Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030794 (pelvic pain)
 4,056 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although leiomyomas (LMs) of the uterus are common, hematopoietic components within these tumors are not. Lymphoid and other hematopoietic elements have been previously recognized, but eosinophilic infiltrates in LMs have received little attention in the literature. The clinical and pathologic features of 3 cases of uterine LM with eosinophilic infiltration were studied. The patients ranged in age from 35 to 62 years and presented with abdominal and/or pelvic pain and abnormal uterine bleeding. None had peripheral blood eosinophilia or clinical evidence of allergy or parasitic infection. One patient had a benign LM, and the other 2 patients had smooth muscle tumors of uncertain malignant potential. The tumors contained variable numbers of eosinophils and Giemsa stains showed variable numbers of mast cells in addition to the eosinophils. We also performed immunohistochemical and in situ hybridization studies to assess for interleukin-5 (IL-5) and eotaxin in these LMs. There was no consistent association between the presence of eosinophils and either IL-5 or eotaxin in smooth muscle cells, suggesting that mechanisms other than IL-5 or eotaxin production may account for the eosinophilia. Because eosinophils are believed to be involved in wound healing, tissue remodeling, and fibrosis, their presence within LMs may reflect a response to tissue injury produced by the neoplasm rather than intrinsic recruitment by chemotactic factors produced by the smooth muscle cells. Their presence, however, does not appear to have any clinical significance.
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PMID:Uterine leiomyomas with Eosinophils: a clinicopathologic study of 3 cases. 1144 99

Experimental autoimmune prostatitis (EAP) is a murine model of chronic prostatitis/chronic pelvic pain syndrome (CPPS) in men, a syndrome characterized by chronic pelvic pain. We have demonstrated that chemokine ligands CCL2 and CCL3 are biomarkers that correlate with pelvic pain symptoms. We postulated that CCL2 and CCL3 play a functional role in CPPS and therefore examined their expression in EAP. Upon examination of the prostate 5 days after induction of EAP, CCL2 mRNA was elevated 2- to 3-fold, CCL8 by 15-fold, CCL12 by 12- to 13-fold, and CXCL9 by 2- to 4-fold compared with control mice. At 10 days the major chemokines were CXCL13 and CXCL2; at 20 days CCL2 (1- to 2-fold), CCL3 (2- to 3-fold) and CCL11 (2- to 3-fold); and at 30 days, CCL12 (20- to 35-fold) and smaller increases in CCL2, CCL3, and XCL1. Chemokine elevations were accompanied by increases in mast cells and B cells at 5 days, monocytes and neutrophils at day 10, CD4+ T cells at day 20, and CD4+ and CD8+ T cells at day 30. Anti-CCL2 and anti-CCL3 neutralizing antibodies administered at EAP onset attenuated pelvic pain development, but only anti-CCL2 antibodies were effective therapeutically. CCL2- and its cognate receptor CCR2-deficient mice were completely protected from development of pain symptoms but assumed susceptibility after reconstitution with wild-type bone marrow. CCL3-deficient mice showed resistance to the maintenance of pelvic pain while CCR5-deficient mice did not show any lessening of pelvic pain severity. These results suggest that the CCL2-CCR2 axis and CCL3 are important mediators of chronic pelvic pain in EAP.
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PMID:CCL2 and CCL3 are essential mediators of pelvic pain in experimental autoimmune prostatitis. 2281 70