Revista espanola de patologia : publicacion oficial de la Sociedad Espanola de Anatomia Patologica y de la Sociedad Espanola de Citologia · 2026
Gastric surgery as an acquired cause of pancreatic alpha-cell hyperplasia.
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Onieva Carbajo Ricard, Casamitjana Laia, Gener Jorge Cristina, Vidal Borrego Marta, Ferreres Piñas Joan Carles
Аннотация
INTRODUCTION: Alpha-cell hyperplasia (ACH) is a rare condition, with only eighteen cases reported in the literature. Its primary cause is Mahvash disease, a hereditary disorder associated with pancreatic neuroendocrine tumours. Based on the experience of our site, previous gastric surgery (GS) is suspected to represent a potential acquired cause of ACH - the first such case described to date.
MATERIAL AND METHODS: A case-control study was designed using pancreatic tissue samples, selecting six patients with a history of gastric surgery (GS) more than six months before, and twelve patients with GS less than six months before or no history of GS. Immunohistochemical staining for chromogranin, insulin and glucagon was performed. The neuroendocrine cellularity (NEC) area, type of cellularity, and distribution pattern were evaluated.
RESULTS: The mean NEC area in the cases was 6.01%, compared to 3.18% in the controls (p=0.047). A history of Billroth I GS was associated with a lower NEC percentage than Billroth II, which in turn was lower than that observed following bariatric surgery. All samples contained at least one islet exceeding 250μm. In five of six cases, more than 50% of islets demonstrated abundant centrally located glucagon-positive cells, compared with two of twelve controls (p=0.013).
CONCLUSIONS: A history of CG may have histological correlates in pancreatic tissue, making it important to recognise these to avoid misdiagnosing a true ACH, which carries associated implications such as a high risk of tumour development and genetic transmission.
MATERIAL AND METHODS: A case-control study was designed using pancreatic tissue samples, selecting six patients with a history of gastric surgery (GS) more than six months before, and twelve patients with GS less than six months before or no history of GS. Immunohistochemical staining for chromogranin, insulin and glucagon was performed. The neuroendocrine cellularity (NEC) area, type of cellularity, and distribution pattern were evaluated.
RESULTS: The mean NEC area in the cases was 6.01%, compared to 3.18% in the controls (p=0.047). A history of Billroth I GS was associated with a lower NEC percentage than Billroth II, which in turn was lower than that observed following bariatric surgery. All samples contained at least one islet exceeding 250μm. In five of six cases, more than 50% of islets demonstrated abundant centrally located glucagon-positive cells, compared with two of twelve controls (p=0.013).
CONCLUSIONS: A history of CG may have histological correlates in pancreatic tissue, making it important to recognise these to avoid misdiagnosing a true ACH, which carries associated implications such as a high risk of tumour development and genetic transmission.