Sarcoidosis is an inflammatory disease characterised by non-caseating granulomas that can affect any organ, although lung involvement is the most common. It is rare to find sarcoidosis isolated to extrapulmonary organs. We describe a case of extrapulmonary sarcoidosis with involvement of the liver in a man in his late 40s. His initial clinical history and investigations were more consistent with a diagnosis of lymphoma until a liver biopsy was performed revealing non-caseating granulomas more suggestive of a diagnosis of sarcoidosis. This patient had a history of young-onset ischaemic heart disease (IHD). We discuss the possible links between sarcoidosis, an inflammatory condition, and IHD, as well as the challenges to treating such patients with concurrent metabolic syndrome. This case also highlights the heterogeneous nature of sarcoidosis, with the diagnosis being important as prompt treatment can prevent complications of end-stage liver disease, including portal hypertension and cirrhosis.

We present a case of a woman in her 20s with inadequately treated systemic lupus erythematosus (SLE). She presented with heavy menstrual bleeding, along with nasal and gum bleeding worsening over 3 months. There was no bleeding history in her family, childhood, dental procedures or childbirth. Evaluation ruled out structural causes, revealing prolonged activated partial thromboplastin time (incomplete correction on mixing studies), normal prothrombin time, moderate thrombocytopenia, and lupus anticoagulant and anti-phosphatidylserine/prothrombin antibody positivity twice, 12 weeks apart. Further evaluation showed very low von Willebrand factor (vWF) levels (<5%). She was treated with pulse methylprednisolone for 3 days, resulting in complete symptom resolution and improvement in vWF levels to 130%. The absence of bleeding history, family history, presence of very low vWF and its response to corticosteroids led to a diagnosis of acquired vWF syndrome as the cause of mucosal bleeding in an SLE patient with concomitant positive antiphospholipid antibody. She was discharged on hydroxychloroquine, mycophenolate mofetil and tapering oral corticosteroids.

T-cell large granular lymphocytic (T-LGL) leukaemia is frequently associated with an autoimmune phenomenon; approximately one-third of patients have rheumatoid arthritis (RA). Intriguingly, one-third of patients with rheumatoid arthritis exhibit clonal T-cell patterns. Here, we present a patient with RA undergoing evaluation for neutropenia and splenomegaly who was later diagnosed with T-LGL leukaemia.

We report a rare case of a patient with Janus kinase 2-positive myelofibrosis on ruxolitinib, presenting with indolent pneumonia and cavitary lung lesions. Initial transthoracic biopsy was non-specific, but thoracoscopic biopsy revealed necrotising granulomatous disease caused by Pneumocystis jirovecii pneumonia (PJP). The patient, initially treated with trimethoprim-sulfamethoxazole, was switched to atovaquone due to gastrointestinal intolerance. Given the patient\'s immunosuppression and extensive cavitary lesions, an extended course of atovaquone was administered, guided by serial imaging, resulting in clinical and radiological improvement. Unfortunately, the patient later passed away from a severe SARS-CoV-2 infection before complete radiographic resolution was observed. This case highlights the importance of recognising atypical PJP presentations causing granulomatous disease in immunosuppressed patients. While rare, documenting such cases may improve diagnosis using less invasive methods and help determine optimal treatment durations for resolution of these atypical infections.

We present a case of atraumatic splenic rupture secondary to Epstein-Barr virus (EBV) infection in a woman in her early 50s. The patient initially presented with sepsis secondary to pneumonia but then developed abdominal pain and distension. CT revealed splenic rupture with a significant perisplenic hematoma. Laboratory tests confirmed an EBV infection. Owing to frailty, she underwent fluoroscopy-guided splenic artery embolisation. This case highlights the rare risk of splenic rupture following EBV infection, even in the absence of typical symptoms of infectious mononucleosis.

