ArticleEndocrinology, diabetes & metabolism case reports2018
An unusual presentation of post gastric bypass hypoglycemia with both postprandial and fasting hypoglycemia
Article in Endocrinology, diabetes & metabolism case reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Post-bariatric Hypoglycemia Management: A Gulf Cooperation Council Consensus Statement.Journal of the Endocrine Society · 2026Article
- Article
- Review
- Fasting hypoglycaemia secondary to carnitine deficiency: a late consequence of gastric bypass.BMJ case reports · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There has been an increasing awareness of post gastric bypass hypoglycemia (PGBH). Histopathologic findings from such patients who underwent partial/total pancreatomy, however, can vary widely from minimal changes to classic nesidioblastosis, making the pathologic diagnosis challenging. PGBH typically presents as postprandial hypoglycemia, as opposed to insulinoma, which presents as fasting hypoglycemia. Herein, we describe an unusual case of a patient with PGBH who initially presented with postprandial hypoglycemia three years after surgery, but later developed fasting hyperinsulinemic hypoglycemia as the disease progressed. Our hypothesis for this phenomenon is that this disease is progressive, and later in its course, the insulin release becomes dissociated from food stimulation and is increased at baseline. Future studies are needed to investigate the prevalence as well as etiology of this progression from postprandial to fasting hypoglycemia. Learning points: •• There has been an increasing awareness of post gastric bypass hypoglycemia (PGBH). •• Histopathologically, PGBH can vary from minimal changes to nesidioblastosis. •• Although uncommon, patients with PGBH after Roux-en-Y gastric bypass may present with both postprandial and fasting hyperinsulinemic hypoglycemia as disease progresses. •• Our hypothesis for this phenomenon is that the insulin release becomes dissociated from food stimulation and is increased at baseline with disease progression.
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Registered trials
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