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A woman in her 80s was brought to the emergency department for acute onset of generalised weakness, lethargy and altered mental state. The emergency medical service found her to have symptomatic bradycardia, and transcutaneous pacing was done. Medical history was notable for hypertension, hyperlipidaemia, type 2 diabetes, and a recently diagnosed SARS-CoV-2 (COVID-19) infection for which she was prescribed ritonavir-boosted nirmatrelvir (Paxlovid) two days before the presentation. On arrival at the hospital, she was found to have marked bradycardia with widened QRS, hyperglycaemia and metabolic acidosis. Transvenous pacing along with pressor support and insulin were initiated, and she was admitted to the intensive care unit. Drug interaction between ritonavir-boosted nirmatrelvir and verapamil leading to verapamil toxicity was suspected of causing her symptoms, and both drugs were withheld. She reverted to sinus rhythm on the fourth day, and the pacemaker was discontinued.

Pembrolizumab, a humanised monoclonal antibody and immune checkpoint inhibitor (ICI) that blocks programmed death receptor 1 and its ligands, is an effective immunotherapy for malignancies such as melanoma , lung, head and neck, cancers, and Hodgkin’s lymphoma. It has an overall response rate between 73% and 83%, with complete response rate of 27%–30%. It is well tolerated with minor side effects in 70% of cases characterised by fatigue, rash, pruritus and diarrhoea. In rare cases, more serious and life-threatening complications can occur at a rate of 0.3%–1.3%. We report a case of a woman in her 70s with non-small-cell lung cancer treated with ICI. She presented to the emergency department with left-sided ptosis and muscle weakness 3 weeks of her first dose of pembrolizumab infusion as a treatment plan of her cancer. She was diagnosed with myasthenia gravis, myocarditis and myositis as ICI-induced immune-related adverse effects resistant to medical intervention. We wish to raise awareness of the triad of life-threatening complication of ICI therapy that accounts for 30%–50% of fatal complications.

Chemotherapy-induced hypertriglyceridaemia (HTG) is a potential serious adverse event. Severe HTG with triglycerides (TG) >11.3 mmol/L (1000 mg/dL) can cause acute pancreatitis in addition to cardiovascular diseases such as coronary artery disease. While the association of capecitabine (5-fluorouracil (5-FU) prodrug) with clinically relevant HTG is a well-known adverse reaction, 5-FU is not typically associated with HTG. We here report the case of a patient who developed 5-FU-associated grade 4 HTG with TG level raising up to 37.1 mmol/L (3286 mg/dL) occurring after the ninth cycle of adjuvant FOLFOX (Fluorouracil and Oxaliplatin) chemotherapy. Fenofibrate treatment and diet were started. Chemotherapy was postponed and then resumed for two additional cycles. However, severe HTG recurred shortly after. Chemotherapy was therefore permanently stopped. Approximately 8 weeks after chemotherapy discontinuation, TG fell back to range at 2.1 mmol/L (189 mg/dL) allowing interruption of fenofibrate without HTG recurrence at 3 months.

A woman in her mid-50s with IgA nephropathy, sarcoidosis and steroid-induced diabetes mellitus presented with generalised paraesthesia and spontaneous tetany. She had received denosumab 60 mg subcutaneously 8 weeks previously for parathyroid hormone independent hypercalcaemia. At admission, she had severe hypocalcaemia (5 mg/dL), hypophosphataemia (1.9 mg/dL), hypomagnesaemia (1.4 mg/dL) and elevated serum creatinine (1.48 mg/dL) with prolonged QTc (corrected QT interval) on electrocardiograph. She initially received intravenous calcium and magnesium followed by oral calcium carbonate and calcitriol. Her prednisolone dose was tapered to 5 mg/day. Evaluation showed secondary hyperparathyroidism (1474 pg/mL) and elevated 1,25-dihydroxy vitamin D (195 pg/mL). After 1 week of oral calcium carbonate (3000 mg/day) and calcitriol (1.5 µg/day), she achieved normocalcaemia (8.1 mg/dL). To conclude, denosumab for hypercalcaemia with renal insufficiency causes prolonged severe symptomatic hypocalcaemia and hypophosphataemia mimicking hungry bone syndrome. It is important to periodically monitor for hypocalcaemia after denosumab.

