New Onset Diabetes and Acute Pancreatitis- A Sequela of Long COVID?

Introduction: The association between worse COVID-19 outcomes and diabetes has been well-established in the literature. However, with more cases of new-onset diabetes and pancreatitis being reported with or after COVID-19 infection, it poses the question if there is a causal relationship between them. Case Description: 31 y/o female with COVID-19 infection 4-6 weeks ago with moderate symptoms (not requiring hospital admission or monoclonal ab), presented to ED with bandlike epigastric pain radiating to back, which is worsened with food, associated with nausea, vomiting, polyuria, and fatigue. Workup showed lipase 232, AST 180, ALT 256. Blood glucose was 281 and HbA1c was 12. CT A/P showed post cholecystectomy status, normal pancreas with mesenteric adenitis. MRCP showed hepatic steatosis with trace fluid around the pancreas s/o inflammation, and no evidence of choledocholithiasis or biliary dilatation. She denied alcohol use and autoimmune workup for pancreatitis was unremarkable. Islet cell antibodies were negative. The patient improved with fluid resuscitation and was discharged home on insulin with plans to transition to oral agents outpatient. Discussion(s): Long COVID is defined as a range of conditions or symptoms in patients recovering from COVID-19, lasting beyond 4 weeks after infection. A retrospective cohort study showed increased new-onset diabetes incidence in patients after COVID-19. This was redemonstrated in a systematic review and meta-analysis that showed a 14.4% increased proportion of new diagnoses of diabetes in patients hospitalized with COVID-19. Possible pathophysiology that have been attributed to this include undiagnosed pre-existing diabetes, hyperglycemia secondary to acute illness and stress from increased inflammatory markers during the cytokine storm, the effect of viral infections on the pancreas, and concurrent steroid use in patients with severe respiratory disease. The binding of SARS-CoV-2 to ACE2 receptors is thought to the other mechanism by which COVID can cause pancreatitis and hyperglycemia. Study showed increased lipase and amylase levels in patients with COVID and the increase in serum levels was proportional to the severity of the disease. Patients who died due to COVID-19 were also found to have degeneration of the islet cells. While, several studies have showed new onset diabetes and pancreatitis during an active COVID infections, we need larger cohort studies to comment on its true association or causation, especially in patients with long COVID symptoms. As more cases of new onset diabetes and pancreatitis with COVID-19 are being reported, there may be a need for more frequent blood sugar monitoring during the recovery phase of COVID-19.Copyright © 2023

New Onset of Type 1 Diabetes After Severe Acute Respiratory Syndrome Coronavirus 2 Vaccination

Introduction: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) poses the greatest threat of our times. SARS-CoV-2 vaccines are one of the most effective strategies against this infection. Diabetic ketoacidosis, hyperglycemic hyperosmolar syndrome, and new-onset diabetes as adverse effects of SARS-CoV-2 vaccination have been infrequently described in the literature. We hereby report a rare case of new-onset type 1 diabetes after SARS-CoV-2 vaccination. Case Description: An 18-year-old male presented to the outpatient office for evaluation of breast pain. On routine laboratory tests, he was noted to have fasting blood glucose of 200 mg/dL. On further questioning, he reported some polyuria, nocturia, and a 10-pound weight loss over the preceding month. He received the initial dose of Pfizer-BioNTech SARS-CoV-2 vaccine in May 2022 and the second dose in June 2022, approximately one month before the onset of symptoms. He denied any earlier viral infections and had no personal or family history of autoimmune conditions. On evaluation, his body mass index was 20 kg/m2, but otherwise, he had a normal physical exam, including a breast exam. Over the next few days, his blood glucose progressively increased to over 300 mg/dl. HbA1c was noted to be elevated at 8.6%, glutamic acid decarboxylase-65 (GAD-65) antibodies were remarkably high >250 IU/ml (normal 5 IU/ml), C-peptide was 1.51 ng/ml (normal 0.80 - 3.85 ng/ml), blood glucose 156 mg/dl, islet-cell antibody titer was 320 (< 1.25 JDF units) and insulin autoantibodies were negative. He was diagnosed with autoimmune Type 1 diabetes and a basal-bolus insulin regimen was initiated to improve glycemic control. On a one-month follow-up, his insulin requirements remained low but persistent and his glycemic control was acceptable. Discussion(s): Various viruses are known to play a fundamental role in the onset of type 1 diabetes via a variety of effects on pancreatic beta-cells because of either the direct lytic effects of viral replication or the inflammatory response to the virus, which is mediated by autoreactive T cells. The limited release of islet cell antigens induces molecular mimicry and paves the way for long-term autoimmunity and the development of type 1 diabetes mellitus. Our patient did not report any viral illnesses before the onset of his symptoms. He also did not have a family or personal history of autoimmune diseases. His onset of diabetic symptoms coincided temporally with receiving the SARS-CoV-2 vaccine. The detection of a considerable titer of GAD-65 antibodies proved autoimmunity. Clinicians must stay vigilant about this potential side effect of SARS-CoV2 vaccine so that a timely diagnosis can be made.Copyright © 2023

