Search

A 90-year-old woman is referred six months after a transient ischaemic attack (TIA) with asymptomatic cholestatic liver function test (LFT) derangement. Following the TIA, atorvastatin and clopidogrel therapy are initiated. This is added to pre-existent once daily nifedipine for hypertension. Nifedipine (a weak inhibitor of CYP3A4 and competing substrate) and clopidogrel (a competitive inhibitor of CYP3A4) may have affected the metabolism of atorvastatin, resulting in the elevation of serum alkaline phosphatase levels to over six times the upper limit of normal. More often, statin therapy elevates serum alanine aminotransferase levels. Drug-induced liver injury (DILI) was deemed ‘probable’ as judged by the Roussel Uclaf Causality Assessment Method score. Statin therapy remains overwhelmingly safe, with benefits outweighing risks in the vast majority. The UK recommended LFT monitoring regime facilitates early recognition of DILI. Case reports are examined where similar drug combinations resulted in severe morbidity and mortality.

Sitagliptin is a dipeptidyl peptidase-4 inhibitor commonly used in the treatment of type 2 diabetes mellitus for glycaemic control. Concerns have arisen regarding adverse events caused by this drug, particularly concerning arthralgias. Here, we report on a 56-year-old man being treated with sitagliptin who developed inflammatory arthritis after taking the drug for 6 months. The patient presented with pain, swelling and erythema in multiple joints and was eventually diagnosed with seronegative rheumatoid arthritis (RA) under the 2010 American College of Rheumatology/European League Against Rheumatism classification criteria. His symptoms continued for several months after stopping sitagliptin and eventually went into remission after a tapered course of steroids, hydroxychloroquine and methotrexate. Furthermore, the patient is HLA-DRB3 positive, a genetic marker that is still being investigated for its role in the pathogenesis of RA and that may have been a predisposing factor in the development of this patient’s inflammatory arthropathy.

A 76-year-old woman was treated with oral bisphosphonate, alendronate, for osteoporosis in an outpatient clinic. Routine blood tests 4 months after alendronate prescription surprisingly revealed severe hypophosphataemia. The patient was hospitalised and treated with intravenous and oral phosphate supplements. Alendronate was later reintroduced as treatment for osteoporosis and the patient once again presented with severe hypophosphataemia in subsequent routine blood tests. The patient had only presented with lower extremity pain, muscle weakness and difficulty walking. Blood tests in the emergency department both times reconfirmed severe hypophosphataemia. Plasma (p-)ionised calcium levels were normal or slightly elevated and p-parathyroid hormone levels were normal or slightly suppressed. The p-25-hydroxyvitamin-D and p-creatine were in the normal range. Critical illness, malabsorption, nutritional issues and genetics were reviewed as potential causes but considered unlikely. Phosphate levels were quickly restored each time on replacement therapy and the case was interpreted as bisphosphonate-induced severe hypophosphataemia.

A man in his early 50s presented with jaundice, mild shortness of breath on exertion and dark urine. He had had coryzal symptoms 2 weeks prior to admission. Medical history included obstructive sleep apnoea and hypertension. His initial blood tests showed a mild hyperbilirubinaemia and acute kidney injury stage 1. Chest X-ray and CT pulmonary angiogram were negative for features suggestive of COVID-19. He later developed a drop in haemoglobin and repeat bloods showed markedly raised lactate dehydrogenase and positive direct antiglobulin test. These results were felt to be consistent with a haemolytic anaemia. A nasopharyngeal swab came back positive for COVID-19. We suspect the cause of his symptoms was an autoimmune haemolytic anaemia secondary to COVID-19 which has recently been described in European cohorts.

A 45-year-old woman was admitted for diabetic ketoacidosis (DKA). Aggressive rehydration and continuous intravenous insulin resulted in improved blood glucose levels; however, metabolic acidosis persisted. One day prior to admission, the patient took a single dose of a sodium–glucose cotransporter 2 (SGLT2) inhibitor and this likely contributed to the prolonged euglycemic DKA. A single dose of this drug remained effective for over 100 hours as evidenced by massive excretion of urine glucose continuing long after blood glucose normalisation. SGLT2 inhibitor use should be refrained in cases in which DKA has already occurred as they may result in increasing severity or prolonged DKA.

Immune-related myositis is one of the rare immune-related adverse events whose underlying precise mechanisms are not fully understood. Here, we describe a case of immune-related myositis that developed after four cycles of combination therapy with nivolumab plus ipilimumab for the treatment of metastatic renal cell carcinoma. Negative results of autoimmune antibodies, including anti-acetylcholine receptor and anti-muscle-specific kinase antibodies suggested a T-cell-mediated mechanism. After recovery with steroid therapy, the patient resumed nivolumab monotherapy and survived without any evidence of disease progression or refractory of myositis. Differential diagnosis between T-cell-mediated and B-cell-mediated immune-related myositis and its impact on optimal management are discussed.

