CD4 Count Does Not Impact Disease Severity In HIV Positive Patients With Ulcerative Colitis

Abstract

Introduction: The relationship between ulcerative colitis (UC) and Human Immunodeficiency Virus (HIV) is poorly studied to date, owing mainly to the relative rarity of both diseases. Considering UC flares are mediated by CD4+ T-cell dysregulation, it has been suggested that the immunosuppressive effects of HIV-mediated T-cell destruction may concomitantly suppress UC inflammatory activity. The aim of our study was to assess the impact of HIV and suppressed CD4 count on UC phenotype and relapse risk with a matched group of UC seronegative patients. Methods: A total of 8 UC/HIV-infected patients and 40 age and gender matched seronegative controls were identified in a 10 year retrospective database of IBD patients seen at an urban medical center. Information regarding patients’ UC, HIV status, and CD4 count was collected. A UC disease flare was defined as bloody diarrhea, increase in stool frequency, and/or tenesmus, with alternate diagnoses ruled out. A value of CD4+ count <500 was used to define immunosuppression. Results: Eight patients were identified that had both HIV and UC. Six were male and 2 were female with a median age of 45 years, range 28-58 years. The seropositive (S+) UC patients were age and gender matched with 40 UC seronegative (S-) patients. Thirty were male and 10 were female with a median age of 47.5 years, range 26-59. Comparing S+ vs. S- patients, pancolitis was present in 50% S+ vs. 32.5% S-, extensive colitis in 12.5% S+ vs. 22.5% S-, left-sided colitis in 25% S+ vs. 25% S-, unknown disease extent in 12.5% S+ vs. 20% S-. No significant difference in disease phenotype was noted. There was a trend toward a higher median flare rate amongst S+ patients (1 flare per year) compared to S- patients (0.67 flares per year). Of the 23 flares documented for the UC S+ patients and 95 flares for S- patients, 39.1% S+ vs. 35.8% S- required systemic corticosteroids, and 8.7% S+ vs. 7.4% S- required anti-TNF therapy while 43.5% S+ vs. 51.6% S- of flares subsided with topical therapy alone. In total, we identified 14/23 UC flare events in the S+ patients where CD4 count was concomitantly recorded. Of these, 9 (64%) had a CD4 count <500. Comparing this group with those CD4 >500, there was no significant difference in rate of use of systemic steroid and anti-TNF therapy. Conclusion: Our findings suggest that UC/HIV+ patients demonstrate a trend toward more frequent flares than UC/HIV- patients. However, UC phenotype (disease extent) and the medications used during disease flares (a surrogate marker of disease severity) did not differ regardless of HIV status. Moreover, a low CD4 count did not alter flare frequency, extent of disease, or severity of disease (based on above surrogates).