Endoscopic transpapillary drainage of pancreatic pseudocysts
1
April 1995 Pancreatic Disorders A343 ENDOSCOPIC TRANSPAPILLARY DRAINAGE OF PANCREATIC PSEUDOCYSTS. M.BARTHET, C.BODIOU- BERTEI,JP.BERNARD ,J.SAHEL. Service d'H~pato- gastroent~rologie, 270 BD Sainte-Marguerite,BP29, 13274 MARSEILLE CEDEX9 Endoscopic drainages of pancreatic pseudocysts are usually, based on cyst-gastrostomy or cyst-duodenostomy. We tried to evaluate the results of endoscopic transpapillary cyst drainage (ETCD). During a period of 40 months, thirty patients with pancreatic pseudocysts were treated with ETCD. There were 24 males and 6 females with an average age of 45 years (SD 16). 28 had chronic pancreatitis (25 alcoholic pancreatitis) and 2 had biliary acute pancreatitis. 6 patients had infected cysf~s. All the pseudocysts Communicated with the pancreatic ductal system and 9 were bulging through the duodenal or gastric wall. The size of the pseudocysts ranged from 15 to 120 mm (average 50 mm)(head of the pancreas in 17 cases, body in 8 cases and tail in 5 cases. Eleven patients had a stenosis of the main pancreatic duct. Pigtail transpapillary cyst-pancreatic stents were inserted in 12 patients. Straight pancreatic stents were inserted in the remaining 18 patients. 10 patients underwent an additional endoscopic 'cystenterostomy (5 cyst-gastrostomy, 5 cyst- duedenostomy). The average duration for pancreatic stenting was 4.4 months (range 15 days-12 months). Patients were followed up for 15 months (range 2-60 months). 5 minor complications occured. There was no mortality. 23 patients (76%) were definetly healed by ETCD. One patient had recurrence but was healed by a new ETCD. Failure of ETCD occured in 6 patients (24 %) requiring surgery: 3 were early recurrences and 3 were definitive failure. ETCD appears as a safe and efficient modality for the drainage of pancreatic pseudocysts communicating with the pancreatic ductal system. PATTERN OF ALCOHOLIC CHRONIC PANCREATITIS IN PATIENTS WITH PANCREAS DIVISUM M.BARTHET, V. VALANTIN,JP. BERNARD,J.SAHEL. Service d'hdpato- gastroenterologie, 270 BD Sainte-Marguerite,BP29, 13274 MARSEILLE CEDEX 9 Pancreas divisum is a probable aetiology of recurrent acute pancreatitis. Nevertheless, clinical and radiological pattern of chronic pancreatitis (CP) associated with pancreas divisum are not described. Pancreas divisum was diagnosed in 20 patients among 310 presenting with alcoholic CP in a period of 48 months. They were matched with 20 patients presenting with alcoholic CP whithout pancreas divisum, for age and sex (Group 2). The age at the onset of the disease, the consumption of alcohol or tobacco did not differ between the two groups. Pancreatic calcifications were seen in 8 cases of the group 1 and in 14 cases of the group 2 (p=0.05). As considering loss of weight (>5 kg), diabetes, portal hypertension, the rate of the complications of the chronic panoreatitis were not significantly different between the both groups. The frequency of the attacks of acute pancreatitis was similar in the both groups (0.9/year vs 1.2/year (range 0.2-6/year (NS)) and the presence of pseudocysts did not differ among the two groups (11 vs 15 (NS)). ERCP were categorised according to the Cambridge classification. No differences could be evidenciated between the two groups (Chi2: p=0.15). In the group 1, pancreatographic abnormalities were located in the sole ventral segment of the pancreas in 3 cases, in the sole dorsal segment of the pancreas in 9 cases; and in the whole pancreas in 6 cases. In 2 patients, the ventral d~ct could not be demonstrated. Pancreas divisum does not appear to modify the natural course of alcoholic CP. In about half of the cases, pancreatographic abnormalities may be segmental. • STRATIFICATION OF SEVERITY IN ACUTE PANCREATITIS BY ASSAY OF TRYPSINOGEN AND 1-PROPHOSPHOLIPASE A2 ACTIVATION PEPTIDES. N.Beechey-Newman, D.Rae, N.Sumar, J.Hermon-Taylor. Depts. of Surgery Guy's Hospital and St.George's Hospital Medical School, London U.K. The activation of trypsinogens and pancreatic type 1-prophospholipase A 2 can be detected and quantified in vivo using sensitive and specific ELISA's for their released activation peptides, DDDDK (TAP) and DSGISPR (PROP). TAP assay specifically reports the activation