Intravenous iron is commonly prescribed for treatment of iron deficiency, with modern formulations demonstrating an acceptable safety profile in the majority of patients. We report the case of a patient who was hospitalised with muscle pain, deteriorating mobility and multiple fractures following repeated ferric carboxymaltose infusions. Investigations revealed severe hypophosphatemia with serum phosphate of 0.27 mmol/L, 25‐hydroxyvitamin D (25OHD) level of 32 nmol/L and insufficiency fractures of the sacrum and L5 transverse process. The patient's hypophosphatemia was corrected with several infusions of intravenous phosphate, as well as oral phosphate and calcitriol, with subsequent resolution of her muscle aches, back pain and immobility. The risk of persistent hypophosphatemia and osteomalacia may be higher with iron carboxymaltose than other iron formulations and a transient increase in intact fibroblast growth factor‐23 with reduced renal tubular phosphate absorption has been postulated as the key mechanism. This risk appears increased by repeated iron infusions, underlying malnutrition, hypophosphatemia at baseline, vitamin D deficiency, hyperparathyroidism or anti‐resorptive medication use. The true risk and incidence of hypophosphatemia need to be clarified so that appropriate monitoring, prevention and treatment strategies can be developed.

DILI commonly occurs in patients with cADRs and is associated with longer inpatient stay. Patients with SJS/TEN and peripheral lymphocytosis appear to be at higher risk for developing associated liver injury.

Introduction Patients with acute pulmonary embolism (PE) are at risk of developing chronic complications including the post-PE syndrome with reduced cardiopulmonary function and chronic thromboembolism pulmonary hypertension (CTEPH). Risk stratification at PE diagnosis is an important tool in predicting early mortality; however, its use in predicting chronic complications has not been evaluated. Objective This study investigates the effect of initial risk stratification of intermediate risk and standard risk PE on the rate of development of chronic complications including right ventricular (RV) dysfunction, residual perfusion defects, and CTEPH. Methods Cases of acute PE (n = 1,524) were identified using International Statistical Classification of Diseases and Related Health Problems, Tenth Revision, Australian Modification discharge diagnosis coding for PE. Evidence of RV dysfunction and systolic blood pressure < 90 mm Hg were used to risk stratify into high, intermediate and standard risk PE. Results There were 508 patients included in the analysis. Intermediate risk PE was associated with higher rates of persistent RV dysfunction as well as residual perfusion defects on repeat imaging. The overall rate of CTEPH was low (0.6%) and there was no difference between the intermediate risk and standard risk PE groups. Conclusion These findings demonstrate that acute intermediate risk PE is associated with higher rates of RV dysfunction on follow-up imaging than standard risk PE. However, the rate of CTEPH was similar between the two groups and overall the CTEPH rate was low among all patients with intermediate and standard risk PE.

Background: Intravenous iron replacement is recommended for iron-deficient patients with inflammatory bowel disease (IBD), but may be associated with hypophosphataemia, predisposing to osteomalacia and fractures. This study aimed to evaluate the incidence and risk factors for hypophosphataemia following intravenous ferric carboxymaltose (FCM) in patients with IBD. Methods: This prospective observational study of patients with and without IBD evaluated serum phosphate for 28 days following intravenous FCM, and assessed associations with symptoms, markers of inflammation and vitamin D status. Results: Twenty-four patients with IBD (11 with Crohn's disease [CD], 13 with ulcerative colitis [UC], mean age 45 years [range 19-90], 7 female), and 20 patients without IBD (mean age 56 [22-88] y, 11 female), were included. Overall, serum phosphate declined by a mean of 36% at Day 7, with a mean fall of 42% (SD 19%) at some time point over 28 days (p < 0.001). Twenty-four of 44 (55%) patients developed moderate to severe hypophosphataemia (serum phosphate < 0.6 mmol/L). No differences between patients with and without IBD were seen, but patients with CD had greater decline in phosphate than those with UC. There was no association between hypophosphataemia and symptomatic adverse events, faecal calprotectin, C-reactive protein, albumin, platelet count, 25(OH) vitamin D, or 1,25(di-OH) vitamin D. Serum phosphate < 1.05 mmol/L on Day 2 predicted susceptibility to moderate-severe hypophosphataemia (OR 7.0). Conclusions: Hypophosphataemia following FCM is common, unrelated to symptomatic adverse events, baseline intestinal or systemic inflammation, or vitamin D status.