Acute pancreatitis: conservative therapy)

Conservative treatment of acute pancreatitis is symptomatic and depends on the severity of the disease. For treatment of mild pancreatitis, fasting and intravenous application of fluids and analgetics is usually sufficient. Patients with severe pancreatitis should be monitored in an Intensive Care Unit and may require antibiotics. For treatment of acute pancreatitis, a large number of interventions has been suggested. They include nasogastric tubes, drugs which reduce pancreatic and gastric secretion, and treatments which inhibit activated proteases. Controlled studies have shown that most of these measures are ineffective. The value of early ERCP in acute pancreatitis is still under debate. ERCP appears to be helpful in biliary pancreatitis, especially if choledocholithiasis is present. Surgery should be reserved to those patients who do not respond to conservative treatment.     

Bayou virus-associated hantavirus pulmonary syndrome in Eastern Texas: identification of the rice rat, Oryzomys palustris, as reservoir host

OBJECTIVE: To validate the safety of gadolinium-diethylenetriamine pentaacetic acid (GD-DTPA) by measuring its effect on pancreatic capillary perfusion and acinar injury in acute pancreatitis. BACKGROUND: Contrast-enhanced computed tomography (CECT) is proposed as a gold standard for early evaluation of acute necrotizing pancreatitis. However, iodinated contrast media used for CECT have been shown in these circumstances to reduce pancreatic capillary flow and increase necrosis and mortality. Recent reports suggest that post-GD MRI provides images comparable to CECT in the assessment of severe acute pancreatitis. METHODS: Necrotizing pancreatitis was induced in 14 Wistar rats by intraductal glycodeoxycholic acid (10 mM/L) and intravenous caerulein (5 microg/kg/h) over 6 hours. Intravital microscopic quantitation of pancreatic capillary blood flow was performed using fluorescein isothiocyanate-labeled erythrocytes after induction of pancreatitis and 30 and 60 minutes after an intravenous bolus of either Ringer's solution or GD-DTPA (0.2 mL/kg). RESULTS: The two study groups were comparable with regard to mean arterial pressure, heart rate, arterial blood gases, hematocrit, amylase, lipase, and trypsinogen activation peptide production throughout the experiment. GD-DTPA did not reduce capillary flow (1.93 +/- 0.05 nL/capillary/min) compared to animals infused with Ringer's solution (1.90 +/- 0.06 nL/capillary/min). CONCLUSIONS: Intravenous injection of GD-DTPA does not further impair pancreatic microcirculation or increase acinar injury in acute necrotizing pancreatitis. Because of this advantage over CT contrast medium, further development of MRI as a staging tool in acute pancreatitis seems desirable.     

What place for endoscopic sphincterotomy in treatment of acute pancreatitis?

STUDY AIM: A prospective study was undertaken in order to evaluate the effects of endoscopic sphincterotomy on the evolution of biliary and idiopathic acute pancreatitis. PATIENTS AND METHODS: Among 320 patients with acute pancreatitis observed from 1986 to 1996, 118 were excluded from the study for etiological reasons and 137 were included for an endoscopic sphincterotomy within 72 hours from their admission. There were nine technical failures and 128 endoscopic sphincterotomies were performed. Sixty-five eligible patients were not included for logistic problems or patients' refusal; they can be considered as a "control group". RESULTS: The mortality rate of endoscopic sphincterotomy was 0 and the morbidity rate 2.1%. The mortality rate of acute pancreatitis was 3.1% in the sphincterotomy group vs 7.6% in the control group (P = 0.1) (NS) and the morbidity rate 25% versus 32% (P > or = 0.1) (NS). CONCLUSION: These results suggest that endoscopic sphincterotomy could be beneficial in acute biliary or idiopathic pancreatitis but they are not statistically significant. Endoscopic sphincterotomy does not increase the severity of acute pancreatitis and can be considered particularly in cases of gallstone pancreatitis but it should be performed less than 48 hours after the onset of acute pancreatitis.     

