scholarly journals Recurrent acute pancreatitis during a ketogenic diet—a case report and literature review

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Joseph Choi ◽  
Tayler L. Young ◽  
Lucas B. Chartier

Abstract Background The ketogenic (“keto”) diet has been gaining more attention lately in the medical literature and the lay media as a potentially effective method for weight control and management of type 2 diabetes. Though rare, there have been case reports of serious side effects. Here, we present a peculiar case of pancreatitis presumably associated with the ketogenic diet. Case presentation A 35-year-old man on a calorie-restricted ketogenic diet presented to the emergency department with weekly abdominal pain on Monday mornings, each time after dietary indiscretions (“cheat days”) on the weekend. It was found that he had a clinical presentation consistent with acute pancreatitis with no associated alcohol use, hypertriglyceridemia, pancreatic obstruction, or other anatomic abnormalities. The patient’s symptoms resolved with conservative management and progressive reintroduction of a standard diet. Conclusion This case indicates that the ketogenic diet could lower the threshold for acute pancreatitis, and that an episodic stressor may trigger an acute attack in the absence of traditional risk factors.

2021 ◽  
Vol 108 (Supplement_6) ◽  
Author(s):  
K A Vijayagopal ◽  
M Issa ◽  
M Fok ◽  
M S Javed

Abstract Myotonic Dystrophy(MD) is an autosomal dominant genetic condition affecting the musculoskeletal system. Recurrent acute pancreatitis(RAP) is a frequent presentation in the emergency surgical scenario with two or more episodes of established acute pancreatitis separated by a minimum of 3 month periods. We report here a case of a patient presenting with a background of Myotonic Dystrophy with a third episode of RAP. Diagnostic work up led to the discovery of microlithiasis as a possible cause of pancreatitis in our patient. Literature review reports two other case reports detailing a potential association between MD and pancreatitis at the time of writing. This could be due to disturbances of the pancreatobiliary system, resulting from the sphincter of Oddi dysfunction (SOD) and gallbladder myotonia as MD affects the smooth and striated muscle of the gastrointestinal tract. In our case report, we highlight the importance of understanding how MD is a rare cause for a common surgical emergency presentation clinicians should be aware of.


2012 ◽  
Vol 2012 ◽  
pp. 1-4 ◽  
Author(s):  
JayaKrishna Chintanaboina ◽  
Deepa Gopavaram

Context. Approximately 1.4–2% of all cases of acute pancreatitis are drug related in general population. The literature on statin-induced pancreatitis consists primarily of anecdotal case reports. We report a case of possible rosuvastatin-induced pancreatitis.Case Report. A 67-year-old female presented with progressively worsening abdominal pain and vomiting for 7 days. Home medications included rosuvastatin and clonidine. CT scan of abdomen, with intravenous contrast, showed findings consistent with acute pancreatitis. She responded to conservative management. Rosuvastatin was resumed at the time of discharge from the hospital, and she presented two months later with recurrence of acute pancreatitis. Further workup ruled out all likely causes of acute pancreatitis. Rosuvastatin was stopped completely when she was discharged the second time, and she did not have any further episodes of acute pancreatitis. She was completely asymptomatic throughout the 18-month follow-up period.Conclusion. This paper reinforces the possible association of rosuvastatin, a novel statin, with acute pancreatitis, even though the exact underlying mechanism of statin-induced pancreatitis remains unknown.


2022 ◽  
Vol 28 (1) ◽  
Author(s):  
Jielin Zhou ◽  
Yao Lu ◽  
Yajing Jia ◽  
Jing Lu ◽  
Zhengxuan Jiang ◽  
...  

