Reports

Background and Clinical Significance: Zolbetuximab, a claudin 18.2-targeted monoclonal antibody, has demonstrated efficacy in advanced gastric cancer. Hypoalbuminemia has emerged as a notable adverse effect, but its underlying mechanism remains unclear. Case Presentation: A 53-year-old male with unresectable advanced gastric cancer received zolbetuximab-based combination therapy, achieving tumor regression enabling conversion surgery. During six cycles of treatment, serum albumin levels decreased from 4.3 g/dL to 3.5-3.6 g/dL (grade 1 hypoalbuminemia). A histopathological examination of the surgical specimen revealed hypertrophic gastritis characterized by marked foveolar hyperplasia, increased mucus secretion, and pyloric gland metaplasia on the lesser curvature. These findings suggest that zolbetuximab-induced mucosal alterations may contribute to hypoalbuminemia through enhanced protein loss. Conclusions: This is the first pathological documentation of hypertrophic gastritis associated with zolbetuximab therapy. Clinicians should monitor albumin levels during treatment and consider nutritional support when indicated. These findings provide important insights for optimizing patient management and ensuring safe conversion surgery planning.

Background and Clinical Significance: Intracerebral hemorrhage (ICH) is a very rare complication following endovascular closure of direct carotid-cavernous fistulas (CCFs). When reported, ICH typically appears within the first 48 h after CCF closure. We performed an extensive literature review, starting from the case of a 48-year-old patient presenting with an intracerebral hemorrhage after CCF closure. Case Presentation: A 48-year-old woman with arterial hypertension developed an intracerebral hemorrhage in the right frontal lobe 12 days after successful closure of a traumatic CCF. The patient exhibited acute neurological deterioration in a previously hypoperfused territory. A narrative review identifies the classical molecular theory of hemodynamic dysregulation, known as Normal Perfusion Pressure Breakthrough (NPPB), as the principal pathophysiological mechanism. Other mechanisms such as oxidative stress, microglial activation, blood–brain barrier disruption, metalloproteinase expression, and possible genetic alterations such as ICA1L variants are also implicated. Conclusions: This case underscores the importance of considering molecular mechanisms in the pathophysiology of delayed post-endovascular treatment of ICH, as well as the need for hemodynamic monitoring and follow-up in patients with vascular comorbidities.

The paper by Mavroudis et al [...]