Dexamethasone perfusion of the labyrinth plus intravenous dexamethasone for Ménière's disease

Recent clinical and laboratory evidence indicates that Meniere's disease is an immune-mediated disease. Dexamethasone perfusion of the inner ear through the round window plus intravenous dexamethasone often will stop the dizzy spells, reduce the fullness and low-frequency tinnitus, and sometimes improve the hearing in patients with Meniere's disease. The dexamethasone must act mostly on the endolymphatic sac and, to a lesser extent, on the stria vascularis and spiral ligament, the known targets of immune response in the inner ear, to reduce the endolymphatic hydrops and restore the fluid dynamics of the endolymph. Despite the good results with streptomycin perfusion, the number of patients with further hearing loss is large, so dexamethasone perfusion with intravenous dexamethasone should be tried first. The initial response to dexamethasone perfusion plus intravenous dexamethasone has been very good, with very little risk of further hearing loss, and it holds great promise for the future.     

Renal biopsy findings in long-term cyclosporin treatment of psoriasis

BACKGROUND: Patients with severe acute pancreatitis die of complications closely related to the systemic activation of protease cascades. AIM: To examine the effects of human C1 esterase inhibitor (C1 INH) and antithrombin III (AT III) on two experimental models of acute pancreatitis. METHODS: Oedematous pancreatitis was induced by continuous intravenous infusion of caerulein and haemorrhagic pancreatitis by retrograde injection of sodium taurocholate into the biliopancreatic duct. C1 INH and AT III were given intravenously, either before or after the induction of pancreatitis. Treatment with C1 INH and AT III had no beneficial effect on oedematous pancreatitis. On the other hand, combined C1 INH and AT III therapy improved the survival in haemorrhagic pancreatitis compared with treatment with human serum albumin. This reduction in mortality was found regardless of whether the treatment was given prophylactically or therapeutically. CONCLUSIONS: Treatment with C1 INH and AT III represents a promising therapeutic concept for patients with severe haemorrhagic pancreatitis.     

Inferior vena caval thrombosis associated with acute pancreatitis: an unusual vascular complication--its presentation and management

Vascular thrombosis and systemic hypercoagulable states are known complications of acute pancreatitis. They are thought to be secondary to the release of proteolytic enzymes of the pancreas. Inferior vena caval thrombosis is an extremely rare complication of chronic pancreatitis and has, to the authors' knowledge, never been reported in acute pancreatitis. The clinical presentation and radiographic findings are reviewed to illustrate the disease spectrum. Early treatment with intravenous heparin appears to be an effective therapy. Familiarity with this complication will aid physicians in its early diagnosis. However, a high degree of suspicion for this complication is necessary to make a diagnosis.     

Gabexate for the prevention of pancreatic damage related to endoscopic retrograde cholangiopancreatography. Gabexate in digestive endoscopy--Italian Group

BACKGROUND: Endoscopic retrograde cholangiopancreatography (ERCP) is associated with elevated levels of pancreatic enzymes and pancreatitis. Gabexate, a protease inhibitor, has been used to prevent pancreatic damage related to ERCP. METHODS: We conducted a multicenter, double-blind comparison of gabexate (1 g given by intravenous infusion starting 30 to 90 minutes before endoscopy and continuing for 12 hours afterward) with placebo (mannitol and sodium chloride, administered in the same fashion). A total of 435 adults scheduled to undergo ERCP and, when indicated, endoscopic sphincterotomy underwent randomization; 17 were excluded from the final analysis for various reasons. The remaining 418 patients (mean age, 60.4 years)--208 in the gabexate group and 210 in the placebo group--were analyzed. Acute pancreatitis was considered to be present if serum amylase or lipase levels (or both) were five times greater than the upper limits of normal in association with the onset of pancreatic pain. RESULTS: After the procedures, 276 patients (66 percent) had elevated pancreatic-enzyme levels; the frequency was similar in the two groups. Mean serum amylase values were higher in the placebo group than in the gabexate group through 24 hours of observation (P=0.03). Twelve patients in the gabexate group and 29 in the placebo group had abdominal pain (6 percent vs. 14 percent, P=0.009). Sixteen patients in the placebo group and five in the gabexate group had acute pancreatitis (8 percent vs. 2 percent, P=0.03). Two patients treated with gabexate and six given placebo had adverse events, all of which resolved. Two patients given placebo died of acute pancreatitis; one was excluded from the evaluation because pancreatitis was present before endoscopy. One patient in the gabexate group died, from a myocardial infarction. CONCLUSION: Prophylactic treatment with gabexate reduced pancreatic damage related to ERCP, as reflected by reductions in the extent but not the frequency of elevated enzyme levels and in the frequency of pancreatic pain and acute pancreatitis.     

