Acute pancreatitis after growth hormone treatment: disease or treatment linked?

Beaufort, Carine de; Beck, Peter; Seligmann, Roland; Meırleır, Linda De; Schepper, Jean De

doi:10.1007/s00431-006-0126-z

Cited by 11 publications

(4 citation statements)

References 6 publications

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“…To the contrary, some clinical reports have shown that prolonged application of GH to the GH-deficient patients could be complicated, in some individuals, by the development of mild acute pancreatitis [22][23][24][25]. This complication of GH therapy was noted in 7 cases per 24,000 patients treated with GH.…”

Section: Discussionmentioning

confidence: 83%

Involvement of sensory nerves in the protective effect of growth hormone on acute pancreatitis

Jaworek

Leja-Szpak

Dembiński

et al. 2009

Growth Hormone & IGF Research

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Section: Discussionmentioning

confidence: 83%

Involvement of sensory nerves in the protective effect of growth hormone on acute pancreatitis

Jaworek

Leja-Szpak

Dembiński

et al. 2009

Growth Hormone & IGF Research

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“…One study showed that the single effects of growth hormone down-regulated apoptosis of intestinal mucosa cells in acute necrotizing pancreatitis, 36 but growth hormone is seldom used on its own; some studies indicate that the excessive application of it may induce or aggravate acute pancreatitis. 37,38 In conclusion, we found that intestinal mucosa was significantly damaged, and the apoptosis of intestinal mucosa cells increased in this SAP model. The application of Saizen in combination with Stilamin could decrease the apoptosis of intestinal mucosa cells and increase intestinal mucosa barrier function, which suggested that Saizen has significant protective effects on intestinal mucosa in experimental SAP.…”

Section: Discussionmentioning

confidence: 91%

Protective Effects of Saizen in Combination With Stilamin on Intestinal Mucosa of a Rabbit Model of Severe Acute Pancreatitis

Lü

Yu²,

Yang³

et al. 2013

Pancreas

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“…The exact effects of AAS [ 20 ] and growth hormone [ 21 ] on DIAP are not well understood. Predictions are that AAS can induce an immune-mediated inflammatory response, direct cellular toxicity, pancreatic ductal constriction, arteriolar thrombosis, and metabolic effects in the pancreas [ 20 ], and it is observed in pediatric studies that growth hormone causes secretion of pancreatic enzymes [ 22 ]. Animal studies have shown that arginine, which is a potent secretagog of growth hormone, causes direct damage to the pancreatic acinar cells and dose-related necrotizing pancreatitis in rats [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

Drug-induced acute pancreatitis in a bodybuilder: a case report

Shabestari

Chaudhary

et al. 2022

J Med Case Reports

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Background Unregulated use of a variety of drugs and supplements by bodybuilders and athletes is common and can lead to severe adverse complications. Only a small proportion of acute pancreatitis cases are drug induced, and case reports are essential for identifying potential drug-related risks for pancreatitis. Here we present the first case report published of acute pancreatitis linked to recreational use of anabolic–androgenic steroids, subcutaneous growth hormone, and clenbuterol in a previously healthy male after excluding all other causes of pancreatitis. Case presentation A 31-year-old Arab male bodybuilder presented with acute abdominal pain associated with nausea and sharp pain radiating to the back. The patient was not using tobacco or alcohol but was using multiple drugs related to bodybuilding, including anabolic–androgenic steroids, subcutaneous growth hormone, clenbuterol, and multiple vitamin supplements. Laboratory studies revealed a normal white blood cell count, elevated C-reactive protein, minimally elevated aspartate aminotransferase and total bilirubin with normal remaining liver tests, and elevated amylase and lipase. The patient had no hypertriglyceridemia or hypercalcemia, and had had no recent infections, abdominal procedures, trauma, or scorpion exposure. Imaging and laboratory investigations were negative for biliary disease and IgG4 disease. Abdominal computed tomography revealed hepatomegaly and diffuse thickening and edema of the body and tail of the pancreas with peripancreatic fat stranding. An abdominal ultrasound showed slight hepatomegaly with no evidence of cholelithiasis. Genetic testing for hereditary pancreatitis-related mutations was negative. A diagnosis of drug-induced acute pancreatitis was made, and he was treated with aggressive intravenous hydration and pain management. The patient has avoided further use of these drugs and supplements and had no further episodes of pancreatitis during 1 year of follow-up. Conclusions This case describes a patient with drug-induced acute pancreatitis after the intake of anabolic–androgenic steroids, subcutaneous growth hormone, and clenbuterol, where all other common causes of acute pancreatitis were excluded. Clinicians should be alert to the possibility of drug-induced acute pancreatitis occurring in bodybuilders and athletes using similar drug combinations.

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Acute pancreatitis after growth hormone treatment: disease or treatment linked?

Cited by 11 publications

References 6 publications

Involvement of sensory nerves in the protective effect of growth hormone on acute pancreatitis

Involvement of sensory nerves in the protective effect of growth hormone on acute pancreatitis

Protective Effects of Saizen in Combination With Stilamin on Intestinal Mucosa of a Rabbit Model of Severe Acute Pancreatitis

Drug-induced acute pancreatitis in a bodybuilder: a case report

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