Abstract Background Previous reports implied a possible link between PES1 and lipid metabolism. However, the role of PES1 in regulating T2DM related lipid metabolism and the effect of ketogenic diet (KD) on PES1 have not been reported. The aim of present study is to explore the role of PES1 in effects of KD on diabetic mice and its mediated mechanism. Methods Male C57BL/6J and KKAy mice were fed with standard diet (SD) and KD, respectively. Simultaneously, McArdle 7777 cells were treated by β-hydroxybutyric acid (β-HB), Pes1 siRNA or Pes1 overexpression plasmid, respectively. Additionally, liver-conditional knockout (CKO) of Pes1 in vivo was applied. Results Hepatic PES1 expression in diabetic mice was markedly increased, which was suppressed by KD feeding with an accompanying reduction of hepatic and plasma triglycerides (TG). In mice with CKO of Pes1, the protein levels of p300, SREBP1c, FASN, SCD1, Caspase1, NLRP3 and GSDMD were dramatically downregulated in livers, and the plasma and hepatic TG, IL-1β and IL-18 were decreased as well. The similar outcomes were also observed in β-HB and Pes1 knockdown treated hepatocytes. By contrast, Pes1 overexpression in cultured hepatocytes showed that these levels were significantly enhanced, which were, however reduced under β-HB treatment. Mechanistically, we discovered that β-HB decreased CHOP binding to the Pes1 promoters, resulting in the downregulation of PES1, thereby reducing PES1 binding to p300 and Caspase1 promoters. The inhibition of p300 and Caspase1 expression elicited the dramatic suppression of acetylation of SREBP1c via its interaction with p300, and the decreased GSDMD levels. Besides, knockdown of Caspase1 also alleviated the TG levels in cultured hepatocytes. Conclusion KD may improve lipid dysregulation in type 2 diabetic mice by downregulating hepatic PES1 expression.


2020 ◽  
Vol 2020 ◽  
pp. 1-4 ◽  
Author(s):  
Sunam M. Sujanani ◽  
Mohanad M. Elfishawi ◽  
Paria Zarghamravanbaksh ◽  
Francisco J. Cuevas Castillo ◽  
David M. Reich

Sodium-glucose cotransporter 2 (SGLT2) inhibitors are increasingly used as add-on therapy in patients with poorly controlled type 2 diabetes mellitus (T2DM). Although pancreatitis is not a known side effect of SGLT-2 inhibitors, there have been case reports of SGLT-2 inhibitor use being associated with pancreatitis. Case Presentation. A 51-year-old male with a history of type 2 diabetes, dyslipidemia, and status-post cholecystectomy presented to the emergency room with a four-day history of periumbilical pain radiating to the back. He denied any history of recent alcohol intake or prior episodes of pancreatitis. On physical examination, his abdomen was diffusely tender to palpation without guarding or rebound. Initial labs were notable for a leukocyte count of 9.3 × 109/L, creatinine level of 0.72 mg/dL, calcium level of 9.5 mg/dL, lipase level of 262 U/L, and triglyceride level of 203 mg/dL. His last HbA1c was 8.5%. CT scan of his abdomen and pelvis showed findings consistent with acute pancreatitis with no biliary ductal dilatation. Careful review of his medications revealed the patient was recently started on dapagliflozin five days prior to admission in addition to his longstanding regimen of insulin detemir, sitagliptin, metformin, and rosuvastatin. His symptoms resolved after discontinuation of sitagliptin and dapagliflozin. A year later, due to increasing HbA1c levels, a decision was made to rechallenge the patient with dapagliflozin, after which he developed another episode of acute pancreatitis. His symptoms resolved upon cessation of dapagliflozin. Conclusion. This case highlights the possible association of SGLT-2 inhibitors and pancreatitis. Patients should be informed about the symptoms of acute pancreatitis and advised to discontinue SGLT-2 inhibitors in case such symptoms occur.


2021 ◽  
Author(s):  
Jielin Zhou ◽  
Yao Lu ◽  
Yajing Jia ◽  
Jing Lu ◽  
Zhengxuan Jiang ◽  
...  