A 53-year-old woman with atypical chest pain underwent a dobutamine stress echocardiogram (DSE) and developed a coronary spasm (CS) with severe pain and dramatic ST-segment elevation 9 min after dobutamine infusion was discontinued. The spasm resolved after sublingual nitroglycerin administration. The same-day coronary angiogram showed non-significant stenosis in the three coronary territories. Retrospectively, we found that the patient had vasospastic angina (VSA), a condition that has been strongly associated with the development of dobutamine-induced CS. Mechanisms of dobutamine-induced CS are not fully understood and include endothelial dysfunction leading to deficient nitric oxide-mediated coronary vasodilation in response to increased myocardial oxygen demand as well as imbalance between β1 and β2 adrenergic effects of dobutamine. Dobutamine-induced CS has also been much more frequently reported in patients from Asian descent with VSA. VSA should be systemically recognised in patients considered for DSE and, if present, other modalities of stress imaging should be discussed.

Intra-articular steroid injections are widely prescribed for management of osteoarthritis when oral medication or physiotherapy treatment fails to relieve patient’s pain. Septic arthritis is an uncommon side effect of steroid injection. Common causal micro-organisms are bacterial with Staphylococcus aureus being the most frequent. Fungal septic arthritis is rare and does not usually present beyond the neonatal period. We present a rare case of septic arthritis secondary to fungal infection.

Certain medications have been implicated in causing acute myocardial infarctions (AMI). Sumatriptan, a medication usually prescribed for acute migraine and cluster headaches has been documented as potentially causing coronary vasospasm, thereby leading to MI. This is usually seen in patients with strong risk factors for coronary artery disease (CAD) or in those with established CAD. Most cases thus far have been reported in patients using the subcutaneous preparation of sumatriptan. Here, we present a case of a patient without prior risk factors for CAD and angiographically unremarkable coronary arteries who presented with evidence of an AMI after oral sumatriptan use for migraines.

Acute ischaemic stroke is a known risk of percutaneous coronary intervention (PCI). The incidence of such complications has increased in frequency over the last decade due to higher comorbidity burden and increased complexity of PCI procedures. The overall incidence of post-PCI ischaemic stroke remains low at 0.56%, but some groups of patients have significantly higher risk. Risk factors include atherosclerotic plaques, atrial fibrillation, cardiogenic shock, older age and arterial disease. Although the overall incidence of acute ischaemic stroke following PCI is low, it can result in lifelong disability and is associated with high morbidity, mortality and significant costs. Spinal infarctions due to PCI are exceedingly rare. Here, we discuss a 71-year-old woman who presented with a non ST-elevation myocardial infarction and developed both stroke and spinal infarction post PCI due to a thromboembolic event resulting in long-term debility.

Drug-induced thrombocytopenia (DITP) is suggested by severe thrombocytopenia with subsequent recovery of platelet count after removal of the offending drug. The diagnosis is ascertained when there is reproducibility of thrombocytopenia with repeated exposure. Filgrastim is used during peripheral blood progenitor cell harvest during autologous stem cell transplantation in the setting of multiple myeloma to prolong event-free survival and overall mortality. The following case illustrates all of the suggestive features of DITP after filgrastim exposure during elective stem cell harvest. Due to the inability to tolerate filgrastim, autologous stem cell transplant was aborted in this patient and he was maintained on induction chemotherapy.

Irinotecan is a novel anticancer drug that has worked wonders in combination with other anticancer drugs. It can be used as a single chemotherapy agent in colonic cancer treatment or in combination with 5-fluorouracil. Irinotecan has been found a better salvage therapy in patients who are resistant to 5-fluorouracil. It is also used in combination with cisplatin and other drugs for cancers such as pleural mesothelioma, Ewing’s sarcoma, lung cancer and others, and has helped reduce tumour burden. Irinotecan is generally associated with gastrointestinal side effects including nausea, vomiting and diarrhoea, while cardiovascular toxicity (5%) has been reported mainly as vasodilatation and possible bradycardia with no known incidence. A case was reported in 1998 by Miya et al of a 65-year-old man with bradycardia which was managed with atropine without modifications in the dosage of irinotecan or in the rate of infusion. We report a case of a patient with small round cell cancer who presented with sinus pause bradycardia after infusion with irinotecan. The patient was managed with atropine during chemotherapy.

Cisplatin is a widely used chemotherapeutic agent for many cancer types. Its toxicity profile includes drug-induced vascular damage. Clinicians should be aware of its varied presentation, including acute and chronic vascular events involving the arterial and venous system. This is a case of an otherwise well 32-year-old man with testicular cancer who received bleomycin/etoposide/cisplatin, and presented following two cycles of chemotherapy with homonymous hemianopia secondary to acute stroke. Acute arterial complications are rare, but clinicians should maintain a high index of suspicion for such events, even in a patient who otherwise has no vascular risk factors. Primary and secondary prevention measures including lifestyle modifications (smoking cessation, diet and exercise), blood pressure and cholesterol management, and antiplatelet therapy should be considered in patients exposed to cisplatin, during and following their treatment.

