Asymptomatic Hyperamylasemia in Stevens-Johnson Syndrome Is Associated with Intestinal Barrier Dysfunction.

METHODS: A retrospective study on SJS patients was conducted at a tertiary medical center. All patients diagnosed as SJS, with available serum amylase index, were included. Clinical data of all subjects were retrospectively collected and analyzed. Colonic mucosal biopsies were obtained to measure tight junction protein expression. RESULTS: A total of nine patients were included in the present study for study analysis. The average serum amylase of the study cohort was 228.78 ± 204.18 U/L. Among which, five patients had a positive fecal occult blood test (FOBT). Colonic mucosal biopsies were obtained and stained with occludin and zonula occludens-1 (ZO-1). The expression of occludin and ZO-1 was significantly downregulated in SJS patients (p < 0.01), which was indicative of intestinal barrier dysfunction. CONCLUSION: Hyperamylasemia often extends beyond pancreatic diseases. Clinical awareness of asymptomatic hyperamylasemia secondary to other systemic diseases can help avoid unnecessary overexamination and overtreatment.

¿Macroamilasemia o hiperamilasemia en un paciente con dolor abdominal? / Macroamylasaemia or hyperamylasaemia in a patient with abdominal pain?

La macroamilasemia debe sospecharse cuando un paciente presenta una concentración catalítica elevada de la α-amilasa plasmática, sin la presencia de datos clínicos que confirmen la existencia de una enfermedad pancreática o parotídea. La macroamilasemia, en la mayoría de los casos, es un complejo formado por la α-amilasa y las inmunoglobulinas plasmáticas que causa una hiperamilasemia con la amilasuria normal o baja. El diagnóstico diferencial con las otras causas de hiperamilasemia es imprescindible para evitar las exploraciones complementarias y los tratamientos invasivos innecesarios. Se presenta el caso de un varón de 53 años con dolor abdominal e hiperamilasemia, diagnosticado inicialmente de pancreatitis aguda. Macroamylasaemia should be suspected when a patient has a high catalytic concentration of plasma α-amylase in the absence of clinical data confirming the existence of a pancreatic or parotid disease (AU)

In most cases, macroamylasaemia is a complex of α-amylase bound to plasma immunoglobulins that cause hyperamylasaemia with low or normal urine amylase. The differential diagnosis with other causes of hyperamylasaemia is essential to avoid unnecessary additional examinations and invasive treatments. The case is presented of a 53 year-old male with abdominal pain and a high plasma amylase, initially diagnosed with acute pancreatitis (AU)

ECTOPIC ACTH SECRETION WITH CONCOMITANT HYPERAMYLASEMIA IN A PATIENT WITH SMALL CELL LUNG CARCINOMA: CASE REPORT.

Histologically confirmed small cell lung cancer associated with Cushing's syndrome and elevated amylase is rarely described in the literature. We present a case of a 63-year-old patient admitted to cardiology department due to shortness of breath, exhaustion, palpitations and nausea. Elevated values of troponin and electrocardiography suggested that he could have acute coronary syndrome. According to the radiologist's opinion, plane lung radiography was normal. Elevated level of amylase was found in both serum (3802 U/L, normal range 28-100) and urine (12012 U/L, normal range 0-450 U/L), as well as elevated sodium (156 mmol/L, normal range 137-147 mmol/L), hyperglycemia (12 mmol/L, normal range 3.8-6.1 mmol/L) and lowered serum potassium (1.7 mmol/L, normal range 3.5-5.3 mmol/L). Computerized tomography (CT) of the abdomen revealed a tumor of the left adrenal gland and enlargement of the right adrenal gland with normal structure of the pancreas. During hospitalization, the patient had blood while coughing and CT scan of the lungs showed a tumor 48x38x51 mm in size localized in the laterobasal segment of the left lung with mediastinal lymphadenopathy. He also had bilateral pleural effusions with signs of pulmonary embolism, which explained elevated troponin values. Biopsy confirmed microcellular lung carcinoma and tumor cells were diffusely positive for TTF-1 and focally for CK7, expressing markers of neuroendocrine differentiation (chromogranin +++, synaptophysin +++, NSE ++). Since neuroendocrine tumor was confirmed and the patient had low potassium and high glucose, hypercortisolism was suspected. High morning cortisol (1784 mmol/L, normal range 171-536) and unsuppressed ACTH (214 pg/L, < 60), as well as a high level of chromogranin (1339 µg/L, < 65) were determined. During hospital stay, the patient developed heart and respiratory failure and died in the second week of hospitalization.

Frequency and risk factors in the post-ERCP pancreatitis in a tertiary care centre.

OBJECTIVE: To evaluate the frequency and associated factors in the post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis. STUDY DESIGN: Cross-sectional analytical study. PLACE AND DURATION OF STUDY: Endoscopy Suite of Surgical Unit IV, Civil Hospital, Karachi, from December 2009 to November 2010. METHODOLOGY: Patients undergoing ERCP were included. Patients who had presented with pancreatitis or raised amylase levels before procedure or patients who had previous history of surgery on the biliary or pancreatic systems were excluded from the study. Pearson chi-square and Fisher's exact test were used for qualitative data and t-test for quantitative data. Significance was taken as p ² 0.05. Odds ratio was calculated for the qualitative data using 95% confidence interval. RESULTS: Age of the study population ranged from 9 to 90 years (mean age 46.5 ± 14.94 years, median 45 years). Male to female ratio was 1:1.87. Pancreatitis was seen in 18 patients (3.6%), mild in 15 (3%), moderate in one (0.2%) and severe in 2 (0.4%). Mean amylase level at 4 hours and 24 hours was 280.93 ± 539.13 and 168.83 ± 338.34 respectively. Pancreatitis was seen in 15/326 (4.6%) females and 3/174 (1.72%) males. Statistically significant increased risk for pancreatitis was seen in difficult cannulation (9.8%, p = 0.006), prolonged cannulation time (7.6 minute, p = 0.002), pancreatic duct cannulation (13.7%, p = 0.001) and pancreatic duct contrast injection (13.4%, p < 0.001). CONCLUSION: The frequency of post-ERCP pancreatitis was 3.6%. Difficult cannulation, pancreatic duct cannulation, pancreatic duct contrast injection and balloon sphincteroplasty were associated with higher frequency of post-ERCP pancreatitis. Reuse of ERCP accessories poses no additional risk to the frequency of pancreatitis.

