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Massimo Raimondo

Publications and source records attributed to Massimo Raimondo.

At least 19 recordsLinked to original sources
PubMed2006

Glucagon for the relief of esophageal food impaction does it really work?

We sought to evaluate our experience with glucagon used in the emergency department setting to relieve esophageal food impaction (EFI). We reviewed the records of patients with food impaction who received glucagon between January 1998 and May 2003 and recorded patient demographics, medical history, symptoms following glucagon administration, and endoscopic findings. There were 92 episodes of food impaction in 85 patients. Thirty-three percent of the episodes resulted in resolution of symptoms following a dose of glucagon. Sixty-seven percent had symptoms of food impaction after glucagon and underwent upper endoscopy in the emergency room. Only previous solid food dysphagia was positively associated with response to glucagon. Patients who received glucagon plus a benzodiazepine were more likely to have resolution of the EFI. In our experience, glucagon appears to relieve food impaction in one third of patients treated. This result is comparable to previously published data examining glucagon and placebo. The lack of advantage over placebo questions the practice of glucagon administration for EFI.

Adolescent↗
PubMed2006

Do cytokine concentrations in pancreatic juice predict the presence of pancreatic diseases?

BACKGROUND & AIMS: Cytokine concentration in pancreatic juice of patients with pancreatic disease is unknown. Secretin stimulation allows endoscopic collection of pancreatic juice secreted into the duodenum. We aimed to evaluate the cytokine concentrations in pancreatic juice of patients with abdominal pain to discriminate presence from absence of pancreatic disease. METHODS: From January 2003-December 2004, consecutive patients with abdominal pain compatible with pancreatic origin were enrolled. Patients underwent upper endoscopy. Intravenous secretin (0.2 mug/kg) was given immediately before scope intubation. Pancreatic juice collected from the duodenum was immediately snap-frozen in liquid nitrogen until assays were performed. Pancreatic juice levels of interleukin-8, interleukin-6, intercellular adhesion molecule 1, and transforming growth factor-beta 1 were measured by modified enzyme-linked immunosorbent assays. The final diagnosis was made by the primary gastroenterologist on the basis of medical history; laboratory, endoscopic, and imaging studies; and clinical follow-up. Fisher exact test and Kruskal-Wallis rank sum test were used for statistical analysis. RESULTS: Of 130 patients screened, 118 met the inclusion criteria. Multivariate analysis revealed that only interleukin-8 was able to discriminate between normal pancreas and chronic pancreatitis (P = .011), pancreatic cancer (P = .044), and the presence of pancreatic diseases (P = .007). Individual cytokine concentrations were not significantly different in chronic pancreatitis compared with pancreatic cancer. CONCLUSIONS: Cytokine levels can be measured in pancreatic juice obtained from the duodenum without direct cannulation of the pancreatic duct. Interleukin-8 concentration in pancreatic juice can be used to discriminate between normal pancreas and patients with pancreatic disease. This is a relatively simple and noninvasive method to aid in the diagnosis of pancreatic diseases.

Abdominal Pain↗
PubMed2006

Endoscopy-based pancreatic function tests.

Direct pancreatic function tests have been the mainstay for the diagnosis of pancreatic exocrine insufficiency. Due to their cumbersome nature and limited availability there is a continuous search for a rapid and inexpensive test of pancreatic function. Endoscopic approaches to evaluate pancreatic function have been assessed. This article critically reviews the current evidence related to this novel approach, outlining some elements for further refinement.

Adult↗
PubMed2005

Is zinc concentration in pancreatic fluid a marker for pancreatic diseases?

