Excellent Accuracy of Glucose Level in Cystic Fluid for Diagnosis of Pancreatic Mucinous Cysts.

BACKGROUND: CEA in pancreatic cystic fluid (PCF) is standard for mucinous cysts diagnosis. Glucose is an alternative, but its accuracy remains poorly described. AIMS: To evaluate PCF glucose using a glucometer and compare its accuracy with CEA for mucinous cysts diagnosis. MATERIALS AND METHODS: In frozen PCF obtained by EUS-FNA, glucose was evaluated using a glucometer. CEA and cytology were available as standard of care. The accuracy of glucose and CEA was calculated using receiver operator (ROC) curves. Definitive diagnoses were surgical or clinicopathological. RESULTS: We evaluated 82 patients with a mean age of 61.3 ± 14.8 years (25-91), predominantly (59%) females. Diagnoses included 17 serous cystadenomas, five pseudocysts, 20 intraductal papillary mucinous neoplasms, three mucinous cystic neoplasms, five adenocarcinomas, four neuroendocrine tumors, two other types, 26 non-defined. The median glucose levels (interquartile range) were 19 mg/dL (19-19) in mucinous and 105 mg/dL (96-127) in non-mucinous cysts (p < 0.0001). The median CEA level was 741 ng/mL (165-28,567) in mucinous and 9 ng/mL (5-19) in non-mucinous cysts (p < 0.0001). For mucinous cyst diagnosis, a CEA > 192 ng/mL had a sensitivity of 72% (95% CI 51-88) and a specificity of 96% (95% CI 82-100), and ROC analysis showed an area under the curve (AUC) of 0.842 (95% CI 0.726-0.959), while glucose < 50 mg/dL had a sensitivity of 89% (95% CI 72-98), a specificity of 86% (95% CI 67-96), and an AUC of 0.86 (95% CI 0.748-0.973). Pseudocysts presented low glucose, identically to mucinous cysts, with CEA allowing differential diagnosis. CONCLUSION: Glucose measured by a glucometer is accurate for mucinous cyst diagnosis, with significantly higher levels in non-mucinous cysts, except pseudocysts.

Peripancreatic fat necrosis worsens acute pancreatitis independent of pancreatic necrosis via unsaturated fatty acids increased in human pancreatic necrosis collections.

BACKGROUND AND AIMS: Peripancreatic fat necrosis occurs frequently in necrotising pancreatitis. Distinguishing markers from mediators of severe acute pancreatitis (SAP) is important since targeting mediators may improve outcomes. We evaluated potential agents in human pancreatic necrotic collections (NCs), pseudocysts (PCs) and pancreatic cystic neoplasms and used pancreatic acini, peripheral blood mononuclear cells (PBMC) and an acute pancreatitis (AP) model to determine SAP mediators. METHODS: We measured acinar and PBMC injury induced by agents increased in NCs and PCs. Outcomes of caerulein pancreatitis were studied in lean rats coadministered interleukin (IL)-1ß and keratinocyte chemoattractant/growth-regulated oncogene, triolein alone or with the lipase inhibitor orlistat. RESULTS: NCs had higher fatty acids, IL-8 and IL-1ß versus other fluids. Lipolysis of unsaturated triglyceride and resulting unsaturated fatty acids (UFA) oleic and linoleic acids induced necro-apoptosis at less than half the concentration in NCs but other agents did not do so at more than two times these concentrations. Cytokine coadministration resulted in higher pancreatic and lung inflammation than caerulein alone, but only triolein coadministration caused peripancreatic fat stranding, higher cytokines, UFAs, multisystem organ failure (MSOF) and mortality in 97% animals, which were prevented by orlistat. CONCLUSIONS: UFAs, IL-1ß and IL-8 are elevated in NCs. However, UFAs generated via peripancreatic fat lipolysis causes worse inflammation and MSOF, converting mild AP to SAP.

Cyst Fluid Glucose is Rapidly Feasible and Accurate in Diagnosing Mucinous Pancreatic Cysts.

