Two cases of acute pancreatitis with leptospirosis are reported in this article. Case 1: A 68-year-old woman, presented initially with abdominal pain, nausea, vomiting, and jaundice. She was in poor general condition, and had acute abdominal signs and symptoms on physical examination. Emergency laparotomy was performed, acute pancreatitis and leptospirosis were diagnosed on the basis of surgical findings and serological tests. The patient died on postoperative d 6. Case 2: A 62-year-old man, presented with fever, jaundice, nausea, vomiting, and malaise. Acute pancreatitis associated with leptospirosis was diagnosed, according to abdominal CT scanning and serological tests. The patient recovered fully with antibiotic treatment and nutritional support within 19 d.

Leptospirosis is a spirochetal bacterial infection and causes clinical illness in animals and humans. This zoonosis is common in some other parts of the world but rather rare in Turkey[1,2]. This disease is predominantly seen in farmers, trappers, veterinarians, and rice-field workers. Leptospirosis mainly affects liver and kidney. Rarely, other organs such as lung, heart, gallbladder, brain, and ophthalmic tissues are involved, mainly due to vasculitis[3,4]. Hyperamylasemia can be present in leptospirosis infection due to renal impairment[5-7]. Therefore, the diagnosis of acute pancreatitis is controversial in this disease.

Pancreatitis is a rare complication of leptospirosis and only a few cases have been reported in literature[1,5,8,9]. We report two cases here.

Leptospirosis is a spirochetal zoonosis that causes clinical illness in humans as well as in animals. The source of infection in humans is usually either direct or indirect contact with the urine of infected animals. These bacteria infect humans by entering through abraded skin, mucous membrane, conjunctivae. Direct transmission between humans is rare[3,4]. Leptospirosis is a common disease in rice-field workers due to prevalence of wild rats[4,8]. Both of our patients were from rural area of the middle Black Sea region of Turkey and have worked in rice fields. Rice field with stagnant water and humid condition is an ideal environment for leptospira.

Leptospirosis is characterized by the development of vasculitis, endothelial damage, and inflammatory infiltration. This disease mostly affects tissues of the liver and kidney. Other tissues such as the pancreas can be affected due to vasculitis[4].

This disease occurs as two clinically recognizable syndromes: the anicteric leptospirosis (80-90% of all cases) and the remainder icteric leptospirosis[3,4]. Icteric leptospirosis is known as Weil's disease, which is characterized by hemorrhage, renal failure, and jaundice. Icteric leptospirosis is a much more severe disease than anicteric form. The clinical course is often rapidly progressing. Our cases seemed to be icteric leptospirosis. Serological tests confirmed on blood samples as L icterohemorrhagica and L samaranga Patoc. First of these is responsible for icteric form of the disease. L samaranga Patoc sero-type is not the cause of Weil's disease but cross-reaction is possible between the serotypes of leptospirosis.

Thrombocytopenia is a common finding in leptospirosis, occurring in 40-85% of this disease. But the exact reason for thrombocytopenia is unknown. Vasculitis, increased peripheral destruction and decreased thrombocyte production have been considered as potential causes of thromboc-ytopenia[4,10]. Thrombocytopenia was also present in the two cases reported here which were remedied by our treatment.

Oliguric and non-oliguric acute renal failure may be observed in icteric leptospirosis[7], as also seen in our cases. It was reported that oliguria was a significant predictor of death in leptospirosis[4]. Urine output was normal in case 1 but case 2 was oliguric. Renal insult was treated with intravenous fluid replacement and other supportive treatment including antibiotic and hemodialysis in case 2.

Jaundice occurring in leptospirosis is not commonly associated with hepatocellular necrosis and impaired liver function. There are moderate rises in transaminase levels, and minor elevation of alkaline phosphatase level usually occurs[3,4]. Hepatic dysfunction occurs but resolves, and it is rarely the cause of death. The serum bilirubin level is usually <20 mg/dL but can be as high as 60-80 mg/dL. The bilirubin level of case 2 was close to this value (48 mg/dL). In case 1, transaminase levels were very high (more than 2 000 U/dL). The elevation of transaminases that is more than threefold of the normal value is not usual. Some sporadic cases with very high transaminase level were reported in the medical literature[11]. Furthermore, hepatocyte degener-ation and liver cell necrosis have been reported in biliary pancreatitis[12,13]. So, elevated transaminases levels as high as that in case I may be seen in leptospirotic hepatitis. Pancreatic and bile tree involvement can be additional factors for liver cell necrosis. Acute cholecystitis was pathologically confirmed and leptospires were seen in bile in case 1. Therefore, we believe that hepatobiliary and pancreatic involvement could be possible in this case.

For the diagnosis of acute pancreatitis, a simultaneous determination of both amylase and lipase is recommended for the evaluation of patient with abdominal pain. The serum amylase test is available in nearly all laboratories and at all hours. Elevation of lipase level with serum amylase is important for the diagnosis of acute pancreatitis. Elevation of pancreatic izoamylase level also supports the diagnosis[14]. Hypera-mylasemia also can be seen in leptospirosis due to renal function alterations or other unknown reasons[5,6]. The serum amylase and lipase levels were elevated more than threefold of normal level in both cases. Pancreatic izoamylase level was also elevated at diagnostic level in case 2.

CT scan is a gold standard in diagnosis of acute pancreatitis, as shown by many authors who use it. This diagnostic test has 100% specificity and over 90% sensitivity for this disease[15-17]. We also routinely use CT for both diagnosis and follow-up of the treatment as in case 2. Because abdominal CT scan was not available in the emergency condition in our hospital, we could not use it in case 1. However, the pathologic findings of acute pancreatitis were clearly observed at laparotomy in this case. So, there is no diagnostic dilemma for both of two presented cases.

The treatment of acute pancreatitis in leptospirosis includes antibiotic treatment against leptospira and supportive treatments for acute pancreatitis (including intravenous fluid resuscitation and nutrition). We preferred the nutritional support (parenterally or enterally but mostly enterally) in severe acute pancreatitis. This regime was successful in case 2. Case 1 also completely recovered after d 5 and she could feed orally. We believe that the reason of mortality was pulmonary embolism in case 1.

In conclusion, pancreatitis may be seen in leptospirosis infection. Leptospirosis should also be considered in the differential diagnosis of hyperamylasemia, pancreatitis, and obstructive jaundice in endemic areas. Early diagnosis and appropriate treatment is essential for life saving.