DIABETIC KETOACIDOSIS IN A NEW ONSET ELDERLY TYPE 1 DIABETES AFTER SARS-CoV-2 VACCINATION: ASSOCIATION OR COINCIDENCE?

Introduction In the era of the COVID-19 pandemic, several cases of new onset diabetes associated with COVID-19 have been reoprted. Additionally, patients with diabetes, a high-risk population, are prioritised for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination. The vaccine against the (SARS-CoV-2) could represent a new environmental trigger for autoimmune disorders such as Graves' disease, immune thrombotic thrombocytopenia, autoimmune liver diseases, Guillain-Barré syndrome, systemic lupus erythematosus and type 1 diabetes. case We report a case of diabetic ketoacidosis in a new onset Type 1 diabetes in an elderly female following SARSCoV- 2 vaccination. A 69-year-old female with a history of treated TB abdomen in 2015 with no history of diabetes received her second dose of SARS-CoV-2 vaccination (COMIRNATY) on 21st August 2021. Two weeks following vaccination, she developed osmotic symptoms, reduce appetite and lethargy. Her random blood glucose (RBS) was 41 mmol/L, serum ketone 4.4 mmol/L, pH of 7.29 mmHg, bicarbonate 12.5 mmol/L and serum osmolarity of 298 mOsm/kg. She was treated for DKA with intravenous insulin infusion and hydration with resolution of DKA within 12 hours. Anti-Glutamic Acid Decarboxylase and anti-Islet Cells antibodies were positive with low fasting C-peptide of 102 pmol/L. She was discharged well with basal bolus insulin. Four months later, HbA1c reduced from 15.6% to 7.7% with a random C-peptide of 152 pmol/L. Conclusion The occurrence of hyperglycaemia crisis following SARSCoV- 2 vaccine in patients with pre-existing diabetes is known but the occurrence of new onset autoimmune diabetes following vaccination is rare. Further studies are needed to better understand the underlying pathogenesis of autoimmune diabetes following SARS-CoV-2 vaccine.