Postoperative changes in the coagulation and fibrinolytic systems in endoluminal stent-graft treatment of thoracic aortic aneurysms

Length of stay (LOS) predictions in acute pancreatitis could be used to stratify patients with severe acute pancreatitis, make treatment and resource allocation decisions, and for quality assurance. Artificial neural networks have been used to predict LOS in other conditions but not acute pancreatitis. The hypothesis of this study was that a neural network could predict LOS in patients with acute pancreatitis. The medical records of 195 patients admitted with acute pancreatitis were reviewed. A backpropagation neural network was developed to predict LOS >7 days. The network was trained on 156 randomly selected cases and tested on the remaining 39 cases. The neural network had the highest sensitivity (75%) for predicting LOS >7 days. Ranson criteria had the highest specificity (94%) for making this prediction. All methods incorrectly predicted LOS in two patients with severe acute pancreatitis who died early in their hospital course. An artificial neural network can predict LOS >7 days. The network and traditional prognostic indices were least accurate for predicting LOS in patients with severe acute pancreatitis who died early in their hospital course. The neural network has the advantage of making this prediction using admission data.     

Computerized tomography versus nuclear magnetic resonance in acute pancreatitis

The aim of the study was to compare Computed Tomography (CT) and Nuclear Magnetic Resonance (MR) scan's diagnostic reliability in acute pancreatitis (AP). During a 44-month period 21 patients with a clinical and laboratory diagnosis of AP were submitted to CT and MR study. The scans were evaluated according to pancreatitis degree and presence and rate of necrosis. Pancreatitis degree was assessed using Balthazar's grading for CT scans; a similar classification was used for MR scans. Thirteen patients had oedematous pancreatitis and 8 necrotic pancreatitis. Necrosis was diagnosed intraoperatively or in non operated patients with CT scan. MR staging was identical to that of the CT ones except for 2 patients who were grade E at CT and grade D at MR. MR identified necrosis in all 8 patients with necrotic AP whereas CT diagnosed only 5 patients properly since 3 scans were performed without contrast medium infusion because of renal failure. MR proved to be a valid alternative in AP diagnosis: it provide the same diagnostic and prognostic information as CT and does not need contrast infusion, which makes it preferable to CT in the follow-up of severe AP evolution.     

Measuring the quality of outpatient treatment for schizophrenia

OBJECTIVE: Usually it is not possible to study the initial systemic response in patients with acute pancreatitis in the first hours after onset of the disease. We used postendoscopic retrograde pancreatography (ERP) pancreatitis as a model to study cytokine and anticytokine release in the early phase of human acute pancreatitis. METHODS: Post-ERP pancreatitis was defined as a threefold increase in serum amylase and at least two of the following clinical symptoms: abdominal pain, nausea, vomiting or peritonism 24 h after ERP. Serum levels of pro-inflammatory cytokines interleukin-1beta (IL-1beta), interleukin-6 (IL-6), interleukin-8 (IL-8), tumour necrosis factor alpha (TNF), as well as endogenous antagonistic mediators of the systemic inflammatory response such as soluble tumour necrosis factor alpha receptors p55 (TNFR p55) and p75 (TNFR p75), and IL-1-receptor antagonist (IL-1-RA) and interleukin-2-receptor (IL-2R) as indicators of lymphocyte activation were measured before and 0, 1, 4, 12, 24 and 48 h after ERP. In nine patients with acute post-ERP pancreatitis, these parameters were monitored daily until C-reactive protein (CRP) was within normal ranges and were compared to patients without pancreatitis after ERP. RESULTS: IL-1beta was not detectable in five patients with and four patients without post-ERP pancreatitis. The values of the remaining patients in both groups were lower than 3.9 pg/ml. IL-8 and IL-1-RA serum concentrations peaked 12 h after ERP (132.9 and 3245.0 pg/ml respectively) compared to patients without post-ERP pancreatitis (25.8 and 389.9 pg/ml respectively). The IL-6 concentration increased to 81.6 pg/ml (8.0 pg/ml in control patients) 24 h after ERP, while the peak values for CRP were measured 72 h after ERP (164.0 versus 7.7 mg/l). IL-2R content was maximally elevated 144 h after ERP (688.8 versus 255.9 U/ml), while concentrations of TNF and its receptors showed no significant change over time. CONCLUSION: The initial response of the cytokine network to damage of the human pancreas leading to acute pancreatitis includes the release of IL-8 and the IL-1 antagonist IL-1-RA, while IL-1beta is not found in the systemic circulation. The TNF system does not seem to be involved as indicated by the lack of detectable changes in TNF and the soluble TNFR p55 and p75 serum concentrations. Lymphocyte activation as indicated by elevated IL-2R levels occurred days after the initial trauma. Even mild post-ERP pancreatitis leads to significant systemic release of cytokines and their biological counterparts.     