Immune checkpoint inhibitors, including antiprogrammed death cell protein 1 (anti-PD-1) and anti cytotoxic T-lymphocyte-associated protein 4 (anti-CTLA-4), have been associated with a range of autoimmune-related side effects since their introduction in cancer treatment. Small vessel digital necrosis, referred to as the acral vascular syndrome, is a rare but serious complication that can result in loss of digits. Here we present a case report of acral vascular syndrome and review possible aetiologies. A 45- year-old woman with invasive ductal carcinoma of the left breast presented to the emergency department during neoadjuvant treatment with carboplatin, docetaxel and pembrolizumab with complaints of severe pain in her right third digit. She had physical findings consistent with ischaemic necrosis and gangrene of the distal phalanx. Angiography demonstrated Raynaud’s phenomenon in the distal portion of the digits. Laboratory testing showed a weakly positive RNA polymerase III antibody level. Her case resulted in surgical amputation of her affected digit after partial resolution of symptoms with prednisone, vasodilators and antibiotics.

Hypersensitivity pneumonitis (HP), also known as extrinsic allergic alveolitis, is a granulomatous, non-IgE-mediated hypersensitivity reaction of the alveoli and distal bronchioles presenting as an acute, subacute or chronic condition. It is most commonly associated with exposure to extrinsic allergens (eg, avian dust, mould and tobacco) and medications including antiarrhythmics (eg, amiodarone), cytotoxics (eg, methotrexate) and antiepileptics (eg, carbamazepine). Individuals diagnosed with this condition can present with severe hypoxia and respiratory failure. The fundamental principle of management is to remove the causative allergen. Evidence implicating selective serotonin reuptake inhibitors as a causative agent is limited, and this case report describes a rare clinical presentation of HP associated with sertraline, how it was diagnosed and subsequently treated. It is anticipated that raising awareness of this interaction will assist multidisciplinary teams, managing patients diagnosed with HP, to be more cognisant of sertraline as being an aetiological factor for this condition.

A patient undergoes intracranial stent insertion for stent-assisted coiling of a basilar tip aneurysm and left middle cerebral artery aneurysm. A flow diverting stent is also placed across an anterior communicating artery aneurysm. Prior to the procedure, the patient takes dual antiplatelet medications, being aspirin and clopidogrel. Because of the concern regarding in-stent thrombus and thromboembolic complications related to intracranial stenting and the high rate of clopidogrel resistance, preoperative platelet function testing (PFT) was undertaken to ensure platelet inhibition. In this case, PFT was performed on a platelet function analyser which demonstrated platelet inhibition. Ten days following the procedure, the patient represented with thromboembolic stroke. Repeat PFT performed with whole blood impedance aggregometry and despite full medication compliance demonstrated clopidogrel resistance. Clopidogrel was then ceased and prasugrel commenced. This case demonstrates the importance of appropriate platelet inhibition in patients with intracranial stents and the controversy surrounding PFT.

The differential diagnosis of shock following percutaneous coronary intervention (PCI) is vast. Access site complications and bleeding can cause hypovolemic shock. Peri-procedural myocardial infarction, abrupt closure, stent thrombosis, coronary dissection and coronary perforation have a stormy presentation. Vasovagal shock is manifested by bradycardia and hypotension and quickly responds to atropine. Anaphylactic shock secondary to contrast administration can be stormy but usually responds to steroids or adrenaline. Septicemia due to unsterile techniques can cause a less dramatic shock. Acute adrenal insufficiency causing shock following PCI has not been described to the best of our knowledge. We report the case of a 54-year-old woman who underwent successful multivessel PCI. She had refractory unexplained shock following the PCI with no much response from inotropic or intra-aortic balloon pump. After ruling out all possible causes of shock and clinical suspicion of adrenal insufficiency, she was treated with steroids resulting in dramatic improvement in her hemodynamics.

Octreotide is a somatostatin analogue used for treating congenital chylothorax and congenital hyperinsulinism in infants. By increasing splanchnic arteriolar resistance and decreasing gastrointestinal blood flow, octreotide indirectly reduces lymphatic flow in chylous effusions.Splanchnic ischaemia following octreotide predisposes infants to necrotising enterocolitis (NEC). Although NEC occurrence in infants treated with octreotide for hyperinsulinaemic hypoglycaemia has been reported widely, its incidence in infants with chylothroax is low. We describe a case of congenital chylothorax in a preterm infant who had poor response to thoracentesis. Although octreotide initiation lead to resolution of chylothorax, he developed NEC. Cessation of octreotide and medical management resulted in rapid resolution of NEC. Since octreotide is generally used as the first-line treatment for chylous effusion, the risk of NEC should be considered, especially when the dosage is increased. Infants on octreotide should be closely observed for early signs and symptoms of NEC to avert surgical emergency.