of trypsinogens in patients with acute pancreatitis (AP). PROP assay has shown that 1-prophospholipase A 2 is abundantly expressed by human granulocytes, but not by lymphocytes or macrophages. PROP release in response to cytokine stimulation is a highly specific marker of granulocyte activation, an event involved in the development of multi- organ system failure and acute lung injury. We measured TAP and PROP concentrations in EDTA plasma and urine samples from 50 patients with amylase positive AP, on admission to hospital and 24h later. Six patients who subsequently developed the complications of severe necrotising AP were all TAP positive in plasma and urine on admission 1.5-29nM in plasma and 1.5-260nM in urine. Mean first symptom to first' sample interval was 37.2h, range 19-103h. Four of these six patients died and five were also PROP positive. One further patient with uncomplicated AP but who died of septicaemia due to septic arthritis was PROP positive and TAP negative. The remaining 43 Patients were al1 PROP negative. TAP assay subdivided this group into 15 TAP positive, 28 TAP negative. Of the 15 TAP positive patients 1 develope d a GI bleed and another had a lung infection. TAP and PROP assays are accurate early markers of disease severity and identify 4 clinicopathological subgroups on the basis of tests which report specific disease processes: severe AP (TAP positive PROP positive), uncomplicated AP (TAP negative PROP negative), severe complications not due to AP despite hyperamylasaemia (TAP negative PROP positive), and a group of intermediate severity (TAP positive PROP negative), who appear to be at greater risk and merit close clinical monitoring. • THE ROLE OF PROTEIN KINASE C (PKC) IN REGULATING ACUTE AND CHRONIC DESENSITIZATION OF THE GASTRIN-RELEASING PEPTIDE RECEPTOR (GRPR). RV Beava. J Mrozinski, T Kusui, JF Battey, RT Jensen. Digestive Diseases Branch, NIH, Bethesda, MD. The role of second messanger-depandeat kineses in regulating the desensitization of pancreatic G protein-coupled receptors is not clear. For example, in the well-studied GRPR data now exists both for and against PKC playing a role in modulating desensitization of this receptor. To address this issue we created a mutant murine GRPR whereby this reeeptor's PKC consensus sequences (one in intracellular loop-3; two in the carboxyl terminus) were eliminated by site-directed mutagenesis. The cDNA for both the wild type receptor (GRPR-WT) and for the PKC elimination mutant (Mutmc) were transfected into Balb/3T3 fibroblasts by CaPO~ precipitation. Both GRPR-WT (I~= 1.4+0.4 riM) and MutPxc (Ka= 1.2+0.2 nM) bound agonist with similar affinity. The ability of either receptor to couple to G proteins and activate phospholipase C, determined by measuring increases in cellular [~H]inositol phosphates ([~H]IP), was similar for wild type GRPR (EC~o=0.9+0.3 nM) and MutPKc (EC50=0.7+0.2 nM). Chronic desensitization was measured by exposing cells to 3 nM bombesin for 24 hours, and then determining the cell's residual ability to increase ~H]IP. Cells expressing GRPR-WT exposed to agonist for 24 hours were markedly attenuated in their ability to increase [3H]IP's (27+1% of control), whereas cells expressing Mut~c were relatively unaffected by prior exposure to agoniat (92+3 % of control). Acute desensitization was assessed by exposing cells to I00 nM bombesin and then measuring [3H]IP at various time points both with and without the selective PKC inhibitor UCN-0L With or without UCN-01, the rate of formation Of [~H]IP decreased rapidly and equally after the addition of bombesin (100 nM), thus PKC activation does not appear to regulate acute desensitization of the GRPR. To explore further the potential role of receptor phosphorylation in the acute regulation of the GRPR, we next investigated receptor phosphorylation using an antibody targeted to the 3rd intracellular loop of the GRPR. 1 #M bombesin not only resulted in brisk phosphorylation of GRPR-WT, but also caused some phosphorylation of MuFKc, suggesting that this was due to a second messenger-independent kinase. These data suggest that PKC primarily regulates chronic desensitization, and that a second messengur-independent kinase primarily regulates acute desensitization of the GRPR.