OBJECTIVES: An imbalance of free radicals and scavenging processes has been implicated in the pathogenesis of pancreatic tissue injury. Gradual decreases in antioxidant enzyme expression in pancreatic cells from normal pancreas to chronic pancreatitis to pancreatic cancer have been reported. Zinc is one of the components of antioxidant enzymes and may play a role in the pathogenesis of pancreatic diseases. A recent report showed a significant decrease in pancreatic zinc output in patients with chronic pancreatitis and proposed that zinc output can be used as an alternative to enzyme output for the diagnosis. We aimed to determine the zinc concentration in pancreatic fluid of patients with chronic pancreatitis and pancreatic cancer compared to normal pancreas. PATIENTS: Seventy-five consecutive patients were prospectively evaluated. Chronic pancreatitis was diagnosed in 20 patients by ERCP (n=16) and histology (n=4). Pancreatic cancer was diagnosed in 17 patients by cytology from EUS-FNA (n=12) or surgical pathology (n=5). Thirty-eight patients were confirmed to have normal pancreas. INTERVENTIONS: Patients underwent esophagogastroduodenoscopy following intravenous secretin injection (0.2 microg/kg). Pancreatic fluid collected for 10 minutes was immediately frozen at -80 degrees C and stored until the assay was performed. MAIN OUTCOME MEASURE: Zinc concentrations were determined by inductively coupled plasma optical emission spectroscopy. RESULTS: Among the three groups, patients with pancreatic cancer were significant older (P<0.001) with a higher prevalence of diabetes mellitus (P=0.002). Gender distribution (P=0.098), body mass index (P=0.925), and history of alcohol use (P=0.997) were similar among groups. Zinc concentrations in pancreatic fluid were not significantly different among groups (P=0.129). CONCLUSIONS: Zinc concentration in pancreatic fluid was comparable in patients with chronic pancreatitis and pancreatic cancer compared to normal pancreas. Zinc concentration in pancreatic fluid collected by our 10-minute endoscopic method cannot reliably be used for the diagnosis of chronic pancreatitis and/or pancreatic cancer.

Acute Disease↗
PubMed2004

Inflammatory myofibroblastic tumor presenting as a pancreatic mass: a case report and review of the literature.

CONTEXT: Inflammatory myofibroblastic tumor is a distinctive lesion of unknown etiology. It has generally been considered a rare benign pseudosarcomatous lesion of admixed inflammatory infiltrates with myofibroblastic spindle cells. Although original case descriptions focused on the pulmonary system, it is now recognized that virtually any anatomic location can be involved. However, an inflammatory myofibroblastic tumor located in the pancreas is rare. CASE REPORT: We report a case of an asymptomatic 70-year-old Caucasian man with a 3.8 cm inflammatory myofibroblastic tumor located in the tail of the pancreas which was discovered incidentally on a computed tomography scan of the abdomen. Endoscopic ultrasonography with fine needle aspiration was negative for malignancy. However, because of worrisome radiographic features, a distal pancreatectomy with splenectomy was performed. The pathology revealed an inflammatory myofibroblastic tumor with focal extension into the peripancreatic soft tissues, but with negative surgical margins. The patient has been followed for 10 months without evidence of recurrence. CONCLUSIONS: To date, there have been only 25 cases of inflammatory myofibroblastic tumor located in the pancreas reported in the English language scientific literature. Even with multimodal pre-surgical investigation, it can be extremely difficult to differentiate inflammatory myofibroblastic tumor from pancreatic malignancies. Most cases require surgical exploration and complete resection to obtain an accurate diagnosis. A review of published case reports is also presented.

Aged↗
PubMed2004

Photodynamic therapy and endoscopic mucosal resection for Barrett's dysplasia and early esophageal adenocarcinoma.

BACKGROUND: Endoscopic mucosal resection (EMR) and endoscopic ablation with porfimer sodium photodynamic therapy (PDT) have recently been combined to improve the accuracy of histologic staging and remove superficial carcinomas. MATERIALS AND METHODS: All patients with Barrett's esophagus and high-grade dysplasia were evaluated with computed tomography and endosonography. Patients with nodular or irregular folds underwent EMR followed by PDT. RESULTS: In three patients, endoscopic mucosal resection upstaged the diagnosis to mucosal adenocarcinoma (T1N0M0). PDT successfully ablated the remaining glandular mucosa. Complications were limited to transient chest discomfort and odynophagia. CONCLUSIONS: The use of EMR resection in Barrett's high-grade dysplasia patients with mucosal irregularities resulted in histologic upstaging to mucosal adenocarcinoma, requiring higher laser light doses for PDT. PDT after EMR appears to be safe and effective for the complete elimination of Barrett's mucosal adenocarcinoma. EMR should be strongly considered for Barrett's dysplasia patients being evaluated for endoscopic ablation therapy.