Abstract Background: Previous reports implied a possible link between PES1 and lipid metabolism. However, the role of PES1 in regulation of T2DM related lipid metabolism and the effect of KD on PES1 have not been reported. The aim of present study is to explore the role of PES1 in effects of ketogenic diet (KD) on diabetic mice and its mediated mechanism.Methods: Male C57BL/6J and KKAy mice were fed with standard diet (SD) and KD, respectively. Simultaneously, McArdle 7777 cells were treated by β-hydroxybutyric acid (β-HB), Pes1 siRNA or Pes1 overexpression plasmid, respectively. Additionally, liver-conditional knockout (CKO) of Pes1 in vivo were used.Results: We unexpectedly found that hepatic PES1 expression in T2DM patients was markedly elevated, but the elevated PES1 was suppressed by KD feeding in T2DM mice with the reduction of hepatic and plasma triglycerides (TG). In mice with CKO of Pes1, the protein levels of p300, SREBP1c, FASN, SCD1, caspase1, NLRP3 and GSDMD were dramatically downregulated in livers, and the plasma and hepatic TG, IL-1β and IL-18 were decreased as well. The similar phenomena were also observed in β-HB and Pes1 knockdown treated hepatocytes. By contrast, Pes1 overexpression in cultured hepatocytes showed that these levels were significantly enhanced, which however were reduced under β-HB treatment. Mechanistically, we discovered that β-HB decreased CHOP binding to the Pes1 promoters, resulting in the downregulation of PES1, thereby reducing PES1 binding to p300 and caspase1 promoters. The inhibition of p300 and caspase1 expressions elicited the dramatic suppression of acetylation of SREBP1c via its interaction with p300, and the decreased GSDMD levels. Besides, knockdown of caspase1 also alleviated the TG levels in cultured hepatocytes.Conclusion: KD may improve lipid dysregulation in type 2 diabetic mice by downregulating hepatic PES1 expression.


2018 ◽  
Vol 27 (2) ◽  
pp. 189-194 ◽  
Author(s):  
Ágnes Meczker ◽  
Alexandra Mikó ◽  
Péter Hegyi

5-aminosalicylic acid has been reported to be able of inducing acute pancreatitis as an adverse reaction. However, in most case reports, rechallenge of the drug is missing; therefore, evidence is still needed to confirm its role in the clinical course of acute pancreatitis and its influence on the outcome. Here, we report a case of recurrent acute pancreatitis secondary to 5-aminosalicylic acid, with positive unintentional rechallenge. A systematic search of the literature was performed and 42 cases from 35 articles were summarized concerning the clinical course of 5-aminosalicylic acid induced acute pancreatitis.


2006 ◽  
Vol 76 (4) ◽  
pp. 208-215 ◽  
Author(s):  
Astrup

The epidemic of both obesity and type 2 diabetes is due to environmental factors, but the individuals developing the conditions possess a strong genetic predisposition. Observational surveys and intervention studies have shown that excess body fatness is the major environmental cause of type 2 diabetes, and that even a minor weight loss can prevent its development in high-risk subjects. Maintenance of a healthy body weight in susceptible individuals requires 45–60 minutes physical activity daily, a fat-reduced diet with plenty of fruit, vegetables, whole grain, and lean meat and dairy products, and moderate consumption of calorie containing beverages. The use of table values to predict the glycemic index of meals is of little – if any – value, and the role of a low-glycemic index diet for body weight control is controversial. The replacement of starchy carbohydrates with protein from lean meat and lean dairy products enhances satiety, and facilitate weight control. It is possible that dairy calcium also promotes weight loss, although the mechanism of action remains unclear. A weight loss of 5–10% can be induced in almost all obese patients providing treatment is offered by a professional team consisting of a physician and dieticians or nurses trained to focus on weight loss and maintenance. Whereas increasing daily physical activity and regular exercise does not significantly effect the rate of weight loss in the induction phase, it plays an important role in the weight maintenance phase due to an impact on daily energy expenditure and also to a direct enhancement of insulin sensitivity.


2014 ◽  
Author(s):  
Abdulghani Al-Saeed ◽  
Ahmad Alobedallah ◽  
Ayman Al-Hayek ◽  
Sohail Inam ◽  
Rim Braham ◽  
...  

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