Alpha-fetoprotein producing carcinoma of the gallbladder associated with anomalous arrangement of the pancreaticobiliary ductal system--early detection through an attack of acute pancreatitis.

A 56-year-old female was admitted to our hospital with a diagnosis of acute pancreatitis. Ultrasonography revealed a hypoechoic tumor in the gallbladder. The serum alpha-fetoprotein (AFP) level was 971 ng/ml. After healing of the acute pancreatitis, the anomalous arrangement of the pancreaticobiliary ductal system (APDS) was demonstrated by ERCP with mild dilatation of the common bile duct. Within one month after admininon, AFP level reached 4390 ng/ml. On operation, a pedunculated tumor, 6.5 x 3 cm in size, was found in the gallbladder. Histological examination revealed a moderately differentiated adenocarcinoma and positive immunohistochemical staining of cancer cells for AFP. After absolutely curative (stage II) resection, normal serum AFP levels were recognized. This is the first report of an AFP-producing cancer of the gallbladder associated with APDS and it was detected as a result of an attack of acute pancreatitis.     

Recurrent cholangitis associated with biliary sludge and Phrygian cap anomaly diagnosed by magnetic resonance imaging and magnetic resonance cholangiopancreatography despite normal ultrasound and computed tomography

A 31-year-old woman presented with a one and half years' history of intermittent right upper quadrant (RUQ) pain, high fever and severely painful, warm and reddish swollen skin lesions on the fingers. Acute attack resolution occurred within 2 weeks after treatment with non-specific antibiotics. Low-grade fever (around 37.5 degrees C) and less painful swellings continued for 6 months after each attack. Abdominal ultrasound and computed tomography (CT) scans did not show any abnormality during the attacks. Biopsy of the skin lesions after the second attack revealed lymphocytic vasculitis. All laboratory studies including rheumatologic serology panel were normal. One month after the complete resolution of the second attack, the patient was observed to have high fever, the same skin lesions on the fingers as at the initial stage, nausea and marked abdominal pain in the RUQ. Routine laboratory studies including complete blood count, liver function tests and serum amylase and lipase levels were normal. An abdominal CT scan revealed a slight thickening of the gallbladder wall (3.9 mm). Two weeks later, abdominal magnetic resonance imaging (MRI) and magnetic resonance cholangiopancreatography (MRCP) were performed because of persistent abdominal pain. They revealed both biliary tract and pancreatic gland alterations consistent with past cholangitis and pancreatitis with coexisting Phrygian cap anomaly and biliary sludge on the neck of the gallbladder.     

Relapsed Acute Pancreatitis as the Initial Presentation of Pancreatic Cancer in a Young Man: A Case Report

In this report, we describe a 31-year-old man in whom acute pancreatitis was the initial feature of a subsequently diagnosed pancreatic adenocarcinoma with multiple metastases. He initially presented at our hospital with acute pancreatitis. Abdominal ultrasonography revealed a mildly dilated pancreatic duct and an enlarged pancreatic head. Although a follow-up abdominal ultrasonography revealed a progressively dilated pancreatic duct and a progressively enlarged pancreatic head, he refused further investigation and was lost to follow-up. Four months later, he returned to our hospital with relapsed acute pancreatitis. Obstructive jaundice was noted and drainage was performed. Because choledochoplasty with multiple balloon catheters was not fully effective, biliary tract bypass surgery was carried out. Intraoperative biopsy confirmed pancreatic adenocarcinoma with multiple metastases. The patient died of massive gastrointestinal bleeding a few weeks later. To our knowledge, this is the youngest case of pancreatic cancer with the uncommon initial presentation of acute pancreatitis reported in the literature. For a patient with acute pancreatitis, particularly recurrent episodes, but with no known risk factors for pancreatitis, a pancreatic neoplasm should be considered as a potential underlying cause, even in a young man.     

Polysplenia syndrome with congenital agenesis of dorsal pancreas presenting as acute pancreatitis and the role of endoscopic ultrasonography in its diagnosis

A 49-year-old female was admitted to our hospital for acute pancreatitis. The abdomen CT scan incidentally showed midline liver with hepatomegaly, centrally located gallbladder, pancreas truncation, right sided small bowel, left sided large bowel, interruption of the inferior vena cava with azygos continuation, preduodenal portal vein, and multiple spleens in the left upper quadrant. In MRCP, the head of pancreas was enlarged and short main pancreatic duct without accessory duct was showed. EUS revealed enlarged ventral pancreas with a main pancreatic duct of normal caliber, absence of the accessory pancreatic duct and the dorsal pancreas. She was diagnosed as polysplenia syndrome with agenesis of dorsal pancreas. It is a rare congenital anomaly frequently associated with various visceral anomalies including multiple spleens, impaired visceral lateralization, congenital heart diseases, gastrointestinal abnormalities and azygos continuation of the inferior vena cava. We report a case of polysplenia syndrome with agenesis of dorsal pancreas presenting acute pancreatitis.     