Is the association of serum lipase with beta2-microglobulin or C-reactive protein useful for establishing the diagnosis and prognosis of patients with acute pancreatitis?

In the Emergency Department it is mandatory to establish the diagnosis and the prognosis of acute pancreatitis as soon as possible. To evaluate whether the association of serum lipase either with serum beta2-microglobulin or with C-reactive protein allows simultaneously to establish the diagnosis and the prognosis of acute pancreatitis, 96 patients with acute abdomen were studied. Fifty-eight patients had non-pancreatic acute abdomen and the remaining 38 had acute pancreatitis: 23 mild acute pancreatitis, and 15 severe acute pancreatitis. Forty healthy subjects were studied as controls. Lipase, beta2-microglobulin and C-reactive protein were determined in the serum of all subjects, using commercial kits. One patient with acute pancreatitis was not correctly classified when lipase was used to discriminate between patients with non-pancreatic acute abdomen and those with acute pancreatitis. For the discrimination of patients with severe acute pancreatitis from those with the mild form of the disease in the remaining 37 acute pancreatitis patients, beta2-microglobulin had a sensitivity of 53.3 %, specificity of 81.8%, and prognostic accuracy of 70.3 % (27 of the 37 patients correctly classified); 87.5 % of the 96 cases were correctly classified. C-reactive protein showed a lower prognostic accuracy than beta2-microglobulin: sensitivity 86.7%, specificity 45.5%, accuracy 62.2 %; 84.4 % of the cases were correctly classified. Using the polychotomous logistic regression analysis we found the same accuracy in discriminating between patients with acute pancreatitis and those with non-pancreatic acute abdomen (99.0%) but a lower accuracy (54.1%) between patients with severe acute pancreatitis and those with the mild form of the disease. Our study shows that the association of serum lipase with beta2-microglobulin or with C-reactive protein is not useful in simultaneously establishing the diagnosis and prognosis of acute pancreatitis.     

A chronic model for experimental investigation of epidural anesthesia in the rabbit

BACKGROUND/AIMS: By contrast with animal models, in most cases it is not possible to examine the systemic response in patients in the first hours after onset of acute pancreatitis. The aim was to determine whether endoscopic retrograde cholangiopancreaticography (ERP)-induced pancreatitis can be used as a human model for the study of cytokine release and acute phase response in the first hours of the disease. PATIENTS AND METHODS: Seventy consecutive patients undergoing ERP for different reasons were prospectively evaluated by sampling blood before and 0, 1, 4, 12, 24, and 48 hours after ERP and, in patients who developed an acute post-ERP pancreatitis, daily until C reactive protein (CRP) was within normal range. A post-ERP pancreatitis was defined as a three-fold increase of amylase or lipase and at least two of the clinical symptoms: abdominal pain, nausea, vomiting, and peritonism during 24 hours after ERP. RESULTS: Nine out of 70 patients developed an acute pancreatitis. Cytokines and other biochemical variables were measured in those nine and in 34 patients out of the 61 not developing pancreatitis. In the nine patients amylase and lipase increased within the first hour after ERP with maximum values between four and 12 hours. Interleukin-6 increased to maximal concentrations after 24-48 hours and the highest CRP concentrations were found 72 hours after ERP. Tumour necrosis factor did not change. CONCLUSION: Post-ERP pancreatitis is an ideal model in which to examine the initial cytokine and acute phase response in the first hours after the initiation of the disease.     

