and hospital charges using STATA 17. Multivariate logistic and linear regression analysis was used accordingly to adjust for confounders. Results: We identified 1,198,839 patients with IBD of which 235,880 patients were matched to those with anxiety. Average age was 52.04 years. There was a significant decrease in inpatient mortality (OR 0.56, CI 0.51-0.62, P , 0.0001) and total cost of hospitalization (-$3,242.13, CI -4,259.55 --2224.70, P , 0.0001), but hospital length of stay increased (0.27 days, CI 0.20-0.34, P , 0.0001) between patients with IBD with cannabis use when compared to IBD patients without cannabis use. Conclusion(s):The different clinical manifestations and symptoms of IBD may cause several psychological changes in patients. Past studies demonstrated that psychological stress and disorders can trigger flares and relapses in patients with IBD. Our study showed that there was a statistically significant decrease in inpatient mortality and hospital LOS for patients with both IBD and anxiety compared to those with only IBD. Anxiety is known to be 2 to 3 times higher in patients with IBD, but it reduces morbidity and mortality. This may be due to the increased surveillance and treatment to this subgroup of patients. Given the known association between IBD and anxiety, clinicians be vigilant in detecting and treating concomitant anxiety as this could lead to better outcomes in this patient population, as our study revealed. Future randomized control trials are needed to further study the impact of anxiety on IBD.
TNF-α producing antigen (Ag)-specific CD8 T cells induce upper genital tract (UGT) pathology following primary C. muridarum infection; therefore, we hypothesized that a vaccine regimen must subvert Ag-specific CD8 T cell response following immunization, and/or challenge to attenuate Chlamydia-induced UGT pathology. We evaluated three immunization regimens: live-chlamydial elementary body intranasal (EB-i.n.), live-EB i.m. (EB-i. m.), and irrelevant antigen bovine serum albumin i.n. (BSA-i.n.) that induced near-total (90%), partial (50%), and no (0% ) protection, respectively against oviduct pathology following i.vag. C. muridarum challenge in C57BL6/J animals. Live-EB-specific IFN-γ, TNF-α, and IL-17 response from purified splenic CD8 T cells was evaluated on days 7, 14, and 21 after immunization. There was no detectable reduction of Ag-specific CD8 T cell response following immunization with protective vaccine regimens. We evaluated splenic live-EB-specific CD8 T cell responses on days 3, 6, 9, and 12 following i.vag. chlamydial challenge. All groups of challenged animals displayed comparable induction of Ag-specific CD8 T cell cytokine responses on day 6 after challenge. As early as day 9 after challenge, Ag-specific IFN-γ and TNF-α production from CD8 T cells was significantly reduced in EB-i.n.-, compared to the EB-i.m.- or BSA-i.n.-immunized animals. On day 12, both EB-i.n.- and EB-i.m.-immunized animals displayed minimal Ag-specific TNF-α production, compared to enhanced TNF-α production from CD8 T cells in BSA-i.n. immunized animals. These results suggest that TNF-α producing CD8 T cell response could serve as a predictive biomarker of anti-chlamydia vaccine efficacy against reproductive pathology.
