Shared medical and environmental risk factors in dry eye syndrome, Sjogren’s syndrome, and B-cell non-Hodgkin lymphoma: A case-control study

Hadas Ben-Eli*, Doron J. Aframian, Eldad Ben-Chetrit, Dror Mevorach, Geffen Kleinstern, Ora Paltiel, Abraham Solomon

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

Objectives. To assess whether there are shared exposures associated with Sjogren’s syndrome (SS), dry eye syndrome (DES), and B-cell non-Hodgkin lymphoma (B-NHL), in order to determine whether they are etiologically related. Methods. In a clinic-based case-control study, 702 participants (91 SS, 120 DES, 211 (age and sex frequency-matched) controls, and 280 B-NHL cases) were recruited and interviewed regarding exposures, medical history, and family history. Results. Female predominance was noted in SS (ratio 9.2: 1). Eye dryness was severest in SS compared to DES and controls (P < 0 001). Compared to controls, alcohol consumption was inversely associated with NHL, DES, and SS (odds ratio OR = 0 47, 95% confidence interval (CI): 0.31-0.71; OR = 0 54, 95% CI: 0.33-0.88; and OR = 0 26, 95% CI: 0.14-0.49, respectively), while a previous history of infection requiring hospitalization was positively associated with all three conditions: NHL (OR = 1 92; 95% CI: 1.23-2.99), DES (OR = 3 29; 95% CI: 1.97-5.47), and SS (OR = 4 74; 95% CI: 2.66-8.44). NHL patients were more likely to report first-degree relatives with hematologic cancer, while having first-degree relatives with an autoimmune disease (AID) was associated with SS (OR = 5 25; 95% CI: 2.59-10.63) and DES (OR = 3 55; 95% CI: 1.83-6.91) compared to controls. Conclusions. Some exposures are associated with all three conditions (such as an inverse association with alcohol consumption and a positive association with serious past infection), while a family history of AID appears to be shared by DES and SS, but not NHL subjects. Shared risk factors for all three conditions indicate possible mutual etiological pathways.

Original languageAmerican English
Article number9060842
JournalJournal of Immunology Research
Volume2019
DOIs
StatePublished - 2019

Bibliographical note

Funding Information:
This work was generously supported by the Israel Cancer Association (grant number 8037815 to O. P.), American people through the United States Agency for International Development (USAID), and MERC (grant numbers TA-MOU-11-M31-025 and 8037812 to O. P.). The authors thank Rivkah Lender for proofreading.

Publisher Copyright:
Copyright © 2019 Hadas Ben-Eli et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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