Recurrent cholangitis associated with biliary sludge and Phrygian cap anomaly diagnosed by magnetic resonance imaging and magnetic resonance cholangiopancreatography despite normal ultrasound and computed tomography

A 31-year-old woman presented with a one and half years’ history of intermittent right upper quadrant (RUQ) pain, high fever and severely painful, warm and reddish swollen skin lesions on the fingers. Acute attack resolution occurred within 2 weeks after treatment with non-specific antibiotics. Low-grade fever (around 37.5°C) and less painful swellings continued for 6 months after each attack. Abdominal ultrasound and computed tomography (CT) scans did not show any abnormality during the attacks. Biopsy of the skin lesions after the second attack revealed lymphocytic vasculitis. All laboratory studies including rheumatologic serology panel were normal. One month after the complete resolution of the second attack, the patient was observed to have high fever, the same skin lesions on the fingers as at the initial stage, nausea and marked abdominal pain in the RUQ. Routine laboratory studies including complete blood count, liver function tests and serum amylase and lipase levels were normal. An abdominal CT scan revealed a slight thickening of the gallbladder wall (3.9?mm). Two weeks later, abdominal magnetic resonance imaging (MRI) and magnetic resonance cholangiopancreatography (MRCP) were performed because of persistent abdominal pain. They revealed both biliary tract and pancreatic gland alterations consistent with past cholangitis and pancreatitis with coexisting Phrygian cap anomaly and biliary sludge on the neck of the gallbladder.     

Alpha-fetoprotein producing carcinoma of the gallbladder associated with anomalous arrangement of the pancreaticobiliary ductal system—Early detection through an attack of acute pancreatitis

A 56-year-old female was admitted to our hospital with a diagnosis of acute pancreatitis. Ultrasonography revealed a hypoechoic tumor in the gallbladder. The serum α-fetoprotein (AFP) level was 971 ng/ml. After healing of the acute pancreatitis, the anomalous arrangement of the pancreaticobiliary ductal system (APDS) was demonstrated by ERCP with mild dilatation of the common bile duct. Within one month after admininon, AFP level reached 4390 ng/ml. On operation, a pedunculated tumor, 6.5 × 3 cm in size, was found in the gallbladder. Histological examination revealed a moderately differentiated adenocarcinoma and positive immunohistochemical staining of cancer cells for AFP. After absolutely curative (stage II) resection, normal serum AFP levels were recognized. This is the first report of an AFP-producing cancer of the gallbladder associated with APDS and it was detected as a result of an attack of acute pancreatitis.     

A case of octreotide acetate-induced acute pancreatitis]

A 56-year-old man was admitted to our hospital in July 2000 because of epigastralgia and back pain with past history of repeated upper abdominal pain due to acute pancreatitis since 1995. Abdominal computed tomography on admission showed a swelling in the pancreas head and several large pancreatic pseudocysts. He was diagnosed as acute pancreatitis based on abdominal pain, elevated pancreatic enzymes and computed tomography finding, and given 50 microg octreotide subcutaneously for the treatment of pancreatic pseudocysts. Within 3 hours after octreotide injection, he complained of upper abdominal pain and had an elevated serum amylase level. Abdominal pain disappeared after cessation of octreotide injection and the patient was discharged free from abdominal pain. Octreotide might cause acute pancreatitis by inducing spasm of the sphincter of Oddi. Careful check-up of the patients might be needed during treatment with octreotide.     

