Acute pancreatitis in Crohn’s disease: diagnostic value of diffusion-weighted MRI

Clinical History

The patient is a male smoker suffering from upper abdominal pain radiating to his back. Medical history included appendectomy, recent diagnosis and surgical treatment of Crohn's disease one year earlier. Physical examination excluded peritonism, fever and bowel obstruction. Laboratory studies revealed leukocytosis (11.600 cells/mmc), elevated C-reactive protein (54 mg/L) and serum lipase (1400 U/L).

Imaging Findings

Twenty months earlier, before diagnosis of Crohn's disease (CD), he experienced mild acute pancreatitis (AP) with near-normal CT (Fig.1) and MR-cholangiopancreatography (Fig.2) findings apart from subtle peripancreatic fat stranding at the tail. Suspected autoimmune pathogenesis was not confirmed by immunologic studies.
Eight months later, the patient was diagnosed with severely active ileo-colonic CD. After initial steroid treatment, infliximab was suspended because of allergy, and surgical ileocecal resection was performed plus cholecystectomy and adhesiolysis.
A year after surgery, this new AP bout was again studied with CT (Fig.3) and MR (Fig.4) with inconclusive imaging findings. The addition of diffusion-weighted (DW) MRI (Fig.5) revealed homogeneously increased pancreatic signal intensity compared to normal control (Fig.6) with corresponding abnormally low apparent diffusion coefficients (ADC). Therefore, DW-MRI confirmed the diagnosis of AP over unspecific enzyme elevation, probably secondary to iatrogenic effect of drugs (probably metronidazole) since cholelithiasis, alcohol and autoimmune (negative autoantibodies) were excluded.

Discussion

Among the varied spectrum of its extraintestinal manifestations, Crohn’s disease (CD) has a well-known association with acute and chronic pancreatic disorders. In patients with CD, the incidence of acute pancreatitis (AP) reaches 1.4% and is 3- to 4-fold higher compared to control populations even after adjusting for other risk factors. Most cases occur in young adults (between 20 and 50 years of age) with a female predominance and smoking as key risk factor. The majority of AP occur within 2 years after CD diagnosis; less than 10% of patients suffer AP before CD diagnosis is established CD or synchronously with the onset of intestinal CD [1-6].
The increased incidence of AP is multifactorial and involves a combination of gallstone disease, adverse effect of medications, and intrinsic immunologic disturbances. Compared to the general population, patients with CD have higher (13-34%) prevalence of cholesterol, mixed and pigment-type gallstones secondary to ileal disease. Several drugs are known to cause AP from possible idiosyncratic mechanism, such as thiopurines, sulfasalazine, 5-aminosalicylic acids, metronidazole and steroids; azathioprine has the higher incidence (7.3%) and strongest causal association with AP. Idiopathic cases are attributed to direct pancreatic damage as a true extraintestinal phenomenon [1-6].
In CD, the diagnosis of AP requires at least 2 out of 3 criteria (a-consistent abdominal pain, b-serum lipase or amylase greater than 3 times the upper normal limit, c-consistent CT or MRI findings). However, recurrent unspecific abdominal pain is common in the setting of CD, and benign increase of pancreatic enzymes without true imaging-confirmed AP are common (9-17%) in CD [1-6].
As in this case, in patients with consistent clinical and laboratory findings but inconclusive sonographic and CT appearances, the use of diffusion-weighted (DW) MRI may help to confirm the diagnosis of mild AP over nonspecific changes since it allows differentiation between normal, inflamed and necrotic pancreas without intravenous contrast. Albeit values are inconsistent between different scanners and protocols, mean apparent diffusion coefficient (ADC) values in AP are significantly decreased in AP compared to healthy glandular parenchyma and cut-off values of 1.5-1.6 have been proposed for diagnosing AP [7-10].
The same would be probably also useful for drug-induced AP, which represents the third cause (5.3%) of AP in the general population after biliary and alcohol [11, 12]. The severity, treatment and prognosis of AP in CD is analogous to those in the general population, and drug-induced occurrences are generally uncomplicated and self-limiting [1-6].

Differential Diagnosis List

Final Diagnosis

Drug-induced mild acute pancreatitis in Crohn’s disease

URL:	https://eurorad.org/case/14183
DOI:	10.1594/EURORAD/CASE.14183
ISSN:	1563-4086