Background: Since the beginning of COVID 19 pandemic, great evidence has emerged regarding higher risk of coronavirus disease, its severity and complications in patients with type 2 diabetes mellitus (DM). Otherwise, it had been postulated that SARS-CoV-2 could induce severe metabolic decompensation of pre-existing or new-onset diabetes. In this report, we explore the possibility of COVID 19 induced diabetes. Results: Case presentation: A 39-year-old man was admitted to a tertiary referral hospital with a 10-day history of thirst, polyuria and feeling generally unwell. He referred fever and cough, and he had lost 3 kg in weight over the past 2 weeks. He did not report dyspnoea, abdominal pain or dysuria. There was no significant past medical history of note. Family history included type 2 diabetes in his mother and uncle. On examination, he was tired, tachycardic at 105 beats/min, had a temperature of 37.6°C, blood pressure of 125/70 mmHg, body mass index (BMI) 28.77 kg/m2 and respiratory rate of 28/min, with otherwise normal chest examination. Cardiac auscultation and abdominal palpation were normal. Arterial blood gas revealed a pH of 7.34, bicarbonate 19 mmol/L, PaO2 of 96 mmHg, PaCO2 of 41 mmHg. Serum glucose was 27.53 mmol/L with strong positive uric ketones. A chest X-ray was performed and reported as normal. He was sent for testing for COVID-19 with a positive result. He was initially managed with insulin intravenous infusion at around 0.1 U/kg/h and fluid and potassium replacement. He received antipyretic and analgesic drugs but no other therapy for COVID-19 infection as he had not respiratory symptoms. The diabetes study was completed in the conventional hospital ward. Haemoglobin A1c was 14.3%. C peptide was at lower limit of normal values and autoantibodies were negative. Those findings were sufficient to establish a diagnosis of ketosis-prone diabetes mellitus (KPDM). He underwent a good evolution and could start during the remaining hospitalization a subcutaneous basal-bolus insulin therapy. His insulin requirement was approximately 1.5 U/kg/d. He was finally discharged with an insulin regimen. During the next weeks of follow-up the insulin requirements were progressively lower so that the prandial insulin was retired, basal insulin dose was decreased and metformin was introduced finally achieving an appropriate metabolic control. Discussion: KPMD is a clinical entity characterized by an acute onset with severe hyperglycemia and ketosis similar to the presenting form of type 1 DM, but without its autoimmune component. Subsequently, its evolution resembles that of type 2 DM. This situation is caused by an acute, reversible dysfunction of the beta cell in individuals with insulin resistance. In our case, KPDM onset is occurring in a patient at the same time he was infected by coronavirus disease. We hypothesize that SARS-CoV-2 could perform a role when triggering the diabetes onset, as coronavirus can induce beta cell damage due to either its direct lytic effects and the host inflammatory response induced. However, there is not enough evidence to say if it was a trigger or simply COVID-19 infection and diabetes onset concurred at the same time.