Colistin-induced nephrotoxicity is commonly associated with elevation of serum creatinine level or a reduction of urine output. Uncommonly, tubulopathy associated with colistin has been reported. Here we present a unique case of a 46-year-old man who developed polyuria, hypokalaemia, hypocalcaemia, hypomagnesemia and metabolic alkalosis after 3 days of therapy with intravenous colistimethate sodium. After ruling out other causes, a diagnosis of colistin-induced acquired Bartter syndrome was made. The patient required daily aggressive intravenous repletion of fluids and electrolytes. However, polyuria and metabolic abnormalities abated only after drug discontinuation.

A 48-year-old male patient requiring extracorporeal membrane oxygenation (ECMO) support for hypoxaemic respiratory failure failed to achieve therapeutic anticoagulation with bivalirudin after continuous dose escalations, and continued to have recurrent fibrin stranding in the circuit over a 6-day course of treatment. Suspecting bivalirudin resistance, the patient was transitioned to argatroban and achieved a therapeutic response in less than 24 hours. The case describes the challenges of anticoagulation in ECMO supported patients. The interplay between bivalirudin metabolism, renal replacement therapy, and immunological effects leading to a heparin-like-effect, inflammatory mediators, and thrombotic burdens may all impact the clinical effect during bivalirudin therapy. The structural biochemistry of thrombin and bivalirudin likely plays a role in the presented patient’s successful response to argatroban. Bivalirudin may fail at achieving therapeutic anticoagulation in patients with genetic thrombin mutations or structural defects that alter the binding pockets at the thrombin exosites.

Transcatheter aortic valve implantations (TAVIs) may be complicated by a need for permanent pacemaker implantation post procedure, usually due to local trauma or compression on the conduction system. There are some features that might help predict that a patient is high risk for developing conduction disease following TAVI, for example, underlying right bundle branch block or use of certain types of TAVI. It might also become apparent during the procedure, or before temporary wire removal post procedure. Higher risk patients may undergo rhythm monitoring for longer periods post TAVI. We present a case where a patient required an unexpected emergency pacemaker following a TAVI, despite low risk clinical features, a low risk baseline ECG, and the use of a low risk TAVI valve. In addition, this very significant conduction disease only became apparent over 72 hours following implantation, despite normal resting ECGs and telemetry up to that point.

A 63-year-old woman with a medical history of chronic myelogenous leukaemia treated with dasatinib, chronic obstructive pulmonary disease and heart failure with preserved ejection fraction presented with difficulty in breathing. Chest X-ray showed large right-sided pleural effusion, which was confirmed on a CT angiogram of the chest. Echocardiogram showed an ejection fraction of 61% with moderate to severely dilated right ventricle and right ventricular systolic pressure of 60 mm Hg. Diagnostic and therapeutic thoracentesis was performed, and 2.2 L of pleural fluid was removed. Pleural fluid analysis was consistent with chylothorax. Significant symptomatic improvement was noted after thoracentesis. In the absence of an alternate explanation, chylothorax was attributed to dasatinib, which was switched to nilotinib. This resulted in resolution of her pleural effusions.

Acute gastrointestinal (GI) immune-related adverse events (irAE) are commonly reported by patients with cancer undergoing treatment with immune checkpoint inhibitors (CPI); however chronic irAEs are rare. We present a case of a 71-year-old woman with metastatic gastro-oesophageal junction (GOJ) adenocarcinoma who developed delayed-onset chronic intestinal pseudo-obstruction (CIPO) while receiving second-line pembrolizumab. Repeated CT scans of the abdomen/pelvis found no small bowel obstruction, and evaluations for bowel inflammation, infection and paraneoplastic syndrome were negative. Bowel rest and glucocorticoids were associated with transient symptom resolution; however, symptoms recurred within 1 month. The patient was ultimately supported with total parenteral nutrition and intestinal motility agents. After 4 months, the GOJ cancer remained stable with no signs of progression. As CPI use expands, the incidence of rare irAEs, such as CIPO, may increase.

A case illustrating significant hyperglycaemia with azacitidine therapy for myelodysplastic syndrome is presented. The significance of treatment-induced hyperglycaemia with regard to increased risk of infection, and possible mechanisms of azacitidine-induced hyperglycaemia are discussed.

In the perioperative setting, norepinephrine is used to increase blood pressure, an effect mediated mostly via arterial and venous vasoconstriction. Thus, norepinephrine is, allegedly, less likely to cause or worsen left ventricular outflow tract obstruction (LVOTO) than other inotropes. We report a case of norepinephrine-associated dynamic LVOTO and systolic anterior movement in a predisposed patient. This report highlights that unrecognised dynamic LVOTO may worsen shock parameters in patients treated with norepinephrine who have underlying myocardial hypertrophy.