OBJECTIVES: Better diagnostic tools are needed to differentiate pancreatic cyst subtypes. A previous metabolomic study showed cyst fluid glucose as a potential marker to differentiate mucinous from non-mucinous pancreatic cysts. This study seeks to validate these earlier findings using a standard laboratory glucose assay, a glucometer, and a glucose reagent strip. METHODS: Using an IRB-approved prospectively collected bio-repository, 65 pancreatic cyst fluid samples (42 mucinous and 23 non-mucinous) with histological correlation were analyzed. RESULTS: Median laboratory glucose, glucometer glucose, and percent reagent strip positive were lower in mucinous vs. non-mucinous cysts (P<0.0001 for all comparisons). Laboratory glucose<50 mg/dl had a sensitivity of 95% and a specificity of 57% (LR+ 2.19, LR- 0.08). Glucometer glucose<50 mg/dl had a sensitivity of 88% and a specificity of 78% (LR+ 4.05, LR- 0.15). Reagent strip glucose had a sensitivity of 81% and a specificity of 74% (LR+ 3.10, LR- 0.26). CEA had a sensitivity of 77% and a specificity of 83% (LR+ 4.67, LR- 0.27). The combination of having either a glucometer glucose<50 mg/dl or a CEA level>192 had a sensitivity of 100% but a low specificity of 33% (LR+ 1.50, LR- 0.00). CONCLUSIONS: Glucose, whether measured by a laboratory assay, a glucometer, or a reagent strip, is significantly lower in mucinous cysts compared with non-mucinous pancreatic cysts.

[The role of matrix metalloproteinases and their inhibitors in pathogenesis of pancreatic pseudocysts].

The investigation was conducted in 47 patients, operated on for pancreatic pseudocysts (PP). Activity of matrix metalloproteinases (MMP-9) and content of their tissue inhibitor (TIMP-2) were determined in the blood serum for estimation of inflammatory factors, hypoxia severity and state of the pancreatic tissue reconstruction. High activity of MMP-9 and TIMP-2 in presence of PP types I and II was noted in patients, what, probably, is caused by compensation reaction, directed towards inhibition of the collagen system destruction (predominantly of collagen type IV) and prevention of further reconstruction of pancreatic connective tissue. While progressing of pancreatic fibrosis the MMP-9 activity and the TIMP-2 level have lowered in comparison with these indices while its absence. In PP type III the MMP-9 activity was by 83.6% higher, than in a control group, but, by 51.4 and 35.1% lower, than in PP types I and IV. In all the patients endothelial dysfunction with endothelial injury was observed, witnessed by significant rising of the VEGF content in the blood serum. It have created favorable conditions for pancreatic tissue remodeling while parenchymal defect have been constituted by tissue, owing lower level of organization, including a cicatricial one. In cases of cellular repeated affection more activation of pancreatic stellate cells and enhancement of production of extracellular matrix component were noted.

Metabolomic-derived novel cyst fluid biomarkers for pancreatic cysts: glucose and kynurenine.

BACKGROUND: Better pancreatic cyst fluid biomarkers are needed. OBJECTIVE: To determine whether metabolomic profiling of pancreatic cyst fluid would yield clinically useful cyst fluid biomarkers. DESIGN: Retrospective study. SETTING: Tertiary-care referral center. PATIENTS: Two independent cohorts of patients (n = 26 and n = 19) with histologically defined pancreatic cysts. INTERVENTION: Exploratory analysis for differentially expressed metabolites between (1) nonmucinous and mucinous cysts and (2) malignant and premalignant cysts was performed in the first cohort. With the second cohort, a validation analysis of promising identified metabolites was performed. MAIN OUTCOME MEASUREMENTS: Identification of differentially expressed metabolites between clinically relevant cyst categories and their diagnostic performance (receiver operating characteristic [ROC] curve). RESULTS: Two metabolites had diagnostic significance-glucose and kynurenine. Metabolomic abundances for both were significantly lower in mucinous cysts compared with nonmucinous cysts in both cohorts (glucose first cohort P = .002, validation P = .006; and kynurenine first cohort P = .002, validation P = .002). The ROC curve for glucose was 0.92 (95% confidence interval [CI], 0.81-1.00) and 0.88 (95% CI, 0.72-1.00) in the first and validation cohorts, respectively. The ROC for kynurenine was 0.94 (95% CI, 0.81-1.00) and 0.92 (95% CI, 0.76-1.00) in the first and validation cohorts, respectively. Neither could differentiate premalignant from malignant cysts. Glucose and kynurenine levels were significantly elevated for serous cystadenomas in both cohorts. LIMITATIONS: Small sample sizes. CONCLUSION: Metabolomic profiling identified glucose and kynurenine to have potential clinical utility for differentiating mucinous from nonmucinous pancreatic cysts. These markers also may diagnose serous cystadenomas.