Case: Hepatic abscesses are a rare extraintestinal manifestation of inflammatory bowel disease (IBD) with only 60 cases reported in the literature, the majority of which being in Crohn's disease (CD) patients. In ulcerative colitis (UC) patients, Streptococcus is the most common pathogen identified in hepatic abscesses followed by Escherichia coli, and Staphylococcus aureus is the most common cultured hepatic abscess aspirate from Crohn's disease patients. In extremely rare cases, however, no pathogen is isolated, and these so-called visceral aseptic hepatic abscesses represent part of the spectrum of neutrophilic disease and an extremely rare manifestation of IBD. Our case illustrates a middle-aged female with Crohn's disease on adalimumab presenting with an aseptic hepatic abscess. A 49-year-old female with a history of longstanding Crohn's disease on adalimumab status-post partial ileal resection, atrial fibrillation on apixaban, chronic obstructive pulmonary disease, lupus, and hypothyroidism presented for 2 days of cramping right hemi-abdominal pain, fever, and vomiting. Her vitals were within normal limits. Labs showed a mild leukocytosis of 11.1 with neutrophilic predominance, an erythrocyte sedimentation rate of 67, and a C-reactive protein of 20.64. The rest of her labs were unremarkable. Computed tomography (CT) of the abdomen/pelvis showed a subcapsular 2.4 x 2.3 x 1.7 cm rim-enhancing abscess within segment 5 of the liver with central and peripheral hypodensity. There was also a short segment of proximal ascending colon wall thickening most consistent with an inflammatory colitis. She was given ceftriaxone and metronidazole in the emergency department. Repeat CT the following day showed an increase in abscess size, now measuring 3.4 x 3.3 x 3.1 cm. The patient was switched to piperacillin-tazobactam per Infectious Disease recommendations due to concerns for hepatic inoculation from Crohn's colitis and underwent an ultrasound-guided placement of a percutaneous drainage catheter into the abscess by Interventional Radiology 2 days later. Fluid cultures were remarkably negative for any organisms. Post-procedure, with continued catheter drainage, the patient reported significant improvement of symptoms. She was discharged along with removal of her catheter on hospital day 14 with instructions to hold her adalimumab until follow-up in clinic. There are only 7 other reports of aseptic abscesses in the literature as the presenting manifestation of Crohn's disease. Multiple theories have been purported regarding the development of hepatic abscesses in IBD patients. One proposes that ulceration and loss of mucosal barrier integrity leads to microbial invasion of the portal venous system with parenchymal seeding. Another suggests that the increased incidence of cholelithiasis and primary sclerosing cholangitis in IBD patients leads to ascending cholangitis and dissemination of bacteria up the biliary tree to seed the liver. Biologics and other immunosuppressives have also been suggested to reactivate chronic inf...
We have demonstrated previously that CD4 T cells are protective whereas CD8 T cells cause reproductive pathology following genital chlamydial infection. In this study, we explored the interactions of these cell types in context of vaccine-mediated protection. We evaluated three immunization regimens: live-chlamydial elementary body intranasal (EB-i.n.), live-EB i.m. (EB-i.m.), and irrelevant antigen bovine serum albumin i.n. (BSA-i.n.) that induced near-total (90%), partial (50%), and no (0%) protection, respectively against oviduct pathology following i.vag. C. muridarum challenge in C57BL6/J animals. We found no differences in Chlamydia-specific IFN-g, TNF-α, or IL-17 response from purified splenic CD8 T cells on days 7, 14, and 21 after immunization. We further evaluated Chlamydia-specific splenic CD8 T cell responses on days 3, 6, 9, and 12 following i.vag. chlamydial challenge. All groups of challenged animals displayed comparable induction of Ag-specific CD8 T cell cytokine responses on day 6 after challenge. As early as day 9 after challenge, Ag-specific IFN-g and TNF-α production from CD8 T cells was significantly reduced in EB-i.n.-immunized mice, and on day 12, both EB-i.n.- and EB-i.m.-immunized animals displayed minimal Ag-specific TNF-a production, compared to enhanced TNF-a production from CD8 T cells in BSA-i.n. immunized animals. Furthermore, adoptive transfer of Chlamydia-specific CD4 T cells at the time of genital infection induced significant reduction in Chlamydia-specific splenic CD8 T cell response on day 12 after challenge. In summary, these results suggest that Ag-specific CD4 T cells subvert a pathogenic Chlamydia-specific CD8 T cell response to protect against reproductive pathology.
Stevens-Johnson syndrome (SJS) is a potentially life-threatening cutaneous disorder that is characterized by skin erosions. It lies on a spectrum of varying severity with toxic epidermal necrolysis (TEN) being the most severe form. An overlap of the syndromes is known as SJS/TEN. These disorders are most often caused by a drug reaction, with anti-epileptic drugs and sulfonamide drugs as the common offending agents. Rarely, the syndrome can be due to a reaction to carbonic anhydrase inhibitors such as methazolamide. When present in association with methazolamide, the syndrome has only been known to occur in patients of Asian descent with human leukocyte antigen (HLA) mutations. We present a case of methazolamide-associated Stevens-Johnson syndrome in a patient of Caucasian descent.
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