Acute pancreatitis in acute viral hepatitis

AIM： To elucidate the frequency and characteristics of pancreatic involvement in the course of acute （nonfulminant） viral hepatitis. METHODS： We prospectively assessed the pancreatic involvement in patients with acute viral hepatitis who presented with severe abdomimanl pain. RESULTS： We studied 124 patients with acute viral hepatitis, of whom 24 presented with severe abdominal pain. Seven patients （5.65%） were diagnosed to have acute pancreatitis. All were young males. Five patients had pancreatitis in the first week and two in the fourth week after the onset of jaundice. The pancreatitis was mild and all had uneventful recovery from both pancreatitis and hepatitis on conservative treatment. The etiology of pancreatitis was hepatitis E virus in 4, hepatitis A virus in 2, and hepatitis B virus in 1 patient. One patient had biliary sludge along with HEV infection. The abdominal pain of remaining seventeen patients was attributed to stretching of Glisson＇s capsule. CONCLUSION： Acute pancreatitis occurs in 5.65% of patients with acute viral hepatitis, it is mild and recovers with conservative management.     

Acute Myeloid Leukemia Developing with Acute Pancreatitis Mimicking Autoimmune Pancreatitis

A 33-year-old man was admitted to our hospital for fever and abdominal pain. A blood analysis revealed pancytopenia and increased serum pancreatic enzymes with disseminated intravascular coagulation. A detailed examination revealed acute pancreatitis, with diffuse swelling of the pancreas and diffuse beaded dilatation of the main pancreatic duct, which mimicked autoimmune pancreatitis complicated by acute myeloid leukemia. Systemic cytotoxic chemotherapy led to the remission of leukemia and pancreatitis. We hypothesized that the etiology of acute pancreatitis was invasion of leukemia cells. Acute pancreatitis is rare as a symptom of leukemia; however, we should consider the possibility of leukemia during the differential diagnosis of acute pancreatitis.     

Functional recovery of the exocrine pancreas after acute pancreatitis

A tubeless pancreatic function test (BTP test) using N-benzoyl-l-tyrosyl-p-aminobenzoic acid was used to assess exocrine function from urinary recovery of p-aminobenzoic acid produced by hydrolysis of the peptide by chymotrypsin. Patients with acute pancreatitis were studied at various time intervals after the acute attack and compared with controls with abdominal pain that was not pancreatic in origin. The initial BTP test carried out in the convalescent period was abnormal in all of 30 patients with acute pancreatitis but normal in 10 patients with non-pancreatic abdominal pain and also in 8 patients who had recovered from an attack of acute pancreatitis 2-6 years previously. Results were improved or normal in 12 of 15 patients re-tested 1 year after the attack of pancreatitis, but 4 out of 6 still had abnormal results 2-6 months after the attack. The data suggest that an attack of acute pancreatitis may impair exocrine pancreatic function for several months.     

A case of acute pancreatitis complicating salmonella enteritis

Summary We report a case of acute pancreatitis complicating Salmonella enteritis. A 43-yr-old woman who was admitted to our department because of Salmonella enteritis developed clinical acute pancreatitis with laboratory and radiographic signs on the fourth hospital day. She was free from symptoms on the eighth hospital day, but her elevated serum amylase and lipase levels persisted for more than 2 mo. In this case, clinical acute pancreatitis was a complication of bacterial enteritis caused by Salmonella enteritidis, and it was characterized by onset a few days after the onset of enteritis and by sustained elevation of serum pancreatic enzyme levels.     

A case of colon obstruction developed as a complication of acute pancreatitis]

In acute pancreatitis, colonic complications such as mechanical obstruction, ischemic necrosis, hemorrhage, and fistula are rare but their outcomes are fatal. It is known that colonic obstruction in acute pancreatitis is more likely found in splenic flexure and transverse colon caused by severe inflammation of body and tail of pancreas leading to pressure necrosis. A 43-year-old man presented with abdominal distension lasting for 2 weeks. The patient had been admitted to our institution 6 weeks prior to the current admission, and the abdominal CT scan performed during the first admission revealed the pancreatic enlargement with peri-pancreatic fatty infiltration and fluid collection. At that time he was diagnosed as acute pancreatitis. The conservative management resulted in clinical improvement so that the patient was discharged. Upon the second admission, abdominal CT scan revealed multiple pseudocysts in the tail portion of pancreas with concominant wall thickening and narrowing of the proximal descending colon, and a dilatation of the bowel proximal to the splenic flexure. An obstruction of the descending colon as a complication of acute pancreatitis was suspected and the patient underwent left hemicolectomy. Abdominal distension was relieved after the operation and he was discharged on the 15th hospital days.     

A case of acute pancreatitis complicating Salmonella enteritis.