Mucin expression pattern in pancreatic diseases: findings from EUS-guided fine-needle aspiration biopsies.

OBJECTIVES: Alterations in mucin (MUC) glycosylation and expression have been described in cancer. Endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) can provide material for molecular biology analysis. This study assessed the feasibility of evaluating MUC expression from material obtained by EUS-FNA and studied the profile of MUC expression in benign and malignant pancreatic lesions. METHODS: A total of 90 patients with solid or cystic pancreatic lesions underwent FNA. The aspirated material was used for cytological analysis and RNA extraction to assess the expression pattern of MUCs by reverse transcription-PCR with primers specific for the MUC1, MUC2, MUC3, MUC4, MUC5A, MUC5B, MUC6, and MUC7 genes. RESULTS: RNA extraction was successful in 81% of the biopsies. The prevalences of MUC1, MUC2, MUC4, and MUC7 in ductal adenocarcinoma were 57.7, 51.4, 18.9, and 73.0%, respectively. Fifty percent of benign lesions and neuroendocrine tumors (NETs), and 63% of intraductal papillary mucinous neoplasms (IPMNs) were positive for MUC1. Twenty-five percent of benign lesions, 86% of NETs, and 47% of IPMNs were positive for MUC2. Of NETs, 50% were positive for MUC1, and 14% were positive for MUC7. None of the benign lesions or NETs expressed MUC4. MUC7 expression was highly significant for adenocarcinoma (P=0.007) and borderline for IPMN (P=0.05). MUC7 was expressed in 37.5% of chronic pancreatitis cases. CONCLUSIONS: RNA can be extracted from samples obtained under EUS-FNA. MUC7 could serve as a potential biological marker to identify malignant lesions, especially pancreatic adenocarcinoma.

New trends in diffusion-weighted magnetic resonance imaging as a tool in differentiation of serous cystadenoma and mucinous cystic tumor: a prospective study.

BACKGROUND/AIMS: Pancreatic cystic lesions are increasingly being recognized. Magnetic resonance imaging (MRI) is the method that brings the greatest amount of information about the morphologic features of pancreatic cystic lesions. To establish if diffusion-weighted MRI (DW-MRI) can be used as a tool to differentiate mucinous from nonmucinous lesions. METHODS: Fifty-six patients with pancreatic cystic lesions (benign, n = 46; malignant, n = 10) were prospectively evaluated with DW-MRI in order to differentiate mucinous from nonmucinous lesions. Final diagnosis was obtained by follow-up (n = 31), surgery (n = 16) or endoscopic ultrasound-guided fine needle aspiration (n = 9). Serous cystadenoma was identified in 32 (57%) patients. RESULTS: The threshold value established for the differentiation of mucinous from nonmucinous lesions was 2,230.06 s/mm(2) for ADC of 700. DWI-MRI behavior between mucinous and nonmucinous groups revealed sensitivity, specificity, positive predictive value, negative predictive value and accuracy to be 80, 98, 92, 93 and 93%, respectively (p < 0.01, power of sample = 1.0). In the comparison of the diffusion behavior between mucinous (n = 13) and serous (n = 32) lesions, the sensitivity, specificity, positive predictive value, negative predictive value and accuracy were 100, 97, 92, 100 and 98%, respectively (p < 0.01, power of sample = 1.0). The results of endoscopic ultrasound-guided fine needle aspiration were similar to those of DW-MRI. CONCLUSIONS: DW-MRI can be included as part of the array of tools to differentiate mucinous from nonmucinous lesions and can help in the management of pancreatic cystic lesions. and IAP.

