COVID Associated Insulitis in Type 1 Diabetes

ABSTRACT

Recent reports suggest a potential relationship between COVID-and onset of diabetes (DM) . We present the case of a 35 yr old female with type 1 DM (T1DM) who following COVID-pneumonia (COVP) developed worsening insulitis suggesting a potential direct effect of COVID-on beta cell function. The patient is a 35 yr old Caucasian female with T1DM first diagnosed 5 yrs ago. She had some residual beta cell secretory function with fasting C-peptide;0.51 (0-8-3.85ng/ml) . She also has hemochromatosis, thyroiditis with thyroid nodular disease and +ve history of T1DM in her older brother and maternal cousin. Since diagnosis she has been on insulin pump therapy and a CGMS device with excellent glycemic control and HBA1c of 6.7-7.1. She had not received the COVID-vaccine and had COVP in July 2021 requiring inpatient care but not intubation. She received oral steroids and Remdesivir with salutary response. She has not had post-acute sequelae of SARS-CoV (PASC) but ˜ 2 months post discharge had acute thyroiditis with no thyroid abscess, elevated sed rate, leucocytosis and peak thyroglobulin;158 (3-40ng/ml) . Since discharge she noted persistent global hyperglycemia requiring increased basal and bolus insulin therapy with peak HBA1c of 8.3. Further evaluation showed active insulitis with reduced C-peptide 0.and increase in islet related antibodies compared to titers obtained at the time of initial diagnosis 5 yrs prior. The clinical presentation of our patient suggests a potential role of COVID-in inducing insulitis with significant implications for at risk patients including T1DM patients with preserved islet function but also type 2 DM and LADA patients. This case provides another compelling reason for advocating COVID-vaccination in at risk patients. The duration of this effect on islet function and whether beta cell functional recovery is possible over time remains to be seen. The insulitis manifests with worsening glycemic profiles as well as possibly impacting islet mediated counterregulatory glycemic responses.