Association of Oral Glucocorticoid Use With an Increased Risk of Acute Pancreatitis

Sadr–Azodi, Omid; Mattsson, Fredrik; Bexlius, Tomas Sjöberg; Lindblad, Mats; Lagergren, Jesper; Ljung, Rickard

doi:10.1001/jamainternmed.2013.2737

Cited by 80 publications

(63 citation statements)

References 33 publications

(37 reference statements)

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“…Cause and effect of this ominous triad are discussed controversially but they seem to be linked in a multidirectional relationship. A recent Swedish nationwide case–control study showed increased risk for acute pancreatitis in patients under oral CS 11. The mechanisms by which CS induce pancreatitis are not yet fully elucidated 10.…”

Section: Discussionmentioning

confidence: 99%

Ominous triad triggered by high-dose glucocorticosteroid therapy

2017

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Glucocorticosteroids (CS) play a key role in the treatment of numerous diseases. Nonetheless, they can be accompanied by several adverse effects. We present the case of a 51-year-old woman who was treated with high-dose CS for a relapse of her multiple sclerosis. After 5 days of treatment, the patient developed severe diabetic ketoacidosis, hypertriglyceridemia and acute pancreatitis-a potentially life-threatening triad which has previously been described, in our case, however, for the first time as a complication of CS therapy. Our patient's condition was further aggravated by a circulatory shock, haemodynamic relevant bleeding from a duodenal ulcer and psychotic symptoms. In the intensive care unit, intravenous insulin infusion, fluid resuscitation, catecholamine support, electrolyte supplementation, endoscopic haemoclipping and antibiotic and antipsychotic treatment were administered, leading to a continuous improvement of the patient's health state.

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Section: Discussionmentioning

confidence: 99%

Ominous triad triggered by high-dose glucocorticosteroid therapy

2017

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“…Treatment with PLT platelet steroids and intravenous pulse methylprednisolone when necessary, combined with immunosuppressive agents, is recommended to block cytokine-induced inflammation and improve organ perfusion [18]. However, some studies have reported an association between glucocorticoid use and an increased risk of AP with unclear pathogenic mechanisms [19], which manifests as an increase in serum amylase level during the first few days of treatment. However, in our cohort, there was no significant difference between serum amylase levels, or in immunosuppressive agents and pulse steroid therapy between CP and AP, or between SAP and MAP patients.…”

Section: Discussionmentioning

confidence: 99%

Prevalence, severity, and clinical features of acute and chronic pancreatitis in patients with systemic lupus erythematosus

et al. 2016

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Pancreatitis is a rare, life-threatening complication of systemic lupus erythematosus (SLE). This study aimed to describe the clinical features of acute pancreatitis (AP) and chronic pancreatitis (CP) in patients with SLE. Data of patients who fulfilled the revised criteria of the American Rheumatism Association for diagnosis of SLE were retrospectively analyzed. SLE activity was graded according to the SLE Disease Activity Index. Logistic regression analysis was conducted to find out independent associations. Survival rates were estimated by using Kaplan-Meier plots. This study included 5665 SLE patients admitted between January 1983 and January 2014, of whom 52 patients were diagnosed with pancreatitis. Pancreatitis prevalence in SLE patients was 0.92 % (52/5665). AP (0.8 %, 46/5665) was more prevalent than CP (0.1 %, 6/5665), presented mostly during active SLE, and affected more organs. Hypertriglyceridemia occurred in 76.9 % of AP patients and in none of the CP patients. AP patients were divided into severe (n = 10) or mild (n = 20) cases. The average triglyceride level in severe AP cases was higher than that in mild AP cases (P = 0.006), and the mortality rate of lupus-associated AP was 32.6 % (15/46). Concomitant infections and thrombocytopenia were independently associated with poor prognosis (P < 0.001, P = 0.028, respectively). There were significant differences in the clinical manifestations of AP and CP. Patients with severe AP were found to have a higher incidence of concomitant infection and serum triglyceride levels. Concomitant infections and thrombocytopenia were independent risk factors for poor prognosis.

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“…Although the pathophysiological mechanism behind corticosteroid-induced pancreatitis remains unclear, recent data suggest it may be related to the systemic effects of these medications, and specific alterations of lipid and calcium metabolism in pancreatic cells 4. The current literature on epidemiological incidence of oral corticosteroid use suggests that the risk of acute pancreatitis was increased among current users compared with non-users, and the risk for development of this condition was highest 4–14 days after the medication was taken 3. This well-described period when acute onset of pancreatitis likely manifests is important for physicians to be aware of when a patient presents with the clinical symptoms of this disease and with recent history of corticosteroid use.…”

Section: Discussionmentioning

confidence: 99%

“…Extensive case reports have described pancreatic anomalies in systemic diseases that require high dosage of oral chronic steroid regiments for treatment or remission. Such conditions, which require the aforementioned glucocorticoid therapy and have documented pancreatitis, include, but are not limited to, systemic lupus erythaematous, inflammatory bowel disease, IgA nephropathy and Wegener's granulomatosis 3. Although the exact dosage of corticosteroid medication to elicit pancreatic damage has not been established, review of reported incidents of drug-induced pancreatitis reveal that these are after significantly high doses of medication.…”

Section: Introductionmentioning

confidence: 99%

Acute necrotising pancreatitis derived from low-dose corticosteroid use: an important reminder of clinical management

2015

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Although the exact mechanism is unknown, incidence of drug-induced pancreatitis from corticosteroids is well established in the medical literature. Commonly reported in chronic steroid-dependent individuals who require large doses for a wide array of pathologies, the incidence of damage to the pancreas from low-doses have not been well described. We report a case of a 68-year-old woman who presented with severe abdominal pain, nausea and vomiting, 3 days after the initiation of low-dose methylprednisolone for osteoarthritis. Inpatient laboratory analysis revealed an elevated lipase of 1770 U/L and CT scan showing extensive necrotising pancreatitis involving the head, body and tail. Cessation of the causative medication and conservative treatment successfully led to resolution of symptoms. We present this case to inform clinicians of the precipitance of pancreatitis from modest strength corticosteroid management, so that more accurate and improved performance in pharmacological decisions can be made for patient care.

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Association of Oral Glucocorticoid Use With an Increased Risk of Acute Pancreatitis

Cited by 80 publications

References 33 publications

Ominous triad triggered by high-dose glucocorticosteroid therapy

Ominous triad triggered by high-dose glucocorticosteroid therapy

Prevalence, severity, and clinical features of acute and chronic pancreatitis in patients with systemic lupus erythematosus

Acute necrotising pancreatitis derived from low-dose corticosteroid use: an important reminder of clinical management

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