We present the case of ceftazidime-induced immune-mediated haemolysis with associated acute kidney injury in a 43-year-old woman. The patient initially presented to the regional cystic fibrosis centre for treatment of an infective exacerbation of cystic fibrosis. After initiation of ceftazidime (a third-generation cephalosporin), renal function rapidly deteriorated and a fall in haemoglobin was noted. On transfer to our care, a haemolysis screen identified immune-mediated haemolysis, and renal biopsy confirmed the finding of acute tubular necrosis secondary to haem pigment. The patient’s renal function deteriorated such that she required haemodialysis, although she subsequently recovered and is now dialysis-independent. Although acute haemolytic reactions are recognised with third-generation cephalosporins, this is the first reported case of ceftazidime-induced immune-mediated haemolysis with acute kidney injury. Given the increased frequency of cephalosporin usage, it is important for both nephrologists and general physicians to be aware of this rare but very serious complication.

Isoniazid preventative therapy is widely used for latent tuberculosis infection. Isoniazid is highly effective but has many adverse effects, including neuropsychiatric. We describe the case of an 80-year-old woman with mania. She had received isoniazid preventative therapy during steroid treatment for rheumatoid arthritis and organising pneumonia for the previous 5 months. Her mania resolved after discontinuation of isoniazid. Adverse effects of isoniazid should be considered even if a long time has elapsed since the start of administration. Physicians other than infectious disease and respiratory specialists also must be aware of the adverse effects of isoniazid preventative therapy.

A 20-year-old college student presented with high grade, intermittent fever for 10 days associated with blood stained loose stools after taking tablet levamisole for 17 days for vitiligo vulgaris. He was febrile, had a toxic appearance and appeared pale. Investigations showed neutropaenia with thrombocytopaenia. Blood cultures were sterile and stool cultures did not grow any enteric pathogens. His bone marrow examination was suggestive of an aplastic anaemia. He was administered empirical antibiotics, granulocyte colony stimulating factor and platelet transfusions. However, his fever and blood stained stools persisted. A repeat bone marrow examination after 2 weeks still revealed a hypoplastic marrow. Hence, a diagnosis of a levamisole induced bone marrow failure was made. While being worked up for an allogeneic stem cell transplantation, he developed neutropaenic enterocolitis and refractory septic shock with carbapenem resistantKlebsiella pneumoniaeand succumbed to his illness.

A 26-year-old Caucasian man with no medical history, except years of oral and intravenous drug abuse, presented with fatigue, shortness of breath, epistaxis and uncontrolled hypertension. He was pale with skin ecchymosis over his thighs and was anaemic, with severe renal failure and metabolic acidosis. Following initial clinical stabilisation of the patient, a renal biopsy was obtained, which showed vascular and glomerular changes consistent with thrombotic microangiopathic injury and advanced glomerulosclerosis. He was treated with antihypertensives and required haemodialysis. He admitted using ‘crystal meth’ regularly for many years, which is likely responsible for his renal failure. We present the case to illustrate methamphetamine-induced renal disease leading to end-stage renal disease and to bring awareness among practising clinicians, ancillary healthcare workers and public health professionals of this often undervalued cause of renal failure, which can be prevented.

Sodium glucose co-transporter-2 inhibitors (SGLT2-i) have become a popular therapeutic strategy in the management of hyperglycaemia in type 2 diabetes mellitus. The primary site of action of SGLT2-i is at the proximal renal convoluted tubule. They work by blocking SGLT2 receptors, sodium-dependent glucose co-transport molecules, which in turn prevents glucose reabsorption, facilitating glucosuria, improving glycaemic control as well as a moderate degree of weight loss. We report the case of a 51-year-old woman admitted to the acute medical unit with abdominal pain and vomiting, who was diagnosed with euglycaemic diabetic ketoacidosis secondary to recent initiation of an SGLT2-i medication (dapagliflozin). Clinicians should be aware of this rare side effect of SGLT2-i, to circumvent delays in patient management.

The authors report a term male neonate who was born in unexpectedly poor condition with low Apgar scores and low venous cord gas pH. He required admission to the neonatal unit and was found to have developed haemolytic anaemia with associated hydrops, following a presumed severe antenatal insult. Antenatally, low levels of anti-E antibodies (titre 8) had been detected at 28 weeks’ gestation. Following the British Society for Haematology and local neonatal team guidance, advice was given for cord direct antiglobulin test, full blood count and bilirubin at delivery. This case highlights the rare case of haemolytic disease of the fetus and newborn on a background of maternal low titre anti-E antibodies.

