Dear Bhupen!

I am pulmonologist. We treat patients with systemat.corticosteroids in exacerbation of obstructive lung diseases, sometimes in severe asthma bronchiale, sarcoidosis, SLE, and have a lot of patients with rheumat.disorders, who receip biolog.therapy, and we must exclude latent tuberculosis.In the last twenty years I didn't see pancreatitis purportedly caused by CS therapy. Paula

Thank you Sir (Dr Paula), my patient was on Azathoprine and corticosteroid and we are not getting other causes for high amylase and lipase. Once we received, I will let you know the details of CT abdomen other blood reports.

In Gastroenterology we commonly use azathioprine and corticosteroid for the treatment of inflammatory bowel diseases. Elevation of blood levels of pancreatic enzymes is a common event after azathioprine so that we check them in the course of treatmkent. Corticosteroid pancreatitis is less common, but I remener a case with a neurologic autoimmune disorders where amylase and lipse raise were constantly related to steroid administration.

Pancreatitis is a typical adverse event. If other causes of pancreatitis (i.e. biliary stones etc.) are excluded, the toxic effect of the thiopurine is highly probable (OR 5.1;95% CI 1.9–13.5 - Aliment Pharmacol Ther 2013; 38: 825–834).

In an IBD cohort of approximately 400 patients, 10 developed azathioprine-induced pancreatitis (Aliment Pharmacol There 2008; 28: 228–238), in a larger cohort of about 4000 patients the rate was 4%, too (Inflamm Bowel Dis. 2013; 19: 1404-1410). Azathioprine should be stopped and usually not reintroduced.

Azothiaprine induced pancreatitis is rare, and I'm not sure if corticosteroids actually cause it. I think its controversial

Thank you all, patient is improving clinically and all her parameters are settling down, but her sonography and CT abdomen were normal. Is it possible to have very high level of pancreatic enzymes with normal imaging?

Absolutely. Amylasemia is not the best test for acute pancreatitis/ Serum lipase levels are more specific

Thank you Sir @Laurence, but my patient had very high level of serum lipase (1632 ) and also serum lipase with normal imaging. Can we still considered it as acute pancreatitis?

If the US or CT scan are done very early at the begining of the pancreatitis, perhaps the changes of oedema and inflamation have not manifested yet.  If you repeat them 24 or 48 hours later there might be a change.

In my experience  AZA has a low incidence of pancreatitis in patients with autoimmune disease. Amilase plus lipase are needed  for the diagnosis of pancreatic. Only increase of amilase is due to other causes (familiar hyperamilasemia, damage of paratiroids of other glandula

the most specific blood test for pancreatitis is trypsin or trypsinogen.  Amylase and lipase can increase from many other acute or chronic conditions in the absence of pancreatitis.  There is a guideline: a lipase that is increased more than 3 times the upper limit for the lab, is consistent with pancreatitis, but proof comes from elevated trypsin levels.  

Non-invasive imaging can be misleading.  it is possible to have a negative ct/mri/us with/without contrast using dynamic sequencing on a pancreas protocol with mild disease.  Enzyme levels do not correlate all that well with disease severity by imaging in the individual patient. If the imaging is consistent with pancreatitis, it doesn't matter what the blood enzyme levels are. The opposite is not consistent correct however.

Aza= associated pancreatitis does occur but it is pretty uncommon. I have managed thousands of patients in GI, Hepatology, and Transplant over the past couple decades and the rate in that experience is less than 0.1% (based on ruling out all other causes, and re-challanging patients (before Cellcept came along).  Those that get pancreatitis on Aza will very likely have recurrant acute panreatitis (RAP) if the drug is restarted.  

If there was ever some reason to think Aza was essential to a patient who gets RAP on the drug,  there should be a comprehensive eval of the panc to rule out any other cause (insect bites, other meds, social (tobacco, alc, otc/rec drugs/herbals, snake handlers, etc), imaging, eus, +/-ercp, genetics) before restarting the drug..

My personal bias is that prednisone does not cause pancreatitis. At least in my experience and the larger institutions I have worked in,  there has been no case I am aware of that had RAP on steroids after ruling out all other causes as best possible for the time.

I agree with you

It is extremely rate to have pancreatitis

High amylase should not be interpreted as acute pancreatitis in absence of clinical symptoms.

Dear Sir @ Dr Hussien, Patient had clinical symptoms of acute pain abdomen, and after withdrawing Azathioprine and Steroid she responded well both clinically and with serum enzymes level, but her USG abdomen and CT abdomen were normal which was done on day 2 of admission.

In our 1989 study (The value of routine pancreatic iso-amylase measurements in the diagnosis of pancreatitis) we found that raised pancreatic iso-amylase (Pi) levels and the P3 index are useful in  the diagnosis and monitoring of acute pancreatitis (AP), reduced Pi is highly suggestive of CP, and the use of total alpha amylase levels alone can be misleading. We recommended that electrophoretic iso-amylase levels be done routinely in cases of suspected pancreatitis.

There are some criteria to establish connection between drug and AP. I agree that without clinical picture, and with normal CT imaging she should be fine. However there is no time to check if reintroducing the drug can re-induce pancreatitis. It is the case of one patient that we had and published (unfortunately in Romanian) that developed severe acute pancreatitis after unique dose of prednison. 

Only electrophoretic isoamylases with the P3 Index provide a definitive non-invasive measure of acute pancreatitis.

AZA may be the cause of acute pancreatitis, but it is not very common. The mild cours of disease is the most common after AZA.

Despite previous reports, GKS are not likely to be the cause of drug-induced acute pancreatitis (casuistry).