In response to the coronavirus disease 2019 (COVID-19) pandemic, the COVID-19 vaccine was rapidly developed, and the effectiveness of the vaccine has been established. However, various adverse effects have been reported, including development of autoimmune diseases. We report a case of new-onset polyarteritis nodosa (PAN) in a 32-year-old male following COVID-19 vaccination. The patient developed limb pain, fever, pulmonary embolism, and multiple subcutaneous nodules and haematomas. Skin biopsy revealed necrotising inflammation accompanied by fibrinoid necrosis and high inflammatory cell infiltration in the walls of medium to small arteries. The symptoms resolved following corticosteroid treatment. Although it is difficult to prove a relationship between the vaccine and PAN, similar cases have been reported, and further reports and analyses are therefore necessary.

A 25-year-old man accidentally fell from a cliff and hit his right flank on the ground while camping. Initially, he was able to barely walk, but he ultimately became unable to walk at all due to severe flank pain. He had no remarkable personal or family history and was a social drinker. Upon arrival, he showed clear consciousness but was in a hemorrhagic shock state. Enhanced computed tomography (CT) revealed extravasation of contrast medium from the injured right kidney with massive retroperitoneal hematoma. He underwent massive blood transfusion and tracheal intubation followed by renal embolization. His vital signs stabilized on hospital day 2, and he was extubated on day 3. On days 4 and 5, a blood examination revealed increased levels of amylase (360 and 904 IU/L, respectively). Enhanced CT on day 5 did not show signs of severe acute pancreatitis. The maximum amylase level was 1041 IU/L on day 6 and decreased day by day without deterioration of the severity of his acute pancreatitis. He was discharged on day 14. The subacute phase of posttraumatic acute pancreatitis in the present case may have been induced not by direct injury to the pancreas but by several causative factors, such as shock, increased pressure of the retroperitoneal space, or the release of inflammatory mediators from injured tissues or hematoma.

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