Abstract
Background: Sanjad Sakati Syndrome (SSS) is an autosomal recessive multisystem disorder characterized by congenital hypoparathyroidism, prenatal and postnatal growth and mental delay, dysmorphic features, and hypocalcemia seizures. It has not been linked with autoimmune disorders such as Type 1 Diabetes (T1D). Viral infections may play a role in triggering the development of T1D. Contracting SARS-CoV-2 virus may induce an autoimmune response by damaging the pancreatic β cells and accelerate the onset of T1D. To the best of our knowledge, no case studies of SSS has been reported to develop T1D were reported. Aim: To present a child with SSS who was newly diagnosed with T1D and SARS-CoV-2 infection (COVID-19). Method: Data on the patient were extracted from the Childhood Onset Diabetes electronic Registry (CODeR) in Kuwait. Results: The child was diagnosed early in life with SSS by tubulin-specific chaperone E (TBCE) gene mutation. The child is under multidisciplinary care and managed by alphacalcidol treatment. In May 2021, she presented with a history of fever, cough, polyuria, polydipsia, and poor appetite which lasted for 6 days. On investigations, random blood sugar level was 22 mmol/l and HbA1c level was 10%. There was no evidence of diabetic ketoacidosis. Autoantibodies to glutamic acid decarboxylase (GAD) and thyroperoxidase antibodies (TPO) were positive, with normal thyroid function results. Serum insulin and c-peptide levels were low (0.93 miu/ml, 28 pmol/l respectively). Thus, T1D diagnosis was made, and insulin therapy was started. No family history of diabetes was reported. On admission, the child tested positive for SARS-CoV-2 PCR and had positive contacts with family members with COVID-19 infection. As per WHO COVID-19 infection severity criteria, the child’s condition was classified as mild. She was discharged home with no short-term sequelae of COVID-19 infection; diabetes and dietary education was provided. Discussion: To the best of our knowledge, this is the first case reported in literature of a patient with SSS who presented with T1D onset along with COVID-19 infection. Viral infections such as SARS-CoV-2 virus may trigger the development of autoimmune diseases such as T1D. Exploring the relationship between COVID-19 infection and T1D onset is needed for better understand the effect of COVID-19 infection and outcome on pediatric patients with comorbidities. Further explorations are also needed to study the relationship of SSS and autoimmune disorders as well; to fully appreciate the impact on such patients.
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