Effect of different immunosuppressive agents on acute pancreatitis: a comparative study in an improved animal model

BACKGROUND: Immunosuppressive drugs have been associated with the development and progression of acute pancreatitis after organ transplantation. Consequently, a reduction or a change in immunosuppressive therapy has been recommended once posttransplantation pancreatitis has been suspected. However, it is not known which of the available immunosuppressive agents is most harmful to the pancreas and which may be used safely in this situation. The objective of this study was to investigate the effect of different immunosuppressive drugs in various dosages on intrapancreatic protease activation, acinar cell necrosis, and mortality in an improved model of acute necrotizing pancreatitis in the rat. The rat model of acute necrotizing pancreatitis, like posttransplantation pancreatitis, is characterized by ischemia and microcirculatory disorders. METHOD: Acute pancreatitis was induced in rats by using a combination of low-dose controlled intraductal glycodeoxycholic acid superimposed on intravenous cerulein hyperstimulation. Six hours thereafter, animals were randomized to intravenous therapy with 2, 10, or 50 mg/kg/day prednisolone (PRED); 3, 15, or 60 mg/kg/day cyclosporine A (CsA); 10 mg/kg/day azathioprine (AZA); 0.6 mg/kg/day orthoclone OKT3 (OKT3); or saline. After 36 hr, surviving animals were killed to determine acinar cell necrosis and trypsinogen activation peptides levels (TAP) in blood and ascites. RESULTS: Compared with saline-treated control rats, animals treated with 60 mg/kg/day CsA developed significantly more acinar cell necrosis and had increased amounts of TAP in ascites. Likewise, there was more extensive acinar cell necrosis in animals subjected to AZA therapy. However, this was not associated with incremental TAP. Animals treated with 3 or 15 mg/kg/day CsA, OKT3, or PRED showed no significant changes in these target parameters. Animals given 10 or 50 mg/kg/day PRED even had decreased hematocrit values and produced significantly less ascites than animals in the other groups. CONCLUSION: The present results suggest that AZA and high doses of CsA aggravate acute pancreatitis and should, therefore, be avoided once posttransplantation pancreatitis has been suspected, whereas lower doses of CsA, OKT3, and PRED may be used safely. PRED can even be used at higher doses as may be required when graft rejection is suspected.     

Acute cholangitis and pancreatitis secondary to common duct stones: management update

Gallstones are found within the main bile duct (MBD) of 7% to 20% of patients undergoing cholecystectomy. MBD stones are the commonest cause of acute cholangitis and acute pancreatitis. Acute cholangitis is the result of infection superimposed on an obstructed biliary system and carries a high mortality rate if left untreated. The mainstay of treatment is a regimen of broad-spectrum intravenous antibiotics followed by prompt decompression of the obstructed biliary tree. Decompression is best accomplished by the endoscopic route, although transhepatic approaches may also be employed. Gallstone pancreatitis may be associated with cholangitis but is also common as a separate entity. Initial treatment is supportive, although new agents designed to suppress the systemic inflammatory response are under development and have proved beneficial in clinical trials. Severe cases should be treated with systemic antibiotics and early removal of the obstructing stones by endoscopic retrograde cholangiopancreatography and endoscopic sphincterotomy. Prophylactic cholecystectomy is recommended to prevent further episodes of gallstone pancreatitis.     

Acute renal failure in patients with acute pancreatitis

We describe five patients with acute pancreatitis in whom acute renal failure developed in the absence of hypotension. Pancreatitis was diagnosed clinically, with mean serum and urinary amylase levels of 766 +/- 197 (SE) and 2,378 +/- 572 units/100 ml, respectively. Acute renal failure developed within 24 hours after admission in all patients. It was manifested by oliguria, elevated levels of serum creatinine (mean, 6.9 +/- 1.1 mg/100 ml) and BUN (105 +/-28 mg/100 ml); a urinary sodium level of 72.0 +/- 6.6 mEq/liter; and isosmotic urine (355 +/- 31 mOsm/liter). The mean uric acid level was 18.6 +/- 1.6 mg/100 ml. Blood pressure was recorded frequently, and the lowest mean diastolic pressure was 96 +/- 6 mm Hg. The duration of the oliguric phase of acute renal failure was 8.2 +/- 1.7 days, and all patients recovered from both the acute pancreatitis and acute renal failure. In summary, acute pancreatitis, per se, can precipitate acute renal failure. It occurs early in the course of the pancreatitis, and extreme hyperuricemia is frequent finding that does not adversely affect the recovery of renal function.     

