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. Author manuscript; available in PMC: 2020 Oct 1.
Published in final edited form as: Pancreas. 2019 Oct;48(9):e66–e68. doi: 10.1097/MPA.0000000000001400

African Americans With Acute Pancreatitis Present With Worsened Kidney Injury and Have Inadequate Access to Care

Cemal Yazici 1, Kyle Geary 2, Angelica Sanchez 1, Brian R Boulay 1, Georgios I Papachristou 3, Nancy Krett 1, Paul J Grippo 1, Barbara Jung 1
PMCID: PMC6801107  NIHMSID: NIHMS1537748  PMID: 31609935

To the Editor:

Acute pancreatitis (AP) is a health care challenge1 and a major cause for gastrointestinal hospitalization. Severe AP1,2 is associated with up to 30% mortality and current management is limited to supportive care.3 Few studies identified alarming trends in the care and outcomes in AP of minority patients including increased rates of organ failure4 and mortality5 and lower rates of patient transfers6 in African Americans (AA) and longer Emergency Department wait times in Hispanics.7 These investigations established a link between health care disparities and clinical outcomes in AP8 including increased inpatient mortality in AA compared to Whites (odds ratio, 1.18, P = 0.025)5, lower transfer rates of AAs to institutions with a higher level of care6 and higher rates of organ failure among AAs with AP compared to the general population.4 However, they did not provide a detailed assessment of socio-demographic, clinical, and management metrics to determine whether specific differences in these variables underlie this disparity thus limiting our ability to address it. In this study, we assessed whether significant differences in socioeconomic status, clinical presentation, or management of AP subjects contribute to AP disparities.

African Americans and Whites 18 years of age or older who were admitted to University of Illinois at Chicago with AP between January 1, 2010 and December 31, 2015 were identified through the International Classification of Disease (ICD)-9 code for AP (577.0). Socio-demographic, clinical, laboratory and management data were collected and analyzed using Statistical Analysis Software version 9.4 (SAS, Cary, NC). T-test or Mann-Whitney U test for continuous variables and Fisher’s exact test or Analysis of Variance for categorical data were used with two-sided tests with a priori significance level of alpha = 0.05. A multivariate regression analysis was completed to determine independent predictors of creatinine by adjusting for race, body mass index (BMI), age, and comorbidities.

There were 253 subjects analyzed, of which 131 were AAs and 122 Whites (Table 1); 135 were female. There were no significant differences among AAs and Whites (Table 1) for many variables including in age, BMI, or sex (P = 0.42, P = 0.14, P = 0.08, respectively); alcohol, tobacco and illicit drug consumption (P = 0.37, P = 0.09 and P = 1.0, respectively); non-steroidal anti-inflammatory, opioid or statin use (P = 0.69, P = 0.48, P = 0.89, respectively); similar rates of diabetes mellitus, chronic kidney disease and hypertension; nor were there differences in family history of AP and underlying etiologies (P = 0.37 and P = 0.19, respectively). However, compared to Whites, AAs were more likely to have coronary artery disease (P = 0.05). In addition, AAs were more likely to live in underserved neighborhoods of Chicago (P = 0.02); had significantly lower predicted mean annual income (P < 0.0001); and the percentage of subjects transferred to UIC for higher level of care was significantly lower in AAs compared to Whites (20.6% versus 36.9%, P = 0.005) (Table).

TABLE 1.

Demographic and Clinical Data Among African Americans (AAs) and Whites With Index Acute Pancreatitis

