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)

Women with irritable bowel syndrome often report premenstrual distress syndrome and dysmenorrhea. A descriptive, four-group comparison design was used to compare the symptoms and psychological distress levels of women with irritable bowel syndrome (age 18-45 years) with and without dysmenorrhea and premenstrual distress syndrome. Data from three studies on women with irritable bowel syndrome (n = 226) collected between 1995 and 2004 were combined. Of these, 38 had self-reported irritable bowel syndrome with dysmenorrhea and premenstrual distress syndrome, 59 had irritable bowel syndrome with premenstrual distress syndrome, 15 had irritable bowel syndrome and dysmenorrhea, and the remaining 114 had irritable bowel syndrome only. Participants completed the Symptom Checklist-90 Revised and a symptom diary. Pain symptoms and computed scales of anxiety, depression, anger, and cognitive difficulties were compared during the luteal phase, menses phase, and for the change from luteal to menses phases. Premenstrual distress syndrome and dysmenorrhea had a strong impact on uterine cramping at menses, and a weaker effect on other pain symptoms at both luteal and menses phases. Premenstrual distress syndrome was associated with higher depression, anger, and cognitive problems at both luteal and menses phases; however, it was not associated with a greater increase from luteal to menses phases for any symptoms other than uterine cramping. The multiple symptoms reported by women with both irritable bowel syndrome and premenstrual distress syndrome suggest that this group may be particularly challenging to treat and may require a multicomponent (e.g., education, diet, relaxation, cognitive restructuring) approach.
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PMID:Increased symptoms in female IBS patients with dysmenorrhea and PMS. 1655 94

Pain symptoms in several chronic pain disorders in women, including irritable bowel syndrome, fluctuate with the menstrual cycle suggesting a gonadal hormone component. In female rats, estrogens modulate visceral sensitivity although the underlying mechanism(s) are unknown. In the present study the effects of 17-beta estradiol on N-methyl-D-aspartate (NMDA) receptor signaling of colorectal nociceptive processing in the spinal cord were examined. Estrogen receptor alpha and the NR1 subunit of the NMDA receptor are co-expressed in dorsal horn neurons, supporting a direct action of estradiol on NMDA receptors. Intrathecal administration of the NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (APV) dose-dependently attenuated the visceromotor response with greater potency in ovariectomized (OVx) rats compared to OVx with estradiol replacement (E2) rats. Estradiol significantly increased protein expression of NR1 in the lumbosacral spinal cord compared to OVx rats. Colorectal distention significantly increased phosphorylation of NR1ser-897, a PKA phosphorylation site on the NR1 subunit in E2, but not OVx rats. Intrathecal administration of a PKA inhibitor significantly attenuated the visceromotor response, decreased NR1 phosphorylation and increased the potency of APV to attenuate the visceromotor response compared to vehicle-treated E2 rats. These data suggest that estradiol increases spinal processing of visceral nociception by increasing NMDA receptor NR1 subunit expression and increasing site-specific receptor phosphorylation on the NR1 subunit contributing to an increase in NMDA receptor activity.
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PMID:Estrogen alters spinal NMDA receptor activity via a PKA signaling pathway in a visceral pain model in the rat. 1806 1

We sought to determine whether a low fermentable substrate diet (LFSD) decreases abdominal pain frequency in children with irritable bowel syndrome (IBS) and to identify potential microbial factors related to diet efficacy. Pain symptoms, stooling characteristics, breath hydrogen and methane, whole intestinal transit time, stool microbiome, and metabolite composition were collected and/or documented in eight children with IBS at baseline and during one week of an LFSD intervention. Pain frequency (P<0.05), pain severity (P<0.05), and pain-related interference with activities (P<0.05) decreased in the subjects while on the LFSD. Responders vs. non-responders: four children (50%) were identified as responders (> 50% decrease in abdominal pain frequency while on the LFSD). There were no differences between responders and non-responders with respect to hydrogen production, methane production, stooling characteristics, or gut transit time. Responders were characterized by increased pre-LFSD abundance of bacterial taxa belonging to the genera Sporobacter (P<0.05) and Subdoligranulum (P<0.02) and decreased abundance of taxa belonging to Bacteroides (P<0.05) relative to non-responders. In parallel, stool metabolites differed between responders and non-responders and were associated with differences in microbiome composition. These pilot study results suggest that an LFSD may be effective in decreasing GI symptoms in children with IBS. Microbial factors such as gut microbiome composition and stool metabolites while on the diet may relate to LFSD efficacy.
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PMID:Gut microbiota influences low fermentable substrate diet efficacy in children with irritable bowel syndrome. 2463 1