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Transcript of Endoscopic transpapillary drainage of pancreatic pseudocysts
April 1995 Pancreatic Disorders A343
ENDOSCOPIC TRANSPAPILLARY DRAINAGE OF PANCREATIC PSEUDOCYSTS. M.BARTHET, C.BODIOU- BERTEI,JP.BERNARD ,J.SAHEL. Service d'H~pato- gastroent~rologie, 270 BD Sainte-Marguerite, BP29, 13274 MARSEILLE CEDEX9
Endoscopic drainages of pancreatic pseudocysts are usually, based on cyst-gastrostomy or cyst-duodenostomy. We tried to evaluate the results of endoscopic transpapillary cyst drainage (ETCD).
During a period of 40 months, thirty patients with pancreatic pseudocysts were treated with ETCD. There were 24 males and 6 females with an average age of 45 years (SD 16). 28 had chronic pancreatitis (25 alcoholic pancreatitis) and 2 had biliary acute pancreatitis. 6 patients had infected cysf~s. All the pseudocysts Communicated with the pancreatic ductal system and 9 were bulging through the duodenal or gastric wall. The size of the pseudocysts ranged from 15 to 120 mm (average 50 mm)(head of the pancreas in 17 cases, body in 8 cases and tail in 5 cases. Eleven patients had a stenosis of the main pancreatic duct.
Pigtail transpapillary cyst-pancreatic stents were inserted in 12 patients. Straight pancreatic stents were inserted in the remaining 18 patients. 10 patients underwent an additional endoscopic 'cystenterostomy (5 cyst-gastrostomy, 5 cyst- duedenostomy). The average duration for pancreatic stenting was 4.4 months (range 15 days-12 months). Patients were followed up for 15 months (range 2-60 months). 5 minor complications occured. There was no mortality. 23 patients (76%) were definetly healed by ETCD. One patient had recurrence but was healed by a new ETCD. Failure of ETCD occured in 6 patients (24 %) requiring surgery: 3 were early recurrences and 3 were definitive failure.
ETCD appears as a safe and efficient modality for the drainage of pancreatic pseudocysts communicating with the pancreatic ductal system.
PATTERN OF ALCOHOLIC CHRONIC PANCREATITIS IN PATIENTS WITH PANCREAS DIVISUM M.BARTHET, V. VALANTIN,JP. BERNARD,J.SAHEL. Service d'hdpato- gastroenterologie, 270 BD Sainte-Marguerite, BP29, 13274 MARSEILLE CEDEX 9
Pancreas divisum is a probable aetiology of recurrent acute pancreatitis. Nevertheless, clinical and radiological pattern of chronic pancreatitis (CP) associated with pancreas divisum are not described.
Pancreas divisum was diagnosed in 20 patients among 310 presenting with alcoholic CP in a period of 48 months. They were matched with 20 patients presenting with alcoholic CP whithout pancreas divisum, for age and sex (Group 2).
The age at the onset of the disease, the consumption of alcohol or tobacco did not differ between the two groups. Pancreatic calcifications were seen in 8 cases of the group 1 and in 14 cases of the group 2 (p=0.05). As considering loss of weight (>5 kg), diabetes, portal hypertension, the rate of the complications of the chronic panoreatitis were not significantly different between the both groups. The frequency of the attacks of acute pancreatitis was similar in the both groups (0.9/year vs 1.2/year (range 0.2-6/year (NS)) and the presence of pseudocysts did not differ among the two groups (11 vs 15 (NS)). ERCP were categorised according to the Cambridge classification. No differences could be evidenciated between the two groups (Chi2: p=0.15). In the group 1, pancreatographic abnormalities were located in the sole ventral segment of the pancreas in 3 cases, in the sole dorsal segment of the pancreas in 9 cases; and in the whole pancreas in 6 cases. In 2 patients, the ventral d~ct could not be demonstrated.
Pancreas divisum does not appear to modify the natural course of alcoholic CP. In about half of the cases, pancreatographic abnormalities may be segmental.
• STRATIFICATION OF SEVERITY IN ACUTE PANCREATITIS BY ASSAY OF TRYPSINOGEN AND 1-PROPHOSPHOLIPASE A2 ACTIVATION PEPTIDES. N.Beechey-Newman, D.Rae, N.Sumar, J.Hermon-Taylor. Depts. of Surgery Guy's Hospital and St.George's Hospital Medical School, London U.K.