New Onset Autoimmune Diabetes Associated with Acute SARS-COV-2 Infection

Introduction: Infection with SARS-CoV-2 has been shown to cause complications affecting nearly all organ systems of the human body. Here, we outline a case of SARS-COV-2 associated with new onset of autoimmune diabetes. Case Description: A 62-year-old female with past medical history of class III obesity, primary hypothyroidism, obstructive sleep apnea, and endometrial cancer established care with a multidisciplinary bariatric team in March 2021. This team included a dietician and psychologist to promote healthful lifestyle intervention with the intent to undergo bariatric surgery in December 2021. At a follow up visit in September 2021 her HbA1c was 6.7% (normal < 5.7 %) and she was diagnosed with type 2 diabetes treated with healthful lifestyle. After lifestyle modification the patient successfully lost 40 pounds. In December 2021, she presented to the ED (Emergency Department) complaining of fatigue and neuropathy. She was found to be hyperglycemic with glucose 369 mg/dL (normal 70-100 mg/dL). β-hydroxybutyrate was 32.1 mg/dL (normal 0.20-2.81 mg/dL) and anion gap was 10 mmol/L (normal 3-13 mmol/L). She was resuscitated with fluid and referred urgently to Endocrinology. One week later, she was seen in the office by her endocrinologist for initial consultation. She was acutely complaining of anosmia and ageusia and found to be positive for acute SARS-COV-2 infection. Bloodwork revealed an increase in HbA1c to 13.9 %, fasting glucose 303 mg/dL (normal 70-100 mg/dL), normal C-peptide 1.6 ng/dL (normal 0.5-3.3 ng/dL), elevated GAD antibody 154.3 IU/mL (normal 0-5 IU/mL), elevated anti-Islet Cell antibody IgG ratio 1:64 (normal < 1: 4), elevated anti-Islet Antigen 2 antibody >120 U/mL (normal 0–7.4U/mL), and elevated anti-Zinc Transporter 8 antibody 500 U/mL (normal 0–15 U/mL). Patient was diagnosed with autoimmune diabetes associated with acute SARS-COV-2 infection and was started on basal-bolus insulin with improvement in her hyperglycemia. She did not require hospital admission or steroid treatment for SARS-COV-2 infection. Discussion: Although viral infections are associated with type I diabetes related autoimmunity in children, this case study is unique regarding its mechanism in association with SARS-CoV-2 infection. Potential mechanisms underlying onset of diabetes in patients with SARS-COV-2 infection are still under investigation. One potential mechanism involves pancreatic beta cell dysfunction with diminished insulin secretion due to a systemic inflammatory cascade. This case is unique in as the patient’s C-peptide was still detectable indicating intact beta cell function. Furthermore, the patient’s diabetes paradoxically worsened after a more healthful lifestyle and 40-pound weight loss. This patient’s case of autoimmune diabetes illustrates the need for further research into the mechanisms underlying the onset of diabetes after SARS-COV-2 infection.

A case of newly diagnosed type 2 diabetes complicated by SARS-CoV-2 infection

Introduction: Covid-19, a novel Coronavirus SARS-COV-2, has caused major morbidity and mortality worldwide most especially in the high-risk population. SARS-COV-2 has caused more unfavorable outcomes and increased insulin resistance in patients with diabetes mellitus. It has been observed that many of these patients require very high doses of insulin to manage hyperglycemia. This will discuss a case of a young male with newly diagnosed type 2 diabetes complicated with Covid-19 infection. Case Description: 38-year-old Hispanic male with no past medical history presented to the emergency department with shortness of breath, cough, and chest congestion. His only medication was azithromycin. He had no family history of diabetes mellitus. There was no acanthosis nigricans on examination and the patient's BMI was 26.7 kg/m 2 . The patient was admitted for severe acute respiratory syndrome and diabetic ketoacidosis. His hba1c level was 13.7%, c-peptide was inappropriately low with a value of 0.31 ng/mL and glucose of 153 mg/dL and GAD-65 and islet cell antibodies were negative. Endocrinology was consulted for diabetic management. The patient was started on basal insulin 5 units at bedtime;however, the dose was increased to 7 to 9 to 12 and then 20 units at bedtime due to uncontrolled sugar levels. The patient was started on short-acting insulin before meals because his glucose ranged from 156 mg/dL to 381 mg/dL. The patient clinically improved and was discharged on hospital day 12. He got discharged on insulin detemir 20 units at bedtime and insulin lispro 8 units before meals. On a visit to the clinic, the patient was weaned off of insulin due to better glycemic control. His hba1c level significantly dropped to 7.2% and his c-peptide level improved to 3.21 ng/mL. He is now been controlled only on metformin 1000mg twice a day. Discussion: There is no definite explanation for why SARS-COV- 2 infection causes new-onset diabetes and worsening insulin resistance. However, there have been some theories attributed to the effects of the SARS-COV-2 coronavirus on angiotensin-converting enzyme 2 (ACE2). ACE2 is present in metabolic organs and tissues including pancreatic beta cells. As a result, an infection with the SARS-COV-2 virus could affect the pathophysiology of glucose metabolism causing increase insulin resistance. Another theory explains that coronavirus could cause ketosis-prone diabetes causing diabetic ketoacidosis in patients with no known history of hyperglycemia. Therefore, Covid-19 has some association with diabetes mellitus management outcomes.

