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)

Spinal cord stimulation (SCS) suppresses visceral response to colon distension in an animal model. In humans, it may be an effective therapy for chronic pain of pelvic origin, irritable bowel syndrome, and persistent unspecified abdominal pain. Described here is the case of SCS for 38-year-old woman with visceral pain secondary to chronic pancreatitis. Previous therapies included numerous endoscopic retrograde cholangiopancreatographies, multiple pancreatic duct stenting, chemical and surgical sympathectomies with short-lasting pain relief. After the initial evaluation, the patient underwent retrograde epidural differential block to determine possible source of pain. Delay in pain recurrence after block suggested that the origin of her pain was visceral. After the psychologic evaluation, the patient underwent SCS trial over 14 days. She had 2 trial leads placed epidurally via T9-T10 paramedian entry with the tips of both leads positioned at T6 vertebral body. During the trial, visual analog scale pain score decreased from 8 to 1 cm, Pain Disability Index from 62 to 14, and opioid use from 150 to 0 mg of morphine sulfate equivalent a day. After the completion of successful SCS trial, she was implanted with dual octrode leads and rechargeable pulse generator. Median pain scores decreased from 8 to 1 at 3 months after the implant. Pain Disability Index changed from 62 to 15. Opiate use decreased to none. It seems that SCS may have a significant therapeutic potential for the treatment of visceral pain secondary to chronic pancreatitis.
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PMID:Spinal cord stimulation for chronic visceral pain secondary to chronic non-alcoholic pancreatitis. 1849 89

Co-existing algogenic conditions in two internal organs in the same patient may mutually enhance pain symptoms (viscero-visceral hyperalgesia). The present study assessed this phenomenon in different models of visceral interaction. In a prospective evaluation, patients with: (a) coronary artery disease (CAD)+gallstone (Gs) (common sensory projection: T5); (b) irritable bowel syndrome (IBS)+dysmenorrhea (Dys) (T10-L1); (c) dysmenorrhea/endometriosis+urinary calculosis (Cal)(T10-L1); and (d) gallstone+left urinary calculosis (Gs+LCal) (unknown common projection) were compared with patients with CAD, Gs, IBS, Dys or Cal only, for spontaneous symptoms (number/intensity of pain episodes) over comparable time periods and for referred symptoms (muscle hyperalgesia; pressure/electrical pain thresholds) from each visceral location. In patients' subgroups, symptoms were also re-assessed after treatment of each condition or after no treatment. (a) CAD+Gs presented more numerous/intense angina/biliary episodes and more referred muscle chest/abdominal hyperalgesia than CAD or Gs; cardiac revascularization or cholecystectomy also reduced biliary or cardiac symptoms, respectively (0.001<p<0.05). (b) IBS+Dys had more intestinal/menstrual pain and abdomino/pelvic muscle hyperalgesia than IBS or Dys; hormonal dysmenorrhea treatment also reduced IBS symptoms; IBS dietary treatment also improved dysmenorrhea (0.001<p<0.05) while no treatment of either conditions resulted in no improvement in time of symptoms from both. (c) Cal+Dys had more urinary/menstrual pain and referred lumbar/abdominal hyperalgesia than Cal or Dys; hormonal dysmenorrhea treatment/laser treatment for endometriosis also improved urinary symptoms; lithotripsy for urinary stone also reduced menstrual symptoms (0.001<p<0.05). (d) In Gs+LCal, cholecystectomy or urinary lithotripsy did not improve urinary or biliary symptoms, respectively. Mechanisms of viscero-visceral hyperalgesia between organs with documented partially common sensory projection probably involve sensitization of viscero-viscero-somatic convergent neurons.
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PMID:Viscero-visceral hyperalgesia: characterization in different clinical models. 2067 12

Irritable bowel syndrome (IBS) is a common functional gastro-intestinal disorder characterized by intractable chronic abdominal pain. In this study, we examined the possible spinal mechanisms underlying colonic hypersensitivity (CHS) using a non-inflammatory rat model of IBS induced by rectal enemas of butyrate, a short-chain fatty acid. We hypothesized that spinal plasticity could be responsible for CHS and that ASIC channels, which are known to support pain-elicited currents in the spinal cord, could contribute to central sensitization in our model of IBS. First, in order to determine if visceral pain relies on changes in spinal activity, we analyzed Fos expression in the spinal cord of rats treated with butyrate following a challenge with repetitive noxious colorectal distension. We found that Fos immunoreactivity was increased in thoracic T10-11-12, lumbar L1-2-6 and sacral S1 spinal segments. In control rats treated with saline, noxious repetitive colorectal distensions evoked Fos expression only in L1-2-6 and S1 spinal segments. Secondly, intrathecal injection of PcTx1, a specific ASIC1A antagonist, in the lumbar spinal cord completely prevented the development of CHS induced by butyrate. ASIC1 and 2 mRNAs, especially ASIC1A, were upregulated in the lumbar spinal cord. ASIC1A could thus contribute to spinal sensitization in our model of IBS, as it is supported by spinal colocalization of ASIC1A and Fos proteins. The whole data pinpoint a potential critical role of thoracic spinal cord in non-inflammatory pain states such as IBS and suggest that ASIC channels are part of the molecular effectors of central sensitization leading to visceral pain.
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PMID:Spinal cord plasticity and acid-sensing ion channels involvement in a rodent model of irritable bowel syndrome. 2088 77