A 61-year-old Caucasian woman presented to the emergency room complaining of left-sided chest pain and altered mentation for 3 days. Her medical history included liver cirrhosis and coronary artery disease. On admission, she was found to have methicillin-resistant Staphylococcus aureus (MRSA) bacteraemia. Due to a decline in mental status, a lumbar puncture was performed and cerebrospinal fluid cultures grew MRSA. She was treated initially with vancomycin. Ceftaroline was later added, due to the high burden of disease and difficulty in clearing her infection. After initiation of ceftaroline, bacteraemia cleared and mental status improved, however, she developed haemolytic anaemia. Ceftaroline was stopped and vancomycin continued. Staphylococcal meningitis is a rare occurrence, estimated at a rate of only 1%–10% of all bacterial meningitis cases. Ceftaroline seems to be a suitable option for disseminated MRSA infection, including MRSA meningitis, when the clinical response to vancomycin is inadequate. Further studies are warranted in order to establish adequate dosing while avoiding adverse effects.

Cancer immunotherapy has been used in several malignancies with clinical benefit. Despite the clinical success, immune-related adverse events are frequent and endocrinopathies can be particularly severe. We report a 55-year-old male patient with stage IV pulmonary carcinoma treated with nivolumab who presented with thyroid dysfunction after the sixth administration of the drug. One year after thyroid dysfunction, the patient complained of severe fatigue, asthenia and weight loss. Laboratory testing showed low morning cortisol with undetected adrenocorticotropic hormone; other pituitary hormones were normal and MRI showed homogeneous enhancement of the pituitary gland and no space-occupying lesions. The diagnosis of nivolumab-induced hypophysitis was made and replacement treatment with hydrocortisone was started with clinical improvement. This case demonstrates that patients under immunotherapy are at risk for a large spectrum of endocrine dysfunctions that may worsen their prognosis. Close monitoring of these patients is warranted.

A 72-year-old woman presented with nephrotic proteinuria and moderate haematuria. Renal pathology was compatible with immunotactoid glomerulopathy (ITG), for which there is no consensus for appropriate therapy. We, therefore, postponed immunosuppressive therapy. After 4 years, the patient’s renal function started to decline and renal pathology was re-evaluated, revealing a pathological change from mesangial proliferative glomerulonephritis to endocapillary proliferative glomerulonephritis. Treatment with oral prednisolone (30 mg/day) was initiated. Within 5 weeks, complete remission of proteinuria was obtained (proteinuria 6.02 g/gCr to 0.12 g/gCr), and the patient’s renal function stabilised. Generally, responsiveness to immunosuppressive therapy is poor in patients with ITG, and the present case represented a very rare clinical course. Some previous cases have indicated susceptibility to the therapy, regardless of the severity of renal damage. As a possible distinct entity that determines susceptibility to immunosuppressive therapy, we suggest the presence of a latent lymphoproliferative disease with no significant haematological symptoms.

Behçet’s disease (BD) is a variable-vessel vasculitis which commonly presents with recurrent orogenital ulceration, skin lesions, visual disturbances and neurodeficits. Arterial involvement is seen variably in 8%–18% cases of BD, with common affliction of the carotid, pulmonary, aortic and iliofemoral arteries. Cardiac involvement in the form of myocarditis, myocardial infarction, pericarditis, cardiac dysrhythmias or valvular disease is also known in BD, although rarely. Sudden-onset chest pain in BD is a medical emergency, with acute coronary syndrome, pulmonary thromboembolism and rupture of aortic or pulmonary artery aneurysms being the commonly implicated causes. Here, we report a rare case of BD who presented with sudden-onset severe chest pain, the cause of which remained elusive despite extensive evaluation for the abovementioned causes. To the best of our knowledge, this is the first reported case of cyclosporine-induced pericarditis in BD in available literature and should be considered in patients on cyclosporine presenting with chest pain.

We report a case of a 74-year-old man who developed myocarditis complicated by atrioventricular (AV) block following two doses of nivolumab for the treatment of non-small cell lung cancer. A diagnosis of drug-induced acute myocarditis with complete AV block was considered on the basis of elevated troponin, new onset left ventricular (LV) systolic dysfunction, absence of acute myocardial infarction and some findings suggestive of myocarditis on cardiac magnetic resonance. The patient was commenced on glucocorticoids, perindopril and carvedilol. AV block and LV dysfunction persisted despite 2 weeks of treatment. He ultimately became hypotensive which prompted an implantation of a cardiac resynchronisation therapy pacemaker. Follow-up echocardiogram at 6 weeks showed resolution of LV systolic dysfunction. However, he continued to have AV block.

Spontaneous cancer regression is a rare event, scarcely reported among gastrointestinal malignancies. Pancreatic adenocarcinoma regression has been documented in five previous cases, none of which included liver metastases, and the mechanism by which this occurs is not known. A 56-year-old woman with history of discoid lupus, homocysteinemia and peripheral vascular disease was diagnosed with stage IV pancreatic ductal adenocarcinoma (PDA) metastatic to the liver. She received palliative chemotherapy with 5-fluorouracil, leucovorin, irinotecan and oxaliplatin (FOLFIRINOX) for 6 months, complicated by mucositis, diarrhoea, vomiting and twoClostridium difficilecolitis episodes. Cancer initially responded to chemotherapy. However, due to substantial toxicities, she decided to discontinue cytotoxic chemotherapy and focus on palliation alone. Thereafter, CT and carbohydrate antigen (CA) 19-9 showed further response and ultimately complete cancer regression that has persisted for 33 months after cessation of chemotherapy. This is the first report in the English literature showing spontaneous regression of a PDA with liver metastases. Two possible mechanisms are proposed: antitumoral autoimmunity and tumour hypoxia related to vascular disease.