Micafungin concentrations from brain tissue and pancreatic pseudocyst fluid.

We report the attainment of micafungin concentrations from brain tissue and pancreatic pseudocyst fluid from two patients with invasive candidiasis. Micafungin was present in low levels at both body sites, indicating limited penetration into central nervous system (CNS) tissue and pancreatic fluid. Further studies are needed to fully characterize its pharmacokinetics at these locations, as micafungin may potentially serve as an alternative antifungal therapy for CNS or pancreatic candidal infections for which the currently recommended first-line therapy fails.

[Milk-of-calcium in a pseudocyst of the pancreas].

A 59-year-old woman with a history of abdominal injury was admitted to our hospital for abdominal discomfort. CT revealed a cyst showing a fluid-calcium level in the pancreatic body. EUS-FNA was performed to aspirate the fluid in a cyst. Aspirated was milky-white odorless material. Chemical analysis showed high amylase level in the fluid. Spectroscopic analysis revealed that the fluid mainly consists of calcium phosphate. To the best of our knowledge, this is the first case of milk-of-calcium in a pancreatic pseudocyst with an analysis of cystic fluid obtained by EUS-FNA.

Anaplastic Carcinoma Arising in a Mucinous Cystic Neoplasm Masquerading as Pancreatic Pseudocyst.

Mucinous cystic neoplasms (MCN) of the pancreas can vary from benign to premalignant and malignant. Preoperative diagnosis is essential to offer the patient appropriate treatment. Occasionally these cases may harbor anaplastic carcinoma while clinically masquerade as a pseudocyst. Here in, we report an unusual case of a 37-year old female presented with recurrent abdominal pain that was suspected clinically and by imaging studies to have a pseudocyst. EUS-FNA with internal drainage of the cyst was performed. Cytological evaluation of the cyst fluid showed numerous inflammatory cells composed mainly of many neutrophils admixed with macrophages reminiscent of the usual pseudocyst content but there were scattered rare dyscohesive malignant cells which were highly pleomorphic with multinucleation. Immunostains on the cell block showed immunoreactivity of these cells including the multinucleated cells for Cam 5.2 and AE1/AE3 and focally for Ber-Ep4, Moc -31, and CA19-9. The subsequent resection confirmed the presence of anaplastic (undifferentiated) carcinoma (AC) arising in a MCN of the pancreas. Diagn. Cytopathol. 2016;44:538-542. © 2016 Wiley Periodicals, Inc.

Three truncated forms of serum albumin associated with pancreatic pseudocyst.

Plasma from a patient with chronic pancreatic pseudocyst showed an additional more negative albumin band (18%) on agarose gel electrophoresis. Both components bound (63)Ni(2+), indicating intact N-terminals; however, electrospray ionisation analysis of the intact proteins showed the mass of more negative albumin was 1254 Da less than the control and that the apparently normal band was 112 Da less. Reverse phase mapping and mass analysis of CNBr peptides showed three proteolytically modified forms of the C-terminal peptide indicating that some 81% of the albumin molecules lacked the C-terminal Leu residue, that 18% lacked the C-terminal KKLVAASQAALGL and that approximately 1% lacked the QAALGL sequence. These findings were further verified by tryptic mapping of the aberrant CNBr peptides. The truncations probably result from exposure of the albumin to 'leaking' pancreatic endo and exoproteases. During less acute phases of the disease, the 13 and 6 residue truncated forms together decreased to less than 1%, while the des-Leu(585) form made up the balance; no normal albumin was detected. This suggested that the des-Leu(585) form might be present at low levels in the plasma of normal individuals and CNBr mapping confirmed that it constituted 4-15% of the albumin from normal plasma.

