Hyperphagia leading to obesity is the most common cause of mortality and morbidity in Prader-Willi syndrome (PWS). It has been classified as the most common genetic cause of the development of life-threatening obesity resulting from a defect in satiety, with an onset during early childhood. Abnormalities in the feedback from gut peptides, including ghrelin, may contribute to the satiety defect; autonomic dysfunction may also play a role in impaired satiety. Usually, pharmacological treatment is ineffective in managing obesity in these patients. A 19-year-old male child with Prader-Willi syndrome presented with morbid obesity, obstructive sleep apnea, and impaired glycemic control. The patient had complained of hyperphagia since early childhood, but food intake increased aggressively in the last few years, which resulted in morbid obesity. The patient was treated with laparoscopic sleeve gastrectomy, and the residual stomach volume was 100 ml. The intervention resulted in a 37.1% weight reduction after one year of surgery with well-controlled blood sugar levels. The patient also reported improved overall quality of life, mood, and functionality. Laparoscopic sleeve gastrectomy can be offered to obese Prader-Willi syndrome patients with heightened mortality, particularly because no other effective alternative therapy is available.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9375055 | PMC |
http://dx.doi.org/10.7759/cureus.27955 | DOI Listing |
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