Akathisia is a subjective feeling of restlessness that often results in a compulsion to move. Drug-related causes are the most common aetiologies. It can often be confused with restless legs syndrome (RLS). We describe a case of valproate-induced akathisia that improved with drug cessation. This case reports a rare but treatable adverse effect of sodium valproate and highlights the importance of differentiating akathisia from RLS.

We report a case of a woman in her 50s with chronic teprotumumab-associated sensorineural hearing loss. The patient presented with chronic thyroid eye disease with proptosis and diplopia despite systemic thyroid control and orbital decompression. She was started on teprotumumab but developed tinnitus after the third dose, followed by frank hearing loss after the fifth dose. Her audiogram showed bilateral mild to moderate-severe hearing loss, which was significantly worse compared with her baseline audiogram obtained prior to treatment. Teprotumumab was immediately stopped, however repeat audiogram 6 weeks later showed no improvement. Given potentially irreversible sensorineural hearing loss, we recommend close monitoring with regular audiometric testing before, during and after teprotumumab therapy and propose potential treatment to reverse its effects in the ear.

Here, we describe a rare case of drug-induced unilateral ciliary body effusion precipitated by topical brinzolamide, presenting acutely with pain, angle closure and myopic shift.Ciliary body effusion was suspected clinically and confirmed by ultrasound biomicroscopy. Brinzolamide was ceased, atropine instilled and the ciliary body effusion promptly resolved without need for further treatment. Brinzolamide is a sulfonamide-derived carbonic anhydrase inhibitor (CAI) commonly used in the treatment of glaucoma. Sulfite derivates can rarely cause ciliary and suprachoroidal effusions, so if ocular pain or visual changes develop, these need to be promptly assessed.

Two postmenopausal women with breast cancer developed acute confusion and seizures, less than 24 hours after the first cycle of neoadjuvant chemotherapy with fluorouracil, epirubicin and low-dose cyclophosphamide. They were found to have severe, life-threatening hyponatraemia with sodium levels of 113 and 115 mEq/L, respectively. Both women made a full recovery within 24 hours of admission with slow correction of sodium levels. Following investigational workup, the most likely diagnosis was cyclophosphamide-associated syndrome of inappropriate antidiuretic hormone secretion (SIADH). Aprepitant - a commonly used antiemetic and moderate cytochromeP450 3A4 inhibitor was identified as the precipitating factor. Aprepitant was discontinued and both women were successfully re-challenged with full dose cyclophosphamide in an outpatient setting with no subsequent adverse events. This is a typical case of a rare cause of a common medical problem. A systematic approach to diagnosis and treatment of hyponatraemia in an oncology patient requires awareness of toxicities of systemic anticancer agents.

Relapsed/refractory (R/R) peripheral T cell lymphoma (PTCL) has a poor prognosis, with limited treatment options and generally no durable response. However, long-term remission with the histone deacetylase (HDAC) inhibitor romidepsin has been reported, especially in angioimmunoblastic T cell lymphoma (AITL). Recently, tucidinostat, a novel oral HDAC inhibitor that selectively inhibits class I and class IIb HDACs, was approved for R/R PTCL in China and Japan. We present the case of a patient with AITL whose gastrointestinal symptoms and health-related quality of life improved after switching from romidepsin to tucidinostat as maintenance therapy. Romidepsin and tucidinostat appear to have different safety profiles; non-haematological toxicities such as nausea, vomiting, constipation, anorexia and fatigue may be reported less frequently with tucidinostat than with romidepsin. This case suggests that switching to tucidinostat therapy may be a viable option for patients with PTCL suffering from severe gastrointestinal adverse events with romidepsin.

We report the case of a previously healthy woman in her 60s who presented to the emergency department with acute confusion, vomiting and fever. She was recently diagnosed with a urinary tract infection as an outpatient and had completed the fifth day of a 7-day course of treatment with nitrofurantoin. We maintained a wide differential diagnosis including infectious, metabolic, autoimmune and medication-related causes. She developed an acute normocytic anaemia in hospital with a haemoglobin drop from 121 g/L to 89 g/L. Further investigation revealed evidence of haemolysis with an elevated bilirubin, lactate dehydrogenase, reticulocyte count and decreased haptoglobin. She was worked up for both inherited and acquired causes of haemolysis and found to have glucose-6-phosphate dehydrogenase deficiency. Her presentation was thought to be secondary to nitrofurantoin-induced haemolysis and she recovered completely with conservative management through intravenous fluids and discontinuation of nitrofurantoin.