Crizotinib-induced pancreatic pseudocyst: a novel adverse event.

Crizotinib is a tyrosine kinase inhibitor that demonstrates a dramatic tumour response in patients with advanced non-small cell lung cancers harbouring anaplastic lymphoma kinase (ALK) rearrangement. The pancreatic cyst has never been reported in patients who received crizotinib, whereas crizotinib-induced renal cysts developed in 4% of patients who were enrolled in clinical trials. We present the case of a 54-year-old man who was diagnosed with non-small cell lung cancer harbouring ALK rearrangement. After the start of treatment with crizotinib, we accidentally encountered the pancreatic pseudocyst without abdominal symptom and elevated serum pancreatic enzymes. In this report, we describe a case of pancreatic pseudocyst that appeared after starting treatment with crizotinib and regressed after treatment withdrawal.

Mucin-secreting tumors of the pancreas.

Mucinous pancreatic neoplasms present diagnostic and therapeutic challenges. These tumors behave in an indolent nature, with frequent overlap of symptoms and radiographic appearance with other forms of pancreatic cysts, pseudocysts, and malignancy. Some authors propose that all mucin-producing tumors of the pancreas are variants of the same basic entity and have subclassified them on the basis of their predominant location within the pancreas. These disorders must be considered in the evaluation of chronic abdominal pain, particularly in the presence of a cystic pancreatic lesion or when associated with idiopathic chronic or acute recurrent pancreatitis. The clinicopathologic features of IMHN overlap to a great extent with classic mucinous cystic neoplasms but are different significantly enough to be distinct clinical entities. These tumors originate from the pancreatic duct epithelium, produce mucin, demonstrate a papillary growth pattern, and are considered premalignant or frankly malignant at the time of diagnosis. Both lesions biologically are much less aggressive than that of pancreatic ductal adenocarcinoma and appear to infiltrate peripancreatic tissue and to metastasize to lymph nodes or other adjacent structures late in the course of disease. Nevertheless, IMHNs are located primarily in the head of the pancreas, commonly affect elderly men, and present clinically with obstructive pancreatitis, often leading to pancreatic insufficiency, whereas mucinous cystic neoplasms are more likely to develop in the pancreatic body or tail, predominate in young women, and present with symptoms referable to tumor compression of adjacent structures. The location of the lesion is the primary differentiating feature because the lining epithelium of the two tumor types is indistinguishable pathologically. In mucinous cystic tumors, the mucus is secreted and retained within the cyst lumen because of the absence of communication between the cyst and the main pancreatic duct. In contrast, mucus produced in MDE flows into the main pancreatic duct, resulting in obstructive pancreatitis and, ultimately, dilatation of the pancreatic duct. Intraductal mucus provides an important clue to the diagnosis of intraductal pancreatic neoplasms and, whenever present, should prompt an aggressive diagnostic evaluation. Both lesions are managed by resectional surgery because the opportunity for cure is high in the absence of metastatic disease.

Vascular endothelial growth factor, a novel and highly accurate pancreatic fluid biomarker for serous pancreatic cysts.

