Mild acute pancreatitis

A 36-year-old man took fluvastatin 40 mg/day for 3 months and developed mild acute pancreatitis, which settled with medical treatment. Other causes were ruled out. Some months later, he started taking fluvastatin again and had a recurrence of pancreatitis within a few days. 

Mild acute pancreatitis Acute pancreatitis associated with minimal organ dysfunction and an uneventful recovery it lacks the described features of severe acute pancreatitis. 

A4. Amano, Y., Oishi, T., Takahashi, M., and Kumazaki, T., Nonenhanced magnetic resonance imaging of mild acute pancreatitis. Abdom. Imaging 26, 59-63 (2001). 

McQave SA, Greene LM, Snider HL, et al. Comparison of the safety of early enteral vs parenteral nutrition in mild acute pancreatitis. JPEN J Parenter Enter Nutr 1996 21 14-20. 

Dibutyltin dichloride induced acute pancreatitis and bile duct lesions in rats, depending on dose (6 and 8 mg/kg body weight intravenously) and time (1-24 weeks) (Merkord Hennighausen, 1989 Merkord et al., 1997, 1999 Sparmann et al., 2001). The lesions in the pancreas developed into a pancreatic fibrosis, and the lesions in the liver into liver cirrhosis. A single intravenous administration of dibutyltin dichloride at 4 mg/kg body weight induced a mild interstitial pancreatitis after 2 days (Merkord et al., 2001). Repeated administration of dibutyltin dichloride (4 mg/kg body weight intravenously) to rats at intervals of 3 weeks induced acute interstitial pancreatitis and, after 9-12 weeks, a pancreatic fibrosis and liver lesions (intrahepatic bile duct hyperplasia) (Merkord et al, 2001). 

Various conditions such as perforated peptic ulcer, cholecystitis, common bile duct and intestinal obstruction, trauma to the abdomen inducing pancreatitis and ruptured ectopic pregnancy may cause an elevated serum amylase but the levels are usually not as high as those found in acute pancreatitis. Mumps and bacterial parotitis, which block the secretion of salivary amylase are associated with mild elevations of serum amylase. 

Empiric antibiotics are not necessary if the patient has mild disease or a non-infectious etiology of acute pancreatitis. Antibiotics have not been shown to prevent the formation of pancreatic abscess or necrosis when given early in the course of acute pancreatitis. 

Given the severity of acute pancreatitis, patients are monitored closely in the intensive care setting. Patients with mild disease can be managed more conservatively with observation and supportive care. Critically ill patients may require surgery and aggressive life support measures.16,28... 

The arylpropionic acid derivatives are useful for the treatment of rheumatoid arthritis and osteoarthritis, for reduction of mild to moderate pain and fever, and for pain associated with dysmenorrhea. Side effects of the drugs are similar to but less severe than those described for the salicylates. Those who are sensitive to salicylates also may be sensitive to and have adverse reactions when taking ibuprofen and related drugs. Acute hypersensitivity to ibuprofen has been reported in patients with lupus. The hypersensitivity reaction to sulindac can be fatal. The use of sulindac has also been linked to cases of acute pancreatitis. The use of dimethylsulfoxide (DMSO) topically in combination with sulindac has been reported to induce severe neuropathies. The concurrent use of ibuprofen with aspirin reduces the antiinflammatory effects of both drugs. Ibuprofen is contraindicated in patients with aspirin sensitivity leading to bronchiolar constriction and in patients with an-gioedema. As with all NSAIDs, renal and liver function should be normal for adequate clearance of the drugs. 

Fire-toxin, as a pathological product as well as a pathogenic factor, can accumulate in the intestines. Fire-toxin should be eliminated as soon as possible, especially before long-term accumulation and when the blood is not strongly disturbed, in order to prevent further development of disease, such as in chronic mild infections of the intestines, or at the primary stage of acute appendicitis, acute pancreatitis, acute cholecystitis, hepatitis and ulcer perforation and inflammation. 

A 33-year-old woman developed acute pancreatitis together with mild cholestatic hepatitis and erythema nodosum 1 month after starting carbimazole for Graves disease rechallenge with a single dose of carbimazole (10 mg) 7 days after initial recovery led to a further episode of acute pancreatitis, from which she recovered (54). 

According to the authors, statin-induced acute pancreatitis can occur on the first day of therapy or after several months. It is generally mild and runs a benign course no deaths have been reported. Its frequency is unknown but it is probably rare. 

In a randomized, multicenter study in 94 patients, mesalazine 4 g/day for 12 weeks in a microgranular formulation was as effective as a standard dose of a glucocorticoid (6-methylpredisolone 40 mg/day) in mild to moderate Crohn s ileitis (Crohn s Disease Activity Index 180-350) (9). The group treated with methylpredisolone had a higher number of adverse events than those given mesalazine. The only adverse effect related to mesalazine was acute pancreatitis, which resolved on withdrawal. 

A 53-year-old woman developed severe central abdominal and epigastric pain 90 minutes after taking codeine for migraine. Pancreatic amylase, lipase, and hver function tests were mildly raised. Abdominal ultrasound was consistent with acute pancreatitis. 

Acute pancreatitis—Acute inflammation of the pancreas which may be mild with minimal or no organ dysfunction or severe with organ failure and local complications. 

Gastrointestinal Mucositis and diarrhea are common and generally mild at standard doses. Nausea and vomiting are also frequent and affect 25% of patients. Other less common adverse reactions include ileus, anal inflammation and ulceration, esophageal ulceration, and gastrointestinal hemorrhage [12 ,20 ]. Acute pancreatitis is rare and usually self-limiting [21 ]. 

The lactic acidosis seen with these drugs has ranged from mild and chronic to acute, severe, and fatal [95-106]. The acidosis generally develops after several months of therapy. Patients with NRTl-associated lactic acidosis present with symptoms of nausea, vomiting and abdominal pain. Other features often include elevated liver enzymes, hepatic steatosis, pancreatitis and elevated creatinine kinase with evidence of a myopathy, and liver failure. The lactic acidosis may persist for many weeks despite discontinuation of the NRTl [95-106]. NRTl-related mitochondrial toxicity may also present with rhabdomyolysis and acute kidney failure [110]. Mortality related to NRTl-induced acute lactic acidosis is high, in the range of 50% to 100%, despite drug discontinuation. 

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