A 22-year-old male presented with a 4-day history of fever, myalgia, arthralgia, and sore throat, alongside a 2-day history of vomiting and diarrhoea. He was a non-smoker, with no regular medications or past medical history. There was no recreational drug history or family history of note. Clinical examination revealed a fever of 38.4°C. His pulse was 89 beats per minute, blood pressure 77/34 mmHg, respiratory rate 18 breaths per minute, and oxygen saturations 98% on room air. He was noted as having a regular pulse with cool peripheries, normal heart sounds with no added sounds, and no evidence of fluid overload. Clinical examination with otherwise unremarkable. Full blood count demonstrated a normal haemoglobin (148 g/L, n = 130–175) with mild thrombocytopaenia (146×10⁹/L, n = 150–400), and a leukocytosis (22.87×10⁹/L, n = 4.0–11.0) with predominant neutrophilia (13.61×10⁹/L, n = 1.9–7.5), monocytosis (2.88×10⁹/L, n = 0.2–1.0), lymphopaenia (0.82×10⁹/L, n = 1.0–4.0), and normal eosinophils (0.17×10⁹/L, n < 0.6) and basophils (0.04×10⁹/L, n = 0.0–0.2). Other laboratory findings included an acute kidney injury [creatinine 333 μmol/L (n = 60–105), urea 22.2 mmol/L (n = 3.2–7.7)], mildly deranged liver function tests [bilirubin 22 μmol/L (n < 25), AST 123 U/L (n < 45), ALT 46 U/L (n < 45), GGT 19 U/L (n = 0–60), ALP 154 U/L (n = 40–110)], high-sensitivity troponin T (hsTnT) of 4550 ng/L (n < 15), and elevated NT-proBNP (1485 pmol/L, n < 35). C-reactive protein was markedly elevated (415 mg/L, n < 5), and lactate raised (3.6 mmol/L, n < 1.9). There was mild hyponatraemia (129 mmol/L, n = 135–145), while potassium (3.7 mmol/L, n = 3.5–5.2) was within normal limits. Electrocardiogram demonstrated sinus rhythm with right-axis deviation and diffuse ST-segment elevation. Chest radiograph was unremarkable. Initial impression was of septic shock from a presumed viral illness complicated by myocarditis, acute kidney injury, and metabolic acidosis. Due to worsening shock, he was transferred to the intensive care unit for vasopressor support, initially with noradrenaline and then dobutamine. He was commenced on empiric broad-spectrum antibiotics, and high-dose intravenous (i.v.) dexamethasone (10 mg four times daily). He responded well to therapy with clinical and biochemical improvement. Transthoracic echocardiography demonstrated severe global left ventricular (LV) systolic impairment (ejection fraction 35%), with normal LV size and wall thickness. The right ventricle had moderate systolic impairment. There was no significant valvular pathology or pericardial effusion. Endomyocardial biopsy demonstrated features of subtle interstitial lymphocytes and oedema, without associated myonecrosis. There were no giant cells, eosinophils, granulomas, or fibrosis, while stains for amyloid and iron were negative. Overall, this was felt to represent possible myocarditis without any specific features. Cardiac MRI performed on Day 4 after steroid commencement showed improved cardiac function (without having received any heart failure therapy), with high myocardial T2 signal indicative of myocardial oedema, as well as extensive circumferential late gadolinium enhancement in a subepicardial distribution, consistent with acute myocarditis (). Two attempts were made to transition to oral steroid therapy (Day 10, Day 14). Both were unsuccessful, with clinical and biochemical deterioration noted within 12 h of steroid de-escalation. This manifested as mild hypotension, fever, chest pain, and rising inflammatory markers (). In both cases, this resolved with reinstatement of i.v. steroid. Extensive testing excluded infectious and immunological causes of myocarditis (). The patient’s ferritin was markedly elevated at 20 233 μg/L (n = 20–320) with a low glycosylated ferritin percentage of 5% (n = 50–80%). Haematology review and bone marrow biopsy did not support a diagnosis of haemophagocytic lymphohistiocytosis. Given the markedly elevated ferritin levels with low glycosylated ferritin, failure to wean i.v. steroids, absence of infection, low/negative antinuclear antibody (ANA) and rheumatoid factor, the diagnosis of AOSD was considered following Rheumatology review. Bedside USS revealed mild extensor tendon oedema of both ankles, as well as bilateral knee joint effusions with synovial thickening supporting the diagnosis of AOSD. He developed a new maculopapular rash over his neck, face, and back; gradually progressing to his arms and trunk. There was no skin peeling or involvement of the oral mucosa. Skin biopsy was consistent with the cutaneous manifestation of Still’s disease and not of a delayed drug reaction (). No lymphadenopathy or organomegaly was noted at any point. The patient received pulsed methylprednisolone for 6 days and given an infusion of tocilizumab (4 mg/kg), with early signs of clinical and biochemical improvement within 1 day (). He was then transitioned to oral prednisone 100 mg once daily. At Day 25, he was discharged home on a tapering regimen of oral prednisone with monthly tocilizumab infusions. Signs of clinical and biochemical relapse on Day 37, just prior to his second infusion, prompted tocilizumab dose escalation to 8 mg/kg for his third infusion, given on Day 63, with immediate improvement (). Six months on, he had weaned off prednisone and continued tocilizumab infusions without any clinical or biochemical signs of active disease (hsTnT 16 ng/L, WCC 3.8×10⁹/L, ferritin 360 μg/L, C-reactive protein < 1 mg/L, and creatinine 96 μmol/L) (see Supplementary material online ). Due to a global tocilizumab shortage during the COVID-19 pandemic, he was transitioned to fortnightly subcutaneous adalimumab 40 mg, an anti-tumour necrosis factor alpha (TNF-α) agent, with continued disease control. Repeat cardiac MRI at 18 months showed no evidence of on-going inflammation ().