BACKGROUND: Mucinous pancreatic cysts (intraductal papillary mucinous neoplasm and mucinous cystic neoplasm) have the potential to progress to invasive pancreatic adenocarcinoma, presenting an opportunity for early detection, prevention, and cure. Serous cystic neoplasms (SCN) have no malignant potential, but can mimic mucinous pancreatic cysts on imaging. Therefore, identification of biomarkers that can distinguish between cystic lesions is critically important. We hypothesize that vascular endothelial growth factor (VEGF)-A levels in pancreatic fluid correlate with pathologic diagnosis. STUDY DESIGN: Pancreatic cyst/duct fluid samples were prospectively collected from patients undergoing pancreatic resection and correlated with surgical pathology. VEGF levels were detected by ELISA. VEGF-A and VEGF receptor 2 expression in pancreatic tissue was localized by immunohistochemistry. Genetic alterations of the von Hippel-Lindau gene were determined by targeted next-generation sequencing. RESULTS: Eighty-seven patients met inclusion criteria for enrollment. Final pathologic diagnoses included pseudocyst (n = 9), SCN (n = 17), mucinous cystic neoplasm (n = 24), low/moderate grade intraductal papillary mucinous neoplasm (n = 16), high-grade/invasive intraductal papillary mucinous neoplasm (n = 10), and pancreatic ductal adenocarcinoma (n = 11). VEGF-A was significantly upregulated in SCN cyst fluid compared with all other diagnoses (p < 0.0001). With a cut-off of 8,500 pg/mL, VEGF-A has 100% sensitivity and 97% specificity as an SCN biomarker. VEGF-A and VEGF receptor 2 are overexpressed in SCN cyst tissue. VEGF-C was also significantly elevated in SCN cyst fluid (p < 0.0001). With a cut-off set at 200 pg/mL, VEGF-C identifies SCN with 100% sensitivity and 90% specificity. The presence of a von Hippel-Lindau mutation in SCN cyst tissue correlates with elevated cyst fluid VEGF levels. CONCLUSIONS: This is the first report of a cyst fluid protein biomarker that can positively identify SCN. The ability to distinguish SCN from premalignant/malignant pancreatic cysts can spare the cost and risk of surveillance and surgical intervention in select patients.

Commercial molecular panels are of limited utility in the classification of pancreatic cystic lesions.

The PathfinderTG biomarker panel is useful in the evaluation of pancreatic cysts that have clinical features suspicious for malignancy, but its utility in classifying fine-needle aspiration biopsies from small pancreatic cystic lesions is yet to be proven. We used morphology to classify 20 pancreatic cyst cytology aspirates, all of which met radiographic criteria for close observation. Cases were cytologically classified as consistent with pseudocyst, serous cystadenoma, or mucinous neoplasm with low-grade, intermediate-grade, or high-grade dysplasia and analyzed for carcinoembryonic antigen. Redpath Integrated Pathology Inc. rendered diagnoses of nonmucinous (reactive/indolent or serous) or mucinous (low-risk or at risk) cyst on the basis of results of the PathfinderTG panel (KRAS mutations, DNA content, and loss of heterozygosity at microsatellites linked to tumor suppressor genes). Cytologic and commercial laboratory diagnoses were concordant in only 7 (35%) cases. Seven cysts classified as mucinous with low-grade dysplasia by cytology were interpreted as nonmucinous on the basis of the PathfinderTG panel, 2 of which were resected mucinous cysts. Two pancreatitis-related pseudocysts were misdiagnosed as low-risk mucinous cysts; 1 mucinous cyst with low-grade dysplasia was considered at risk for neoplastic progression using the PathfinderTG panel. Only 1 cyst misclassified as pseudocyst by cytology, but low-risk mucinous cyst by molecular analysis, proved to be a mucinous cystic neoplasm with low-grade dysplasia after surgical resection. We conclude that the PathfinderTG panel may aid the classification of pancreatic lesions, but is often inaccurate and should not replace cytologic evaluation of these lesions.

Pseudocyst of the pancreas: the role of cytology and special stains for mucin.