New onset diabetes in a boy with multi-system inflammatory syndrome in children (MIS-C) following SARS-CoV-2 infection

Introduction: Case report Objectives: During the past year, COVID-19 infection was recognized as a potential trigger for new onset diabetes in children. A rare but severe complication of COVID-19 infection in children and adolescents is multisystem inflammatory sindrome in children (MIS-C). We describe a case of newly diagnosed diabetes mellitus (DM) in a tenyear old patient during the course of MIS-C. Methods: Case report Results: A ten-year-old previously healthy male presented with vomiting and painful and enlarged lymph nodes. He was febrile to 39.4°C and tachycardic to 124 beats/minute. Initial laboratory evaluation was notable for acute infection, but the child also had hyperglycemia, ketonuria, glycosuria. Empiric antibiotic therapy was started, but he was persistently febrile, had lymphadenopathy with redness of the surrounding skin and developed conjunctival injection and a discrete livid erythema on the trunk. His follow up labs showed leukopenia with lymphocytopenia and neutrophilia, anemia and thrombocytopenia and upsurge of inflammation markers. Other possible causes of his condition were excluded and he tested positive for anti-SARS-CoV-2 IgM and IgG via immunochromatographic assay. Criteria for MIS-C was met, and intravenous immunoglobulin treatment was started which yielded immediate recovery. During the acute course of MIS-C his blood glucose levels were up to 15.5 mmoL/L, with no disturbances in acid-base status. Since high glucose levels and glucosuria persisted beyond resolution of the MIS-C, and HbA1c was elevated (7.8%), the patient was started on intensified therapy with insulin analogues. Islet-cells autoantibodies were only marginally elevated (GAD-65 1.9 and IA-2A 1.8 kIU/L) and C-peptide was normal. Conclusions: In pediatric population inflammatory syndromes like MIS-C can raise the risk for diabetes development or presentation. Therefore it is important to monitor glycemia during the course of MIS-C and also during post-inflammatory follow-up.

COVID-19 and new-onset type 1 diabetes mellitus in a large Portuguese pediatric diabetes center: What changed?

Introduction: On 12th March 2020, a national lockdown was imposed in Portugal, as a response to rising COVID-19 cases. Since then healthcare access patterns were deeply modified. Objectives: In this study, we tried to understand what shifted from prior years in new-onset type 1 diabetes mellitus (T1D). Methods: It was performed a retrospective analysis of patients referred to a level III pediatric hospital from March 2020 until March 2021. Patients admitted during the same period in the 3 previous years were set as control group. Results: Since lockdown imposition, 44 children and adolescents were diagnosed T1D, contrasting with prior mean incidence of 32 cases/ year. Median age was 9,9 years (min. 0,5 - max. 15,8). Children under 2 years-old represented 4,9% of cases, contrasting with only 2,1% in previous years. All subjects were tested for SARS CoV-2 but only 2 were positive. When comparing to prior years, subjects presenting with less than one week of symptoms almost doubled in 2020, (19,5% vs. 10,4%), and a higher rate of diabetic ketoacidosis (DKA) was also observed (53,7%, vs. 38,5%). DKA severity was also higher (40,9% vs. 21,6%;p=0,02 and 14,6% subjects required admission to intensive care unit. Conclusions: Similarly to other reports, a higher number of new-onset T1D was observed, with a comparable increase in severity. In contrast to what might have been expected, DKA prevalence and severity was not necessarily linked to delayed diagnosis. We estimate that such severity may be related to a higher proportion of younger patients. While the role of SARS CoV-2 exposure in pancreatic islet cells destruction is still under investigation, antibody assessment and detailed contact history could help to explain the increased prevalence and severity of new-onset T1D during the pandemic period.