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Cerebral proliferative angiopathy (CPA) is a rare subtype of cerebral arteriovenous malformation, characterized by unique angiographic features and clinical presentations. Although the clinical and angiographic characteristics of CPA have been well described, their impact on the surrounding tissues remains underexplored. Herein, we investigated the presence of calvarial thickening in patients with CPA, and discuss its potential pathogenesis.

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Rationale: Temporary central venous catheters are commonly used for patients who require emergency hemodialysis. In rare instances, this procedure can result in a very serious complication known as arteriovenous fistula (AVF). Although some cases of femoral arteriovenous fistula have been reported previously in the literature; however, the incidence of iliac AVF precipitated by a hemodialysis catheter is exceedingly uncommon.

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Hereditary haemorrhagic telangiectasia (HHT) is a rare genetic disease characterised by mucocutaneous telangiectasias and arteriovenous malformations that can affect multiple organs. Although rare, ischaemic cholangiopathy can occur, a serious complication that can even lead to death. We present the case of a patient with HHT disease with previous mucocutaneous and gastrointestinal manifestations in whom 8 weeks after cholecystectomy a saccular dilatation of the intrahepatic bile duct was observed.

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Unlabelled: Right-to-left shunt may be a cause of paradoxical embolization (and cryptogenic cerebral ischemic events). Patent foramen ovale and pulmonary arterio-venous malformations are the most common cause of paradoxical embolization; however, some rare cardiovascular lesions may cause a right-to-left shunt with consequent paradoxical embolization. We describe a case of a young child with superior sinus venosus atrial septal defect who underwent surgical closure and developed a cryptogenic cerebral ischemic attack due to a rare cause of paradoxical embolization, during a long-term follow-up.

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Hereditary hemorrhagic telangiectasia is an autosomal dominant disorder caused by mutations in the bone morphogenetic protein signaling pathway, leading to arteriovenous malformations. While previously thought to share molecular and cellular dysregulation, this study reveals highly distinct mechanisms depending on whether mutations occur in Alk1 or SMAD4. Loss of SMAD4 enhances endothelial cell responses to flow, including flow-regulated transcription and cell migration against blood flow, causing excessive pruning of capillaries and the formation of single large shunts.

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