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R B Ness,
D E Soper,
R L Holley,
J Peipert,
H Randall,
R L Sweet,
S J Sondheimer,
S L Hendrix,
A Amortegui, G Trucco,
D C Bass,
S F Kelsey
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ABSTRACT: Among women diagnosed with pelvic inflammatory disease, we examined the associations between hormonal or barrier methods of contraception and upper genital tract infection or inflammation.
Participants were 563 patients from a treatment trial for pelvic inflammatory disease. All had pelvic pain; pelvic organ tenderness; and leukorrhea, mucopurulent cervicitis, or untreated cervicitis. Contraceptive use within the prior 4 weeks was compared among women with baseline upper genital tract gonorrhea or chlamydia, women with endometritis without upper genital tract gonorrhea or chlamydia, and women with neither upper genital tract gonorrhea or chlamydia nor endometritis.
Inconsistent condom use was significantly and independently associated with a 2 to 3 times elevated risk for upper genital tract infection. Upper genital tract gonorrhea or chlamydia was not significantly associated with use of oral contraceptives, use of medroxyprogesterone, condoms used consistently, nor other barrier methods.
No hormonal or barrier contraceptive method was related to a reduction in upper genital tract disease among women with clinical pelvic inflammatory diseases.
American Journal of Obstetrics and Gynecology 08/2001; 185(1):121-7. · 3.47 Impact Factor
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J F Peipert,
R B Ness,
J Blume,
D E Soper,
R Holley,
H Randall,
R L Sweet,
S J Sondheimer,
S L Hendrix,
A Amortegui, G Trucco,
D C Bass
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ABSTRACT: Careful detection and treatment of pelvic inflammatory disease are essential for the prevention of adverse sequelae. The purpose of this study was to evaluate the diagnostic test characteristics of clinical criteria for the diagnosis of pelvic inflammatory disease.
We performed a cross-sectional analysis of the baseline characteristics of 651 patients enrolled in a multicenter randomized treatment trial for pelvic inflammatory disease. Clinical and laboratory findings were recorded for all patients, and endometrial sampling was performed. We calculated sensitivity and specificity and performed receiver operating characteristic curve analysis and multivariate logistic regression, using histologic endometritis as the criterion standard.
The minimal criteria for pelvic inflammatory disease, as recommended by the Centers for Disease Control and Prevention, had a sensitivity of 83%, in comparison with a 95% sensitivity for adnexal tenderness (P =.001). Of the supportive clinical criteria, the finding most highly associated with endometritis was a positive test result for Chlamydia trachomatis or Neisseria gonorrhoeae (adjusted odds ratio, 4.3; 95% confidence interval, 2.89--6.63). A multivariate logistic regression model indicated that combinations of criteria significantly improve the prediction of endometritis.
Sensitivity can be maximized by using the presence of adnexal tenderness as a minimal criterion for the diagnosis of pelvic inflammatory disease, and supportive criteria are helpful in estimating the probability of endometritis.
American Journal of Obstetrics and Gynecology 05/2001; 184(5):856-63; discussion 863-4. · 3.47 Impact Factor
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ABSTRACT: Although the etiopathogenesis of idiopathic dilated cardiomyopathy (IDC) is still unclear, it is widely accepted that a complex interplay between viral infections and immune mechanisms is the basis of disease genesis. Previously, we showed that heart-infiltrating T cells of patients suffering from acute, fulminant Coxsackie virus B3+-IDC shared a preferential usage of three variable gene segments of the T cell receptor beta chain-(TCR-Vbeta) encoding families Vbeta3, 7 and 13.1. This indicated the possible presence of a superantigen-driven immune response. Here, we further investigated the IDC immunological scenario by analysing different phenotypes of heart-infiltrating cells: TCR repertoires, cytokine expression and presence of enterovirus-specific antigens. IDC patients who underwent heart transplantation at different times after the onset of heart failure were studied. A cardiac infiltrate of CD4+ and CD8+ T cells was present together with activated macrophages. Furthermore, the same Vbeta gene families, previously found to be skewed in hearts from fulminant cases of CVB3+-IDC, together with two additional Vbeta gene families, Vbeta1 and 5B, were increased. IL-1beta, IL-2, IL-6 and IFN-gamma were expressed in the myocardium while others, like IL-4 were not. In conclusion, an orchestrated complex of immune mechanisms seems to be the basis of IDC etiopathogenesis.
Journal of Autoimmunity 03/2001; 16(1):3-13. · 7.37 Impact Factor
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ABSTRACT: Many cases of idiopathic dilated cardiomyopathy (IDC) result from an inflammatory myocarditis. The specific immunological mechanisms are not yet defined. Various autoimmune diseases are associated with superantigen-triggered immune responses, resulting in massive T-cell activation and tissue damage. We studied 3 cases in a search for evidence that such a phenomenon is also implicated in IDC.
Myocardial, lymph node, and thymic tissue samples were obtained from IDC patients who were undergoing heart transplantation. Infiltrating immune-cell phenotypes and gene expression of T-cell receptor (TCR) alpha- and beta-chain variable (Valpha and Vbeta) regions were analyzed by immunostaining and polymerase chain reaction. Similar technical approaches were used to assay the tissues for the presence of coxsackievirus B (CVB). In all the specimens analyzed, an overexpression of the TCR Vbeta3, Vbeta7, and Vbeta13.1 gene families was detected among the infiltrating T cells. These tissues were also found to be CVB3-positive. In vitro exposure of peripheral blood mononuclear cells to lysates of cells infected with CVB3 was capable of stimulating expansion of the same TCR Vbeta families. The TCR Valpha repertoire was never found to be skewed.
