To our knowledge, our report represents the first case of SIADH due to a single oral dose of cyclophosphamide. Clinicians should be aware of this rare adverse event, as it can have life-threatening consequences.

The adult zebrafish brain, unlike mammals, has a remarkable regenerative capacity. Although inflammation inhibits regeneration in mammals, it is necessary for zebrafish brain repair. Microglia are resident brain immune cells that regulate the inflammatory response. To explore the microglial role in repair, we used liposomal clodronate and colony stimulating factor-1 receptor (csf1r) inhibition to suppress microglia during brain injury. We found that microglial ablation inhibited injury-induced neurogenesis and regeneration. Microglial suppression specifically attenuated cell proliferation at the progenitor cell amplification stage of neurogenesis. Notably, the loss of microglia impaired phospho-stat3 (signal transducer and activator of transcription 3) and ß-catenin signaling by altering tumor necrosis factor-α expression after injury, and the ectopic activation of stat3 and ß-catenin rescued neurogenesis defects caused by microglial loss. Leukocytes also accumulated after microglial ablation, potentially hindering the resolution of inflammation. These findings reveal specific roles of microglia and inflammatory signaling during zebrafish telencephalic regeneration that should provide strategies to improve mammalian brain repair.

Thrombotic microangiopathy (TMA) is a microvascular occlusive disorder characterised by platelet aggregation, thrombocytopenia and end-organ damage. It is commonly idiopathic, although several drug classes, including cytotoxic chemotherapy, have been implicated. Several of cases of gemcitabine-induced TMA have been documented with incidence likely to increase with the escalating use of gemcitabine. We report the cases of two patients who developed TMA while on gemcitabine chemotherapy.

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Novelty statement:1. What is the new aspect of your work?• Acquired haemophilia A (AHA) typically occurs in elderly patients with multiple comorbidities. Immunosuppression has demonstrated improved overall survival and remission rates; however, treatment-related complications in this cohort often occur. Efficacious but dose-reduced immunosuppression for this rare condition will hopefully reduce morbidity and is an important area for further research. What is the central finding of your work?• Universal immunosuppression in AHA patients improves overall survival, and 87.5% of patients achieved a complete remission in a median of 48 days. The use of upfront rituximab with corticosteroids is increasing and is associated with shorter times to complete remission. Low-dose rituximab (100 mg/m 2 weekly IV for 4 doses) is emerging as an alternative and appears non-inferior in this case series.