The activation of trypsinogens and pancreatic type 1-prophospholipase A 2 can be detected and quantified in vivo using sensitive and specific ELISA's for their released activation peptides, DDDDK (TAP) and DSGISPR (PROP). TAP assay specifically reports the activation of trypsinogens in patients with acute pancreatitis (AP). PROP assay has shown that 1-prophospholipase A 2 is abundantly expressed by human granulocytes, but not by lymphocytes or macrophages. PROP release in response to cytokine stimulation is a highly specific marker of granulocyte activation, an event involved in the development of multi- organ system failure and acute lung injury. We measured TAP and PROP concentrations in EDTA plasma and urine samples from 50 patients with amylase positive AP, on admission to hospital and 24h later. Six patients who subsequently developed the complications of severe necrotising AP were all TAP positive in plasma and urine on admission 1.5-29nM in plasma and 1.5-260nM in urine. Mean first symptom to first' sample interval was 37.2h, range 19-103h. Four of these six patients died and five were also PROP positive. One further patient with uncomplicated AP but who died of septicaemia due to septic arthritis was PROP positive and TAP negative. The remaining 43 Patients were al1 PROP negative. TAP assay subdivided this group into 15 TAP positive, 28 TAP negative. Of the 15 TAP positive patients 1 develope d a GI bleed and another had a lung infection. TAP and PROP assays are accurate early markers of disease severity and identify 4 clinicopathological subgroups on the basis of tests which report specific disease processes: severe AP (TAP positive PROP positive), uncomplicated AP (TAP negative PROP negative), severe complications not due to AP despite hyperamylasaemia (TAP negative PROP positive), and a group of intermediate severity (TAP positive PROP negative), who appear to be at greater risk and merit close clinical monitoring.
• THE ROLE OF PROTEIN KINASE C (PKC) IN REGULATING ACUTE AND CHRONIC DESENSITIZATION OF THE GASTRIN-RELEASING PEPTIDE RECEPTOR (GRPR). RV Beava. J Mrozinski, T Kusui, JF Battey, RT Jensen. Digestive Diseases Branch, NIH, Bethesda, MD.
The role of second messanger-depandeat kineses in regulating the desensitization of pancreatic G protein-coupled receptors is not clear. For example, in the well-studied GRPR data now exists both for and against PKC playing a role in modulating desensitization of this receptor. To address this issue we created a mutant murine GRPR whereby this reeeptor's PKC consensus sequences (one in intracellular loop-3; two in the carboxyl terminus) were eliminated by site-directed mutagenesis. The cDNA for both the wild type receptor (GRPR-WT) and for the PKC elimination mutant (Mut mc) were transfected into Balb/3T3 fibroblasts by CaPO~ precipitation. Both GRPR-WT (I~= 1.4+0.4 riM) and Mut Pxc (Ka= 1.2+0.2 nM) bound agonist with similar affinity. The ability of either receptor to couple to G proteins and activate phospholipase C, determined by measuring increases in cellular [~H]inositol phosphates ([~H]IP), was similar for wild type GRPR (EC~o=0.9+0.3 nM) and Mut PKc (EC50=0.7+0.2 nM). Chronic desensitization was measured by exposing cells to 3 nM bombesin for 24 hours, and then determining the cell's residual ability to increase ~H]IP. Cells expressing GRPR-WT exposed to agonist for 24 hours were markedly attenuated in their ability to increase [3H]IP's (27+1% of control), whereas cells expressing Mut ~c were relatively unaffected by prior exposure to agoniat (92+3 % of control). Acute desensitization was assessed by exposing cells to I00 nM bombesin and then measuring [3H]IP at various time points both with and without the selective PKC inhibitor UCN-0L With or without UCN-01, the rate of formation Of [~H]IP decreased rapidly and equally after the addition of bombesin (100 nM), thus PKC activation does not appear to regulate acute desensitization of the GRPR. To explore further the potential role of receptor phosphorylation in the acute regulation of the GRPR, we next investigated receptor phosphorylation using an antibody targeted to the 3rd intracellular loop of the GRPR. 1 #M bombesin not only resulted in brisk phosphorylation of GRPR-WT, but also caused some phosphorylation of MuF Kc, suggesting that this was due to a second messenger-independent kinase. These data suggest that PKC primarily regulates chronic desensitization, and that a second messengur-independent kinase primarily regulates acute desensitization of the GRPR.