Adenocarcinoma↗
PubMed2004

Diagnosis of early chronic pancreatitis by endoscopic ultrasound. Are we there yet?

The diagnosis of chronic pancreatitis at an early stage is a clinical challenge. A major limitation is the inability of clinicians to obtain a tissue or histological sample to confirm the clinical diagnosis. Currently available imaging modalities have limited sensitivity or specificity for diagnosing early chronic pancreatitis. Endoscopic ultrasonography (EUS), introduced in the early 1980's, was first developed to image the pancreas. It overcame many of the limitations (abdominal gas and fat) of transabdominal ultrasonography when evaluating patients for possible pancreatic diseases. To date, EUS represents the most promising imaging modality for diagnosing chronic pancreatitis. Contrary to endoscopic retrograde pancreatography (ERCP), EUS has a very low risk of complications and can detect abnormalities suggestive of chronic pancreatitis in the pancreatic parenchyma and ductal system which are not visible on any other imaging modality. The minimal changes in echotexture are difficult to interpret because there is no reliable gold standard confirmatory test. There is now some evidence in the literature suggesting that these early changes detected by EUS correlate with the histological changes of chronic pancreatitis and may predict progression to more advanced disease. The EUS diagnosis of chronic pancreatitis relies on quantitative (more than qualitative) parenchymal and ductal criteria found during evaluation of the pancreas. It is generally accepted that, in the absence of any criteria, chronic pancreatitis is unlikely, whereas in the presence of 5 or more criteria (out of 9-11) chronic pancreatitis is likely although ERCP and pancreatic function tests may still be normal. The diagnostic significance of patients with fewer (1-4) criteria found on EUS is currently unclear, particularly when other diagnostic tests such as ERCP and function testing are normal. In these cases, there is a potential for "over-diagnosis" of chronic pancreatitis, since the EUS changes cannot be confirmed by other modalities. How can we better understand the implications of EUS detected changes when other tests are normal?

Biopsy, Fine-Needle↗
PubMed2004

Recurrent pancreatitis due to a cystic pancreatic tumor: a rare presentation of acinar cell carcinoma.

CONTEXT: Acinar cell carcinoma is an uncommon malignancy of the pancreas. It has characteristic histomorphology, immunohistochemistry profile, and clinicopathological behavior. CASE REPORT: We report a rare case of recurrent pancreatitis secondary to acinar cell carcinoma of the pancreas. We describe the endoscopic ultrasound characteristic, treatment and the surgical outcome. CONCLUSIONS: Acinar cell carcinoma should be considered in the differential diagnosis of cystic pancreatic tumors presenting with recurrent pancreatitis.

Aged↗
PubMed2003

Rapid endoscopic secretin stimulation test and discrimination of chronic pancreatitis and pancreatic cancer from disease controls.

BACKGROUND & AIMS: The cholecystokinin (CCK)/secretin pancreatic function tests to diagnose pancreatic exocrine insufficiency are time consuming and invasive. Our aim was to develop a rapid pancreatic function test performed during upper endoscopy that could discriminate between patients with normal from impaired exocrine pancreatic secretion. METHODS: We prospectively evaluated 412 patients for possible pancreatic diseases. During upper endoscopy, 1 CU/kg of secretin was given intravenously and duodenal juice (collected for 10 min) was assayed for concentrations of bicarbonate and lipolytic and trypsin activity. Final diagnosis was by histology, imaging, and a previously validated scoring system (for chronic pancreatitis). Of 412 patients, 117 patients had normal pancreas, 72 patients had chronic pancreatitis, and 116 patients had pancreatic adenocarcinoma. The remaining 107 patients had miscellaneous disease of the peripancreatic region. In 28 patients we also validated the secretin test with the standard CCK pancreatic function test. RESULTS: There was no difference between bicarbonate or trypsin concentrations among the groups. Lipolytic concentration was significantly lower in chronic pancreatitis (115 +/- 18) and in pancreatic adenocarcinoma (87 +/- 10) compared with patients with normal pancreas (229 +/- 23; P < 0.03 and P < 0.0001, respectively). The overall accuracy of the endoscopic secretin test was 79%, with positive and negative predictive values of 73% and 85%, respectively. The concentration of lipolytic activity obtained by the endoscopic secretin test in 28 patients correlated moderately well (r = 0.41, P < 0.03) with lipolytic output obtained by the CCK pancreatic function test. CONCLUSIONS: Lipolytic concentration in duodenal juice after intravenous secretin collected for 10 minutes during upper endoscopy was significantly lower in chronic pancreatitis and pancreatic adenocarcinoma compared with patients with normal pancreas, but was not accurate enough for routine clinical use.