We report a case of acute pancreatitis complicating Salmonella enteritis. A 43-yr-old woman who was admitted to our department because of Salmonella enteritis developed clinical acute pancreatitis with laboratory and radiographic signs on the fourth hospital day. She was free from symptoms on the eighth hospital day, but her elevated serum amylase and lipase levels persisted for more than 2 m.o. In this case, clinical acute pancreatitis was a complication of bacterial enteritis caused by Salmonella enteritidis, and it was characterized by onset a few days after the onset of enteritis and by sustained elevation of serum pancreatic enzyme levels.     

How often are liver function tests normal in acute biliary pancreatitis?

BACKGROUND: The biochemical markers of a biliary etiology of acute pancreatitis (AP) include an ALT elevation of more than 3 times the upper range of normal (ULN) and a serum total bilirubin greater than 3 mg%. OBJECTIVES: To analyze the frequency of normal LFTs (Bilirubin, ALP, ALT, and AST) in patients with biliary AP. DESIGN: In this prospective study data collected for other ongoing studies on AP in the division of Gastroenterology in the last 20 years were analyzed. MATERIAL AND METHODS: Serum total Bilirubin, AST, ALT, and ALP levels in 269 patients with biliary AP out of 728 cases of AP of various etiologies were analyzed. The biliary etiology was confirmed on the basis of gallstones documented by transabdominal US or at surgery. RESULTS: We noted normal bilirubin, AST, ALT, and ALP levels in 14.5%, 12.3%, 11.2%, and 26.4% of cases of acute biliary pancreatitis respectively. When all the 4 laboratory tests were considered collectively, the incidence of normal values was 10.4%. We also noted an ALT elevation of <3 x ULN in 16.7% of cases of biliary AP and 43.5% of cases had a T. Bilirubin level of less than 3 mg %. CONCLUSIONS: Almost 15 to 20% of patients with biliary AP manifest with normal LFTs. The clinician should not exclude a biliary etiology solely on the basis of normal LFTs.     

New diagnostic criteria of acute pancreatitis

Practical guidelines for the diagnosis of acute pancreatitis are presented so that a rapid and adequate diagnosis can be made. When acute pancreatitis is suspected in patients with acute onset of abdominal pain and tenderness mainly in the upper abdomen, the diagnosis of acute pancreatitis is made on the basis of elevated levels of pancreatic enzymes in the blood and/or urine. Furthermore, other acute abdominal diseases are ruled out if local findings associated with pancreatitis are confirmed by diagnostic imaging. According to the diagnostic criteria established in Japan, patients who present with two of the following three manifestations are diagnosed as having acute pancreatitis: characteristic upper abdominal pain, elevated levels of pancreatic enzymes, and findings of ultrasonography (US), CT or MRI suggesting acute pancreatitis. Detection of elevated levels of blood pancreatic enzymes is crucial in the diagnosis of acute pancreatitis. Measurement of blood lipase is recommended, because it is reported to be superior to all other pancreatic enzymes in terms of sensitivity and specificity. For measurements of the blood amylase level widely used in Japan, it should be cautioned that, because of its low specificity, abnormal high values are also often obtained in diseases other than pancreatitis. The cut-off level of blood pancreatic enzymes for the diagnosis of acute pancreatitis is not able to be set because of lack of sufficient evidence and consensus to date. CT study is the most appropriate procedure to confirm image findings of acute pancreatitis. Elucidation of the etiology of acute pancreatitis should be continued after a diagnosis of acute pancreatitis. In the process of the etiologic elucidation of acute pancreatitis, judgment whether it is gallstone-induced or not is most urgent and crucial for deciding treatment policy including the assessment of whether endoscopic papillary treatment should be conducted or not. The diagnosis of gallstone-induced acute pancreatitis can be made by combining detection of elevated levels of bilirubin, transamylase (ALT, AST) and ALP detected by hematological examination and the visualization of gallstones by US.     

Atypical eating disorder masquerading as recurrent acute pancreatitis: the value of multiple pancreatic serological markers.

A 28-year-old woman with nausea, vomiting, and abdominal pain had been hospitalized elsewhere on 13 separate occasions over the year before this admission for similar episodes thought to be secondary to acute pancreatitis. She had undergone repeated work-ups including endoscopic retrograde cholangiopancreatography, computed tomographic scan, and exploratory laparotomy. There was a discrepancy between her unremarkable physical examination and extremely elevated amylase (3,210 U/L) which suggested nonpancreatic hyperamylasemia; normal serum pancreatic isoamylase, trypsinogen, and lipase confirmed this suspicion. The patient was noted to have self-induced vomiting in the hospital which she admitted was frequent behavior. her psychiatric disturbance was characterized as an atypical eating disorder. This case illustrates that hyperamylasemia in association with abdominal pain, nausea, and vomiting may not be secondary to pancreatitis and that use of a second serum marker (such as trypsinogen, lipase, or isoamylase) helps to establish a definitive diagnosis.     