A superantigen-mediated immune response is involved in human heart disease. CVB3 may directly or indirectly trigger this response, suggesting a possible mechanistic link between CVB infection and myocarditis development progressing to IDC.
Circulation 09/1998; 98(8):777-85. · 14.74 Impact Factor
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ABSTRACT: Fas is an apoptosis-inducing surface receptor involved in controlling tissue homeostasis and function at multiple sites. Here we show that beta cells from the pancreata of newly diagnosed insulin-dependent diabetes mellitus (IDDM) patients express Fas and show extensive apoptosis among those cells located in proximity to Fas ligand-expressing T lymphocytes infiltrating the IDDM islets. Normal human pancreatic beta cells that do not constitutively express Fas, become strongly Fas positive after interleuken (IL)-1beta exposure, and are then susceptible to Fas-mediated apoptosis. NG-monomethyl-L-arginine, an inhibitor of nitric oxide (NO) synthase, prevents IL-1beta-induced Fas expression, whereas the NO donors sodium nitroprusside and nitric oxide releasing compound (NOC)-18, induce functional Fas expression in normal pancreatic beta cells. These findings suggest that NO-mediated upregulation of Fas contributes to pancreatic beta cell damage in IDDM.
Journal of Experimental Medicine 11/1997; 186(8):1193-200. · 13.85 Impact Factor
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ABSTRACT: FK-506 is an immunosuppressive agent used mainly to prevent allograft rejection in organ transplant patients. Recently, it has been applied as a treatment for patients with autoimmune disorders. An entity called posttransplant lymphoproliferative disorder (PTLD) is a well-recognized result of immunosuppression in transplant patients receiving long-term immunosuppression. This disorder is a complication of treatment with FK-506 in 0.7 to 1.6% of transplant patients and is usually of B-cell origin. A majority of patients have serologic evidence of EBV infection. We report a case of a patient receiving long-term FK-506 therapy for multiple sclerosis who developed lymphoproliferative disorder involving the cervix. We will discuss the possible role of FK-506 initiation of this tumor.
Gynecologic Oncology 09/1996; 62(2):301-3. · 3.89 Impact Factor
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ABSTRACT: Insulin-dependent diabetes mellitus (IDDM) is a T-cell-mediated autoimmune disease whose onset is believed to be triggered by unknown environmental factors acting on a predisposing genetic background. Islet-infiltrating T (IIT) cells from two IDDM patients, who had died at the onset of the disease from brain swelling as a complication of ketoacidosis, were analysed. The results provided evidence for the involvement of a pancreatic islet cell membrane-bound superantigen as a diabetes aetiopathogenetic factor. There was a selective expansion of a T-cell receptor (TCR) variable segment of the beta-chain (V beta 7) in these IIT cells in association with unselected V alpha-chain segments; extensive junctional diversity of the TCR V beta 7 chains; and evidence of positive selection, after exposure to diabetic islet cell membrane preparations, of V beta 7+ T-cell clones among peripheral blood lymphocytes from non-diabetic individuals.
Nature 10/1994; 371(6495):351-5. · 36.28 Impact Factor
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Transplantation Proceedings 05/1994; 26(2):598. · 1.00 Impact Factor
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ABSTRACT: To ascertain why HLA-DR2 seems to confer only a moderate resistance to insulin-dependent diabetes mellitus (IDDM) in the high-incidence population of Sardinia, Italy, 32 families having one individual affected with IDDM (the proband) and 31 families without IDDM history were randomly selected from the same geographical area and serologically and molecularly HLA typed. The 64 haplotypes of the probands were then compared with the 122 haplotypes determined in the parents from the control families. Two haplotypes were found to have the highest percentage in the general population (12.3% and 7.3%, respectively). The first is the already described "Sardinian" extended haplotype A30, Cw5, B18, 3F130, DR3, DRw52, DQw2 (39.0% in IDDM patients). The second is an extended haplotype that has not been identified before (A2, Cw7, B17, 3F31, DR2, DQw1), and, due to the DR2 allele, we expected it to be decreased in IDDM. However, a stratified analysis performed by removing the DR3 and DR4 haplotypes showed that the frequency of this haplotype is significantly increased in IDDM patients. A peculiar feature of this haplotype is its DQw1 allele, which is DQB1*0502 and has serine in position 57 of the DQ beta chain. The absence of an aspartic acid in this position seems to confer susceptibility to IDDM and not resistance. The fact that DQB1*0502 was present in 75% of the Sardinian DR2 haplotypes may explain why, in Sardinia, DR2 is not providing the commonly recognized resistance to IDDM.
Human Immunology 08/1991; 31(3):159-64. · 2.84 Impact Factor
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ABSTRACT: The allelic forms of the human leukocyte antigen (HLA)-DQ beta-chain (DQB1) have been recognized as the best markers of insulin-dependent diabetes mellitus (IDDM) susceptibility. We describe a method that allows the recognition of these DQB1 alleles without the use of either allele-specific oligonucleotide probes or radioactive material. This method determines these alleles by electrophoretically separating restriction enzyme-generated fragments from the polymerase chain-reaction-amplified second exon of the HLA-DQB1 gene, which encodes the first domain of the protein chain. This digestion method, which is simpler and more rapid than the previously adopted hybridization method, is described in detail to enable individuals at any clinical laboratory to quickly ascertain IDDM susceptibility.
Diabetes 01/1990; 38(12):1617-22. · 8.29 Impact Factor