Adenocarcinoma↗
PubMed2002

Study of recurrence after surgical resection of intraductal papillary mucinous neoplasm of the pancreas.

BACKGROUND & AIMS: The aim of this study was to determine recurrence and long-term survival after resection of pancreatic intraductal papillary mucinous neoplasm and to correlate recurrence and survival with histology, extent of resection, and duration of follow-up. METHODS: A single pathologist, without knowledge of previous interpretations of histology or clinical data, retrospectively reviewed and classified 113 resected intraductal papillary mucinous neoplasms as invasive carcinoma (n = 40) or as noninvasive neoplasms (adenoma, borderline, or carcinoma in situ; n = 73). Data on recurrence (locoregional or metastatic), follow-up, and cause of death were obtained from patient records and/or by contacting patients and their physicians. RESULTS: In invasive intraductal papillary mucinous neoplasm, recurrence was similar after partial pancreatectomy (18/27; 67%) and total pancreatectomy (8/13; 62%) and occurred within 3 years of resection in 91%. Among noninvasive neoplasms, 5 of 60 (8%) recurred after partial pancreatectomy (median follow-up, 37 months); none recurred after total pancreatectomy (n = 13; median follow-up, 32 months). Recurrence after resection in noninvasive neoplasms was diagnosed after a median of 40 months (range, 23-75 months); recurrence was noninvasive in 3 and invasive cancer in 2. Five-year survival was better for noninvasive compared with invasive intraductal papillary mucinous neoplasm (84.5% vs. 36%; P < 0.001). CONCLUSIONS: Invasive intraductal papillary mucinous neoplasm recurs frequently even after a complete "curative" resection and portends poor survival. In contrast, noninvasive intraductal papillary mucinous neoplasm recurs infrequently after resection, and survival is excellent regardless of the degree of epithelial dysplasia in the tumor.

Adenocarcinoma, Mucinous↗
PubMed2002

Invasive cancer and survival of intraductal papillary mucinous tumors of the pancreas.

OBJECTIVES: Intraductal papillary mucinous tumor (IPMT) is frequently associated with pancreatic cancer. We hypothesized that IPMT progresses to invasive cancer with K-ras mutations as an early event, and that invasive cancer affects survival. We compared survival after resection and determined whether K-ras mutations predicted survival in IPMT patients without or with invasive cancer. METHODS: Records of 47 patients with IPMT who were seen between 1983 and 1998 were reviewed retrospectively in 15 cases and prospectively in 32. All histological material was reviewed to confirm the diagnosis of IPMT and to assess invasion. Kaplan-Meier survival curves were analyzed by the log-rank test. The chi2 test was used for differences in K-ras between groups. RESULTS: There were 30 men and 17 women, with a mean age of 65 yr (range 36-90 yr). Of the patients, 26 had IPMT without invasive cancer and 19 had IPMT with invasion. Tissue diagnosis was available in 45 patients. K-ras was analyzed in 40 patients. Mutations were present in 15 of 23 patients (65%) without invasive cancer and in 14 of 17 patients (82%) with invasive cancer (p = ns). At 2.5 yr, the overall cumulative survival of IPMT patients without invasive cancer was 94% compared to 24% of patients with invasive cancer (p < 0.001). The 5-yr survival of IPMT patients without invasive cancer was 94%. K-ras mutations did not correlate with survival. CONCLUSIONS: Invasive cancer in IPMT reduces the 2.5-yr survival after surgery from 93% to 24%. K-ras mutations occur before invasive cancer, and do not predict postoperative survival.

Adult↗