BACKGROUND: Currently, the preoperative diagnosis of a pancreatic cyst is based on clinical and imaging findings, frequently in conjunction with chemical analysis of cyst fluid and cytologic evaluation. The purpose of these diagnostic tests is to distinguish benign from malignant cysts of the pancreas. Accordingly, it is imperative to distinguish pancreatic pseudocysts from their mimics. In this study, the authors explored the cytomorphologic features of pseudocyst of the pancreas and evaluated the role of Alcian blue and mucicarmine stains in the cytologic evaluation of pancreatic cysts. METHODS: Forty-two patients were identified who had an eventual diagnosis of pancreatic pseudocyst and had an endoscopic ultrasound-guided fine-needle aspirate available. Clinical and imaging findings and chemical analyses of cyst fluid were recorded. The cytologic preparations were evaluated for gastrointestinal contamination, inflammatory cells, mucin, and pigmented material. The cytomorphologic features of 110 neoplastic mucinous cysts (intraductal papillary-mucinous neoplasms/mucinous cystic neoplasms of the pancreas) were evaluated and compared with the pseudocysts. RESULTS: The majority of patients (95%) had a prior episode of pancreatitis. On imaging, the pseudocysts were unilocular (92%). In 69% of cases, the endosonographic diagnosis was that of a pseudocyst. The mean carcinoembryonic antigen level was 41 ng/mL. In contrast, the cytopathologist rendered a definitive diagnosis of pseudocyst in only 10% of cases. The majority of smears (75%) revealed neutrophils and/or histiocytes. Atypical epithelial clusters were identified in 3 cases, 1 of which was diagnosed as suspicious for carcinoma. Yellow pigmented material, which was identified in 13 pseudocysts (31%), was not observed in neoplastic mucinous cysts. Alcian blue- and mucicarmine-positive material was identified in 64% and 40% of pseudocysts, respectively, and in 57% and 38% of neoplastic mucinous cysts, respectively. CONCLUSIONS: The diagnosis of a pseudocyst depended primarily on clinical and imaging findings and on chemical analysis of cyst fluid. The cytologic features frequently were nonspecific. The presence of yellow pigmented material served as a surrogate marker of a pseudocyst. Special stains for mucin did not distinguish pseudocysts from neoplastic mucinous cysts.

Biochemical analysis of pancreatic fluid collections predicts bacterial infection.

BACKGROUND AND AIMS: Despite our understanding of the pathophysiology of different types of pancreatic fluid collections (PFC), few studies have attempted to correlate the biochemical analysis of PFC contents with clinical and radiological characteristics. The aim of this study was to assess the predictive value of fluid analysis for discerning collection type (pseudocyst vs acute fluid collection with necrosis), presence of infection or communication with the pancreatic duct in the setting of acute and chronic pancreatitis. METHODS: Pancreatic fluid from 34 consecutive patients undergoing endotherapy of PFC was prospectively analyzed for seven variables: lactate dehydrogenase (LDH), total protein, albumin, glucose, amylase, lipase and specific gravity. RESULTS: In multivariate analysis, adjusting for age and gender, high intracystic levels of protein (OR 6.2; 95% CI 1.3-37.0), LDH (OR 6.8 [2.3-38.3]), and albumin (OR 7.8 [1.3-67.4]), and low levels of glucose (OR 0.2 [0.03-0.9]) predicted the presence of PFC infection. The optimal threshold value for protein was 1000 g/dL, which achieved a sensitivity of 73% and specificity of 75% for detecting infection; the optimal cut-off for LDH was 1000 U/L (sensitivity 64%, specificity 85%), and the cut-off for albumin was 500 g/dL (sensitivity 75%, specificity 85%). There were no statistically significant differences in biochemical fluid analysis with respect to fluid collection type (pseudocysts vs acute fluid collection with necrosis) and the presence of pancreatic duct communication. CONCLUSIONS: Biochemical analysis of PFC fluid is clinically helpful in detecting fluid infection in patients with bacteria on Gram stain or positive fluid cultures. Our findings fail to support the utility of fluid analysis in characterizing cyst type, and we caution against its use in distinguishing pseudocysts from acute fluid collection with necrosis.

Penetration of cefotaxime into the pancreas.

After intravenous injection of cefotaxime, higher pancreatic concentrations of the antibiotic were found in rats with experimental pancreatitis than in control animals. Also in human pancreatic pseudocysts, high and persistent concentrations of cefotaxime were found following intravenous injection. The results justify the use of cefotaxime in acute pancreatitis, whenever an antibiotic is indicated.