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Autoimmune pancreatitis: An incidental detection on FDG PET/CT with response to steroid therapy
Address for correspondence: Dr. Venkatesh Rangarajan, Department of Nuclear Medicine and Molecular Imaging, Tata Memorial Hospital, Parel, Mumbai - 400 057, Maharashtra, India. E-mail: drvrangarajan@gmail.com
This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
This article was originally published by Medknow Publications & Media Pvt Ltd and was migrated to Scientific Scholar after the change of Publisher.
Abstract
Autoimmune pancreatitis (AIP) is most often incidentally detected, with the diagnosis being based on radiological characteristics. A steroid regimen for 6 weeks is the standard line of treatment for AIP. In our case, AIP was incidentally suspected on fluorodeoxyglucose positron emission tomography/computed tomography (PET/CT) performed for staging a malignancy, and a follow-up PET/CT study after steroid treatment, showed complete metabolic and morphological response; thus confirming the imaging diagnosis of AIP.
Keywords
Autoimmune
CT
FDG PET
pancreatitis
steroid
INTRODUCTION
Autoimmune pancreatitis (AIP) is a rare pancreatic disorder, diagnosed radiologically on the basis of classical imaging hallmarks and biochemically by raised serum markers. It is known to respond well to steroid therapy. We report a case of incidentally detected AIP on fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) performed for staging of lung cancer. In addition to classical CT findings, diffuse pattern of FDG uptake was seen. Patient also had raised serum IgG4 levels. This favored an autoimmune etiology. Importantly, after steroid therapy, there was response seen both morphologically and metabolically; thus retrospectively, confirming it to be AIP.
CASE REPORT
A 72-year-old gentleman, a diagnosed case of small cell lung cancer stage IIIA, was referred for a whole body 18F-FDG PET/CT study, for pre-treatment staging. Patient was breathless, but had no abdominal complaints. Maximum intensity projection (MIP) image showed intense mediastinal tracer concentration at the site of primary [Figure 1a-arrow]; however also seen was moderately increased tracer uptake in the mid-abdomen [Figure 1a-arrow head]. On axial CT [Figure 2a-arrow] and PET/CT [Figure 2b-arrow] image, a large enhancing FDG avid mediastinal mass was seen, predominantly to the right, encasing the right main bronchus and causing vascular compression. Also, PET/CT image showed diffusely increased tracer uptake in the pancreas [Figure 3a-arrow]. Axial contrast enhanced CT image revealed featureless pancreas with diffuse, homogenous, sausage-shaped enlargement, with minimal post-contrast enhancement, associated with diffuse narrowing of main pancreatic duct [Figure 3b-arrow]. No focal lesion or mass was noted in the pancreas. No calcification, peripancreatic fluid or perilesional adenopathy was seen. Liver function tests and CA-19.9 levels were normal. Though, patient was asymptomatic, based on the imaging features, a suspicion of AIP was raised. This was confirmed by raised serum lipase and amylase levels, and raised IgG4 titer (230 mg/L, normal value < 135 mg/L). Small cell lung cancer was managed with a chemotherapy regimen of four cycles of cisplatin with etoposide (Cisplatin 60-80 mg/m2 on day 1 and etoposide 80-120 mg/m2 on days 1-3, every 21 days). Oral corticosteroid (prednisolone 40 mg/week for 4 weeks, tapering by 5 mg/week for 12 weeks) was given for AIP and thereafter, a follow-up PET/CT study was performed. MIP image showed a significant reduction in mediastinal tracer uptake [Figure 1b-arrow] suggestive of response to chemotherapy, with no tracer uptake in the mid-abdomen. Axial PET/CT [Figure 3c-arrow] and CT image [Figure 3d-arrow] showed no pancreatic tracer uptake, with restoration of normal size and architecture of pancreas. Also normal levels of serum amylase, lipase, and IgG4 were seen. These findings, in retrospect, confirmed the presence of AIP.
DISCUSSION
In this case, one could argue that morphologic and metabolic regression of the pancreatic pathology after chemotherapy could also represent metastatic disease from lung cancer. However, the characteristic imaging features of AIP, absence of a focal pancreatic mass coupled with restoration of normal pancreatic architecture and serum levels (lipase, amylase, and IgG) after steroid therapy, were strong pointers toward the diagnosis of AIP. This indirect approach of diagnosing AIP without actual histopathological diagnosis has been followed in most of the imaging data on AIP, except for a single retrospective study.[1] Although, there are diagnostic criteria proposed for AIP,[2] differentiating AIP from other pancreatic conditions can sometimes pose a dilemma. CT is the preferred modality, with features such as diffuse enlargement and ductal narrowing favoring autoimmune etiology.[3] FDG PET/CT often shows diffuse pancreatic tracer uptake due to immune mediated active inflammation of pancreas, in addition to the morphological features on CT component of PET/CT.[4] This metabolic criteria can be used as a baseline and patients can be followed-up after a steroid regimen with PET/CT to assess metabolic response in pancreas, which in itself is a surrogate indicator of autoimmune phenomenon.[35] Though an incidental finding in this case, AIP can be diagnosed on FDG PET/CT in cases where clinical and morphological imaging features are overlapping with other pancreatic conditions.
Source of Support: Nil
Conflict of Interest: None declared.
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