Diagnostic evaluation of acute pancreatitis in two patients with hypertriglyceridemia

We present two diagnostically challenging cases of acute pancreatitis with hypertriglyceridemia accompanied with chylomicronemia caused with a deficiency of lipoprotein lipase and with the presence of type V hyperlipidemia. Both cases suffered from acute abdomen following the ingestion of fatty food and revealed the increase in parameters of inflammation without significant elevation of serum amylase levels. The imaging examination of ultrasonography could not detect significant findings of acute pancreatitis and a computer tomography scan eventually confirmed the findings of acute pancreatitis. Both cases responded to a low fat diet and administration of a cholecystokinin receptor antagonist, exhibiting a relief of abdominal symptoms. As in the present cases with acute abdomen following the ingestion of fatty food, the identification of serum hypertriglyceridemia and an abdominal computer tomography scan might be useful in establishing the diagnosis of acute pancreatitis and in developing the therapeutic regimen, when hypertriglyceridemia interferes with the evaluation of pancreatic enzyme activities and ultrasound examination provides poor pancreatic visualization.     

Emphysematous cholecystitis due to Salmonella derby

We present the case of a woman with diabetes mellitus who developed symptoms and signs consistent with gastroenteritis. After admission for hydration, the patient rapidly became critically ill and an abdominal catastrophe was suspected as the cause of her deterioration. Computed tomography of her abdomen was done and revealed gas in the lumen of the gallbladder consistent with emphysematous cholecystitis. She underwent emergent cholecystectomy, which revealed that the gallbladder had already ruptured. Blood cultures grew Salmonella derby. After a prolonged hospitalisation she eventually recovered and was discharged home. Emphysematous cholecystitis, thought to be a variant of acute cholecystitis, is a medical and surgical emergency. Diagnosis relies heavily on imaging findings by ultrasound or computed tomography since the clinical presentation is often non-specific. Cholecystectomy remains the treatment of choice in addition to broad spectrum antibiotics and other supportive measures.     

A case of splenic artery aneurysm simulating a pancreas tumor

A 46-year-old man was admitted to our hospital for further evaluation of a hypoechogenic mass in the pancreatic body. He had no history of hypertension, pancreatitis, abdominal trauma, or portal hypertension. He had no abdominal symptoms. A contrast-enhanced CT scan demonstrated a hypodense, round shaped mass. EUS and MRI also showed it to be a pancreatic mass. Because of the tumor size of more than 30mm and the possibility of malignancy, distal pancreatectomy was performed. Microscopic findings showed the mass was the dissection of the proximal splenic artery. The true lumen of the dissecting aneurysm was occluded and the false lumen developed fusiform dilatation. Moreover, microscopic findings revealed the rupture of the false lumen complicated by pseudoaneurysm. We finally diagnosed the lesion simulating a pancreatic tumor as the pseudoaneurysm of the splenic artery.     

Resectable gallbladder cancer presenting with acute pancreatitis caused by hemobilia

A 79-year-old female was transferred to our hospital because of suspicion that her acute pancreatitis was caused by stone impaction in the common bile duct (CBD). Laboratory examination showed aspartate aminotransferase, 1645 U/l; alanine aminotransferase, 476 U/l; amylase, 1365 U/l; and white blood cells, 10700/μl. Computed tomography (CT) showed an enhanced tumor in the neck of the gallbladder, an abnormal CBD filled with a high-density area, and localized swelling in the head of the pancreas. Magnetic resonance cholangiopancreatography also showed a low-intensity area in the CBD. Endoscopic retrograde cholangiopancreatography showed coagulated blood discharged from the papilla of Vater. The diagnosis was acute pancreatitis caused by impaction of coagulated blood from a gallbladder tumor. A curative operation was performed 10 days after endoscopic bile duct drainage. Gallbladder cancer (GBCa) has no special symptoms and is usually diagnosed at an advanced stage; however, hemobilia and acute pancreatitis are unusual as an initial presentation of GBCa.