Macroamilasemia en pediatría / Macroamylasemia in paediatrics

No disponible

Incidence of postoperative pancreatic fistula and hyperamylasemia after cytoreductive surgery and hyperthermic intraperitoneal chemotherapy.

INTRODUCTION: The purpose of this study was to analyze the postoperative pancreatic morbidity of cytoreductive surgery (CRS) and hyperthermic intraperitoneal chemotherapy (HIPEC) in the treatment of peritoneal surface malignancies (PSM). PATIENTS AND METHODS: Two hundred and sixty five patients (87M/178F) with PSM underwent 270 consecutive procedures. The mean age was 52 years (range: 22-79 years). CRS was performed using peritonectomy procedures. HIPEC through the closed abdomen technique was conducted using cisplatin (CDDP 25 mg/m2/L of perfusate)+mitomycin C (MMC 3.3 mg/m2/L of perfusate) or CDDP (43 mg/L of perfusate)+doxorubicin (Dx 15.25 mg/L of perfusate), at 42.5 degrees C. Diagnosis and classification of postoperative pancreatic fistula (POPF) were performed according to the international study group on pancreatic fistula criteria. Serum amylase alterations were graded according to the National Cancer Institute (NCI) common terminology criteria for adverse events (CTCAE) v3. RESULTS: POPF was observed in 13 (4.8%) cases. Three cases were classified as major (grade C). Two cases presented postoperative pancreatitis. G3-4 alteration of amylase was observed in 12.3% of the cases. Performing splenectomy and CDDP dosage for HIPEC >240 mg were proven to be independent risk factors for both G3-4 hyperamylasemia and POPF. CONCLUSIONS: CRS+HIPEC presented an acceptable rate of pancreatic morbidity which did not contribute to the mortality related to the procedure. Most of the POPF were mild and/or easily controlled by conservative measures. Although not specific a normal amylasemia could be a useful marker of pancreatic integrity after CRS+HIPEC.

Pro- and anti-inflammatory response of acinar cells during acute pancreatitis. Effect of N-acetyl cysteine.

We investigate the ability of acinar cells to produce tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) at different stages of acute pancreatitis (AP). Since oxidative stress is involved in the inflammatory response, the effect of N-acetyl cysteine (NAC) has also been evaluated. AP was induced in rats by bile-pancreatic duct obstruction (BPDO). NAC (50 mg/kg) was administered 1h before and 1h after BPDO. Acinar cells were incubated for 4 h at 37 degrees C in 5% CO2 atmosphere in absence and presence of 24-h BPDO-PAAF (20%, v/v) as stimulant agent. Acinar production of TNF-alpha and IL-10 was analysed by flow cytometry. Plasma amylase activity and histological studies of the pancreas indicated the severity of AP. PAAF significantly stimulated the acinar production of TNF-alpha and IL-10 in control rats. TNF-alpha production was also significantly stimulated in acinar cells of rats with AP, although a decrease in the pro-inflammatory response was found from 6 h after BPDO onwards. However, acinar cells failed to produce IL-10 from 3 h after BPDO. The protective effect of NAC treatment against oxidative cell damage reduced the pancreatic injury and maintained and enhanced the ability of acinar cells to produce IL-10 at early AP stages. As long as acinar cells were not severely damaged in the course of AP, greater ability to produce cytokines in response to PAAF was found in those with higher forward scatter (R2 cells). We suggest that the capability of acinar cells to maintain an appropriate balance between the production of pro- and anti-inflammatory mediators could contribute to determine the degree of severity of AP.

Clinical significance of chronic hyperamylasemia.

A longitudinal study of patients with persistent hyperamylasemia was carried out to evaluate the clinical significance of this condition. Twenty-five outpatients were studied by means of serum amylase, isoamylase (wheat germ-inhibition method), and lipase determination; macroamylase detection; and abdominal ultrasonography over a one-year period. Cellulose acetate electrophoresis was carried out to validate the wheat germ-inhibition tests; the results of the two assays were closely correlated, except in three patients with macroamylasemia. At the time of the study, none of the patients had evident signs or symptoms of pancreatic disease. At initial evaluation, wheat germ test demonstrated an elevation of only salivary isoamylase in 16 patients, both pancreatic and salivary isoenzyme in two, and only pancreatic isoamylase in six patients (three with macroamylasemia). Normal salivary and pancreatic isoenzymes were found in one with predominantly pancreatic isoamylase. At the 12-month follow-up, hyperamylasemia had disappeared in six cases and salivary isoamylase elevation in three; pancreatic isoamylase remained abnormally high in all eight patients in whom it was elevated at initial evaluation, and lipase was abnormally high in three patients with elevated pancreatic isoamylase. Of the five patients with true pancreatic hyperamylasemia, one had a juxtapapillary duodenal diverticulum, one showed a slight ultrasound alteration of the pancreas, and one had a past history of acute pancreatitis. In our study, most cases of chronic hyperamylasemia were of nonpancreatic origin. In the patients with elevated pancreatic isoamylase, there was no clinical evidence of pancreatic damage, although a subclinical pancreatic involvement could not be excluded in some.