'foggy mind', headache, fatigue, joint and muscle pain, leg or arm numbness, dermatitis (eczema or skin rash), depression, and anemia. In recent years, several studies explored the relationship between the ingestion of gluten-containing food and the appearance of neurological and psychiatric disorders/symptoms like ataxia, peripheral neuropathy, schizophrenia, autism, depression, anxiety, and hallucinations (so-called gluten psychosis). The diagnosis of NCGS should be considered in patients with persistent intestinal and/or extraintestinal complaints showing a normal result of the CD and WA serological markers on a gluten-containing diet, usually reporting worsening of symptoms after eating gluten-rich food. NCGS should not be an exclusion diagnosis only. Unfortunately, no biomarker is sensitive and specific enough for diagnostic purposes; therefore, the diagnosis of NCGS is currently based on establishing a clear-cut cause-effect relationship between the ingestion of gluten and the appearance of symptoms by a standardized double-blind, placebo-controlled gluten challenge.
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PMID:Gluten Sensitivity. 2660 37