AAs (n = 131) Whites (n = 122) P
Age, mean (SD), y 48.9 (15.8) 50.8 (17.6) 0.42
Sex, female, n (%) 77 (58.8) 58 (47.5) 0.08
Body mass index, mean (SD), kg/m2 29.8 (15.8) 29.7 (8.5) 0.14
Location of residence, n (%) 0.02
 Southern suburbs 74 (56.5) 58 (47.5)
 Northern suburbs 43 (32.8) 36 (29.5)
 Western suburbs 14 (10.7) 28 (23)
Predicted mean income, mean (SD), $ 37,924 (16,111) 58,502 (24,978) <0.0001
Transferred to UIC for higher level of care, n (%) 27 (20.6) 45 (36.9) 0.005
Past medical history, n (%)
 Diabetes mellitus 22 (16.8) 27 (22.1) 0.34
 Coronary artery disease 21 (16) 9 (7.4) 0.05
 Chronic kidney disease 10 (7.6) 9 (7.4) 1.0
 Hypertension 57 (43.5) 39 (32) 0.07
Family history of pancreatitis, n (%) 4 (3.1) 1 (0.8) 0.37
No. alcoholic drinks per week, mean (SD) 11 (20) 13 (28) 0.37
Duration of tobacco exposure, mean (SD), y 6 (10.4) 4.7 (10.9) 0.09
Etiologies, n (%) 0.19
 Gallstones 43 (33.1) 51 (41.8)
 Alcoholic 33 (25.4) 22 (18.0)
 Idiopathic 40 (30.8) 29 (23.8)
 Hypertriglyceridemia-induced 2 (1.5) 7 (5.7)
 Post-ERCP 2 (1.5) 3 (2.5)
 Other 10 (7.7) 10 (8.2)
SBP at presentation, mean (SD), mmHg 141 (23) 132 (24) (n = 121) 0.003
DBP at presentation, mean (SD), mmHg 81 (15) 74 (12) (n = 121) <0.001
Creatinine level, mean (SD), mg/dL 1.6 (2.2) 1.2 (1.2) 0.02
Disease Severity, n (%)* 0.66
 Mild 90 (68.7) 70.5 (86)
 Moderate 33 (25.2) 21.3 (26)
 Severe 8 (6.1) 8.2 (10)
Mortality, n (%) 5 (3.8) 3 (2.5) 0.15
Intensive care unit (ICU) admission rate, n (%) 21 (16.0) 14.8 (18) 0.86
ICU length of stay, mean (SD), d 1 (3.8) 1.1 (3.5) 0.87
Hospital length of stay, mean (SD), d 6 (5.9) 6.8 (7.6) 0.21
30-day readmission rate, n (%) 25 (19) 15 (12.3) 0.14

Bold value are statistically significant.

*

Disease severity based on the Revised Atlanta Classification.

SD, standard deviation; UIC, University of Illinois at Chicago; ERCP, endoscopic retrograde cholangiopancreatography, SBP, systolic blood pressure; DBP, diastolic blood pressure

Despite having higher mean systolic and diastolic blood pressures at presentation (P = 0.003, P < 0.001, respectively), AAs had significantly higher creatinine level at admission compared to Whites (1.6 mg/dL vs 1.2 mg/dL, P = 0.02). In a multivariate regression analysis, only race was found to be an independent predictor of creatinine (P = 0.037) when additional adjustments were made for age, BMI, and comorbidities.

African Americans and Whites received similar amounts of intravenous fluids within 8 hours (1.3 [standard deviation {SD}, 0.6] versus 1.4 [SD, 0.8] liters, P = 0.77) and 24 hours of admission (5.3 [SD, 2] versus 5.0 [SD, 2.1] liters, P = 0.19). Disease severity was similar between two groups (P = 0.66). Mortality rate was numerically higher in AAs compared to Whites (3.8% versus 1.6%, P = 0.29) and there were no significant differences in intensive care unit (ICU) admission rate, ICU length of stay and hospital length of stay (P = 0.86, P = 0.87, P = 0.21, respectively) between two groups. However, there was a positive correlation between creatinine levels and ICU admissions (P = 0.002) and AAs had higher 30-day re-admission rate compared to Whites (18.9% versus 12.3%, P = 0.14).

We identified significantly higher creatinine levels on admission in AAs compared to Whites. Race remained an independent predictor of creatinine in the multivariate regression analysis when adjusted for covariables. Therefore, this finding truly reflects the presence of end-organ damage in an acute setting. There were no significant differences in total intravenous fluids administration and disease severity between two groups. African Americans had higher mortality and 30-day re-admission rates compared to Whites but these did not reach statistical significance, most likely due to small study size.

African Americans with AP were more likely to live in underserved neighborhoods and have significantly lower predicted income levels. In addition, percentage of transfer among subjects who received care at our institution for AP was significantly lower in AAs compared to Whites and this is consistent with previous reports.6 This finding along with limited access to care in disadvantaged, lower income populations can explain part of existing disparities.

Our study has several limitations. It is i) a retrospective study which prevented longitudinal collection of key variables, ii) utilized ICD codes which may have resulted in under detection of AP cases,9 iii) focused on AAs and Whites, which decreased the study size. A larger study with an increased power may allow more in depth investigation of actionable factors which can be utilized to develop preventive strategies, improve access to care and optimize delivery of the care especially at high-risk groups.

Acknowledgments

Financial support: The project described was supported by the National Center for Advancing Translational Sciences, National Institutes of Health, through Grant UL1TR002003. In addition, the project described was supported by the National Center for Advancing Translational Sciences, National Institutes of Health, pilot grant to BJ through a pilot grant supported by Grant UL1TR002003 and career development grant to CY by Grant KL2TR002002. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Footnotes

Conflict of Interest Disclosure: The authors declare no conflict of interest.

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