Introduction: Eosinophilic esophagitis (EoE) has been historically more associated with Caucasians. There is currently increased evidence that this disease is underreported in other races especially African American population. In addition, other reports have suggested that EoE may manifest differently in the African American population. The aim of this study is to examine outcomes of EoE based on different racial backgrounds. Methods: Patients hospitalized between 2016 and 2019 who were admitted primarily with EoE or with EoE associated complication (Food impaction, refractory GERD, Dysphagia) and with known EoE diagnosis were identified using International Classification of Diseases Code,10 th Revision Clinical Modification (ICD-10) identified from the Healthcare Cost and Utilization Project databases (HCUP) using the National inpatient sample (NIS). Those patients were stratified according to race. Our primary outcome was in hospital mortality. Secondary outcomes were length of hospital stay (LOS),whether Esophagogastroduodenoscopy (EGD) was performed and time to EGD. Results: After exclusion of other races, a total of 5610 hospitalizations were identified. 4935 (87.97%) patients identified as white while 675 (12.03%) identified as African American. The mean age was 33.1360.79 for the white patients as compared to 32.3962.15 for the African American patients (p50.79). Patients from African American origin had increase Length of stay, 4.04 days (95% CI 3.24-4.84) as compared to 3.14 days (95% CI 2.86-3.42) for white patients, p, 0.001. The mortality rate for white patients was 0.001% as compared to 0% for African American patients (p50.71). 2790 (95% CI 2614.96-2965.04) white patients had EGD as compared to 360 (95% CI 280.26-439.73) African American patients. The median time to EGD was 1 day (IQR51) for white patients and 2 days (IQR52) for African American patients. Log rank test showed x 2 (2) 53.88 and p50.04 Conclusion: Patient from African American descent admitted with EoE appear to have similar mortality as compared to white patients but higher morbidity in the form of longer LOS and longer time to EGD. Further prospective studies are needed to examine these differences and identify possible causes for it.
During the surgery the patient was noted to have extensive thrombus involving the portal system including the main portal vein as well as the superior mesenteric vein, and thrombus in the hepatic veins. Testing for hypercoagulable state was positive for JAK2 V617F mutation, and he was begun on treatment with hydroxyurea. Discussion: His development of Budd-Chiari syndrome is felt to be due to this hypercoagulable state combined with dehydration from strenuous exertion. There was no hepatomegaly noted on imaging which had led to confusion regarding the diagnosis of Budd-Chiari syndrome, but the occlusion of the portal vein in this patient resulted in decreased blood flow to the liver and prevented the development of hepatomegaly. His initial development of lactic acidosis, leukocytosis, and elevated ferritin is felt to be the result of marked hepatic necrosis from the Budd-Chiari syndrome but had led to confusion over the possibility of septic shock or bowel ischemia.
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