We present a teetotaler with compensated non-alcoholic fatty-liver-disease related cirrhosis who presented with acute worsening of his chronic liver disease. The acute event was not discernible even after extensive work up and finally a transjugular liver biopsy revealed features suggestive of severe alcoholic hepatitis. The patient and the family denied occult alcohol use when questioned over multiple times and finally, the culprit ‘alcohol’ was found to be the homoeopathy medicines that the patient was consuming over a month for treatment of Gilbert’s syndrome. We retrieved and tested the homoeopathy drug for alcohol content and found an alarming 18% ethanol in the same, confirming our diagnosis.

The combination of glecaprevir and pibrentasvir was recently approved for chronic hepatitis C virus (HCV) infection with recommended treatment duration of 8–12 weeks depending on previous treatments, viral genotype and cirrhosis status. Although liver injury was reported with other protease inhibitors in the presence of cirrhosis or hepatitis B virus (HBV) co-infection, glecaprevir/pibrentasvir treatment is not known to cause liver injury. We report a patient with chronic HCV infection who despite the absence of cirrhosis and HBV co-infection developed acute liver injury that completely resolved after glecaprevir/pibrentasvir withdrawal. Interestingly, sustained HCV virologic response was achieved after only 3 weeks of glecaprevir/pibrentasvir treatment.

Anthracyclines are an effective chemotherapy agent. However, very few cases of idarubicin-induced cardiomyopathy exist. Herein, we describe a case of first-dose idarubicin-related acute heart failure in a woman with a history of myelodysplastic syndrome converted to acute myeloid leukaemia.

Tranexamic acid (TXA) is an antifibrinolytic which minimises bleeding and transfusions, with thrombotic risk. Our patient had known coronary artery disease with post-TXA acute ST-elevation myocardial infarction (STEMI) due to in-stent thrombosis. He had five drug-eluting stents (DES): two overlapping DES in mid-LAD (3 years ago), and two overlapping DES in distal right coronary artery and one DES in obtuse-marginal (1.5 years ago). After TXA, both overlapping stent locations thrombosed. Of nine reports of post-TXA acute MI, only one had complex stent anatomy (bifurcation stent to left circumflex/first obtuse-marginal) with other single stents, and only the complex stent thrombosed. Post-TXA MI was more often STEMI caused by arterial thrombosis, rather than non-STEMI caused by blood loss, hypotension or demand ischaemia. Overlapping and bifurcation stents thrombosed; single stents remained patent. In conclusion, overlapping stents, bifurcation stents, excessive stent length and previous in-stent restenosis/thrombosis may increase thrombotic risk. TXA should be administered cautiously with complex stent anatomy.

Aortoiliac bypass surgery is the gold standard strategy for removing persistent ischaemia resulting from bilateral aortoiliac occlusive disease, a condition known as Leriche syndrome. However, the impact of aortoiliac bypass surgery on the blood flow of the renal artery is not fully understood. Here, we report a case of worsening renal failure caused by renal steal immediately after aortoiliac bypass for Leriche syndrome. The revascularisation of bilateral renal arteries dramatically improved the patient’s renal function and allowed us to discontinue both haemodialysis and diuretics. This case demonstrates that in rare instances, haemodynamic change induced by aortoiliac bypass surgery affects the arteries feeding other organs. Careful preoperative evaluation for the corresponding branches of the aorta is indispensable. Optimal revascularisation should be performed to avoid serious complications after aortoiliac bypass if the patient is at risk of developing critical ischaemia.

Clozapine is the most effective treatment for patients with refractory schizophrenia. Clozapine is also associated with serious and potentially lethal side effects including drug induced lupus (DIL). There have been four previous published case reports describing clozapine inducing a lupus-like syndrome including one previous case where a clozapine rechallenge was attempted without success. This case report describes a successful clozapine rechallenge in a patient with suspected DIL.

Immunoglobulin A nephropathy (IgAN) is the most commonly diagnosed glomerulonephritis worldwide. It is usually idiopathic and may be associated with many other diseases. Recently, biological agents including tumour necrosis factor alpha (TNFα) inhibitors have been identified as a potential cause for IgAN. We report the case of a 39-year-old woman who presented with renal dysfunction and visible haematuria. She had a background of Crohn’s disease (CD) and had been on adalimumab for 4 years following a right hemicolectomy. Subsequently, she underwent a renal biopsy that demonstrated IgAN and adalimumab was ceased. Following a flare in her CD, she was commenced on infliximab, which led to remission of the IgAN and CD. This is the first case to demonstrate the occurrence of IgAN as a complication of a TNFα inhibitor (adalimumab) that remained in remission despite the commencement of a second TNFα inhibitor (infliximab).