We report the case of a man in his 50s who developed acute respiratory distress syndrome and right heart failure, necessitating intubation and initiation of inhaled nitric oxide (iNO) to decrease right ventricular afterload and improve the right heart function. The course was complicated by acute anaemia, with a diagnostic workup revealing methaemoglobinaemia and evidence of oxidative haemolysis indicated by blister and bite cells on peripheral blood film. The patient received conservative management, including successive red blood cell transfusion and gradual iNO weaning due to suspected glucose-6-phosphate dehydrogenase (G6PD) deficiency. Discontinuation of iNO led to the resolution of both oxidative haemolysis and methaemoglobinaemia. Subsequent enzymatic assay, conducted 4 months later, confirmed G6PD deficiency. This case highlights a rare instance of concurrent methaemoglobinaemia and oxidative haemolytic anaemia following iNO in a patient with underlying G6PD deficiency.

A woman in her 40s with no medical history presented on hospital day #0 with 3 days of epigastric pain, nausea, vomiting and bloody diarrhoea. Initial blood work demonstrated acute kidney injury with metabolic acidosis with an elevated anion gap, thrombocytopenia, an elevated lactate dehydrogenase, and an undetectable haptoglobin. She was quickly diagnosed with haemolytic uraemic syndrome from Shiga toxin-producing O157:H7 Escherichia coli Her microangiopathic haemolytic anaemia and renal failure progressively worsened and only improved after the initiation of eculizumab, a monoclonal antibody directed against complement component C5. We report a case of Shiga toxin-producing E. coli-haemolytic uraemia syndrome with a complement-mediated component.

A woman in her 20s with no medical history was diagnosed with bulky stage II classic Hodgkin\'s lymphoma after an 8-week history of shortness of breath, cough and lethargy. A regimen of doxorubicin (Adriamycin), bleomycin, vinblastine and dacarbazine (ABVD) was commenced with six cycles planned. During the first cycle, the patient was profoundly hypertensive. She then suffered two self-terminating tonic-clonic seizures.Examination and investigations diagnosed posterior reversible encephalopathy syndrome (PRES), which resolved completely in 11 days with strict blood pressure control and withholding chemotherapy. Treatment was further complicated by anthracycline-induced cardiomyopathy, requiring a switch in regimen to gemcitabine BVD.The patient made a full recovery from neurology and cardiology perspectives and completed six cycles of chemotherapy, achieving a complete metabolic response by the tumour. We illustrate the case, describe differential diagnoses and management of PRES, its association with chemotherapy and the successful chemotherapy rechallenge.

Clozapine is the most effective medication for the management of treatment-resistant schizophrenia and schizoaffective disorder, and its discontinuation can pose significant challenges in treatment. We present a patient with a diagnosis of schizoaffective disorder who was stable on clozapine for a decade until discontinuation due to thrombocytopenia. She experienced a relapse of her illness, presenting with psychotic and catatonic features with poor oral intake and physical health complications requiring a lengthy admission to the hospital. There was a poor response to alternative antipsychotics and a full course of electroconvulsive therapy. Intramuscular (IM) clozapine was initiated due to catatonia and refusal to accept oral medications. After receiving 10 doses of IM clozapine, she started accepting oral clozapine and made a full recovery within a few weeks. The low platelet count was persistent, and a bone marrow biopsy showed results consistent with immune thrombocytopenia being the cause of that low platelet count.

Vitamin K is an essential dietary cofactor required for the synthesis of active forms of vitamin K-dependent procoagulant proteins. Vitamin K deficiency, particularly late-onset deficiency occurring between 1 week and 6 months of age, can cause a life-threatening bleeding disorder. An exclusively breastfed, full-term, 6-week-old infant male presented with severe haemorrhagic shock and multi-system organ failure related to caregiver refusal of intramuscular vitamin K after birth. Coagulation studies were normalised within 8 hours of intramuscular vitamin K administration. An increasing number of caregivers are refusing intramuscular vitamin K which has led to a rise in the incidence of vitamin K deficiency bleeding. Health policy organisations around the world emphasise the benefits of intramuscular vitamin K and risks of refusal, particularly in exclusively breastfed infants who are at higher risk due to low vitamin K levels in breast milk. This case highlights the multi-system severity of this life-threatening yet preventable disorder.