Lanthanum carbonate is a phosphate binder that is used to reduce serum phosphate levels in patients with end-stage renal disease (ESRD). Lanthanum forms insoluble lanthanum phosphate complexes that are supposed to pass through the gastrointestinal (GI) tract unabsorbed. Phosphate binders have been reported to deposit in the GI tract and can cause mucosal injury. There are few case reports of GI bleeding associated with phosphate binder deposits. This case report presents a patient with iron deficiency anaemia secondary to biopsy-proven lanthanum deposits in the upper GI tract. There were no overt signs of active GI bleeding. Patient’s anaemia improved with discontinuation of the phosphate binder. Lanthanum could be a hidden cause of resistant anaemia among patients with ESRD through asymptomatic GI blood loss.

Panitumumab is a recombinant human IgG2 monoclonal antibody which is used for the treatment of patients with metastatic colorectal cancer (mCRC) with disease progression on or following FOLFIRI (fluoropyrimidine, oxaliplatin and irinotecan) containing chemotherapy regimen. We report a case of an 83-year-old Hispanic man, non-smoker, with KRAS/NRAS wild-type mCRC of the liver who was treated with 9 cycles of FOLFOX4 (fluorouracil, leucovorin and oxaliplatin) and cetuximab. Follow-up abdominal imaging showed progression of CRC, requiring initiation of panitumumab in addition to FOLFIRI. After 2 cycles of this combination chemotherapy, he presented with acute hypoxaemic respiratory failure. Pulmonary imaging showed new onset of interstitial lung disease (ILD). He was treated with systemic corticosteroids with marked improvement of ILD. We aim to highlight the risk of severe life-threatening ILD associated with panitumumab. Early recognition of this serious adverse event helps avoid unnecessary administration of systemic antibiotics and prevent mortality.

Dofetilide is a class III antiarrhythmic drug that has proven efficacious in maintaining sinus rhythm in up to 60% of patients with persistent atrial fibrillation. Dofetilide’s most concerning adverse effect is QT prolongation and polymorphic VT, but providers should be aware of other rare significant side effects. We report a case of dofetilide associated Bell’s palsy masquerading as stroke that developed shortly after a cardioversion. The patient’s facial weakness, a side effect of dofetilide, resolved relatively quickly after discontinuation of the medication and a short course of oral corticosteroids.

We present a case of azacitidine-induced pneumonitis which is a rare adverse drug reaction and reported in less than 0.1% of cases. Common side effects of azacitidine are weakness, nausea, vomiting, constipation, injection site reactions, insomnia, among others. Our patient received azacitidine to treat her acute myeloid leukaemia and began to develop shortness of breath which progressed to dyspnoea at rest after completing a 7-day course of azacitidine and venetoclax. Initial chest X-ray revealed severe airspace disease for which the patient began receiving broad spectrum antibiotics, antifungals and antivirals therapy. Although infectious workup revealed invasive aspergillosis she did not clinically and radiologically improve despite being on isavuconazole until high-dose glucocorticoids were initiated. This case illustrates the importance of recognising and understanding the potential side effects of azacitidine and other chemotherapy agents as some adverse drug reactions can be life-threatening.

A 67-year-old postmenopausal African American woman presented with biventricular takotsubo cardiomyopathy (TTC)—evidenced by transthoracic echocardiography (TTE) showing apical akinesis of both left and right ventricles in the absence of obstructive coronary artery disease on left heart catheterisation. On the 4th hospital day, she experienced acute left facial droop, dysarthria and dysphagia. CT of the head showed a wedge infarct of the right middle cerebral artery territory. Cardioembolism was presumed after intracranial and extracranial sources of thromboembolism were ruled out. Intravenous tissue plasminogen activator (tPA) was administered with resolution of symptoms. She was later discharged without neurological deficits. Crucially, repeat TTE after tPA infusion revealed a left ventricular mass concerning for thrombus. TTE 150 min prior to stroke onset was devoid of a mass. This case uniquely illustrates the potential for rapid thrombus formation and embolism in patients with TTC. As such, it emphasises the high index of suspicion required for management of these patients.

Recent studies have shown that BRAF inhibitors, such as vemurafenib, are effective in inducing long periods of remission in relapsed hairy cell leukaemia. Acute pancreatitis is one of the rare complications that is reported with vemurafenib use. As severe pancreatitis can be life threatening, physicians should be vigilant of this side effect and promptly treat patients that develop clinical signs and symptoms while receiving vemurafenib. We present an interesting case of vemurafenib-induced pancreatitis that not only resolved but also did not recur after reintroduction of the drug at a reduced dose.