Clinical significance of the tests used in the diagnosis of pancreatic diseases

Different methods available for investigating patients for pancreatic disease are discussed. They first include measurement of pancreatic enzymes in biological fluids. Basal amylase and/or lipase in blood are truly diagnostic in acute pancreatitis but their utility is low in chronic pancreatic diseases. Evocative tests have been performed to increase the sensitivity of blood enzyme measurement. The procedure is based on enzyme determination following administration of pancreozymin and secretin, and offers a valuable aid in diagnosis of chronic pancreatitis and cancer of the pancreas. They are capable of discerning pancreatic lesions but are not really discriminatory because similar changes are observed in both diseases. The measurement of urinary enzyme levels in patients with acute pancreatitis is a sensitive indicator of disease. The urinary amylase excretion rises to abnormal levels and persists at significant values for a longer period of time than the serum amylase in acute pancreatitis. The fractional urinary amylase escretion seems to be more sensitive than daily urinary measurement. The pancreatic exocrin function can be assessed by examining the duodenal contents after intravenous administration of pancreozymin and secretin. Different abnormal secretory patterns can be determinated. Total secretory deficiency is observed in patients with obstruction of excretory ducts by tumors of the head of the pancreas and in the end stage of chronic pancreatitis. Low volume with normal bicarbonate and enzyme concentration is another typical pattern seen in neoplastic obstruction of escretory ducts. In chronic pancreatitis the chief defect is the inability of the gland to secrete a juice with a high bicarbonate concentration; but in the advanced stage diminution of enzyme and volume is also evident. Diagnostic procedures for pancreatic diseases include digestion and absorption tests. The microscopic examination and chemical estimation of the fats in stool specimens in different conditions of intake are still important screening tests. Isotopic estimates of steatorrhea and distinction between labeled triolein and oleic acid absorption do not provide greater diagnostic discrimination than traditional procedures. 131I labeled proteins permit a good evaluation of a negative nitrogen balance. Sophisticated procedures to estimate exocrine pancreatic insufficiency are based on the study of endoluminal digestive processes at several times and different level of the small intestine. They permite esclusion of extrapancreatic factors interfering in digestion and absorption functions. The endocrin pancreatic function is evaluated by mean of oral tolerance test an radioimmunoassay of blood insulin. It is generally agreed that "diabetes" caused by insulin deficiency and digestion and absorption defects are the result of diffuse pancreatic destruction. Many methods are now available investigating patients with pancreatic disease but the single use of one of them is never satisfactory...     

Mucinous cystadenoma of the pancreas as a cause of acute pancreatitis

Acute pancreatitis is only rarely the first presentation of a cystic neoplasm of the pancreas. Mucinous cystadenomas have not been reported to be a cause of acute pancreatitis; however, we present two cases of mucinous cystadenoma of the pancreas which have caused acute pancreatitis. Both patients (female) presented acute abdominal pain, with serum amylase elevation and ultrasound scan (US) and computed tomography (CT) evidence of moderate pancreatitis, which resolved with medical treatment; fluid collection in the distal pancreas had been misinterpreted as a pseudocyst. There was no history of alcohol abuse or gallstone disease. After distal pancreatectomy the diagnosis of mucinous cystadenoma was confirmed; in one case a large pseudocyst was associated with this diagnosis. Pre-operative differential diagnosis between inflammatory and neoplastic cysts is difficult, especially when the patient's first presentation is due to an episode of acute pancreatitis. A neoplastic cyst should be considered when acute pancreatitis attacks occur in non-alcoholic women, who do not have gallstone disease.     

Suitable fixation condition for rat liver using microwave irradiation and its application to the immunohistochemistry of glutamate dehydrogenase

In 50 patients auditory threshold and brain stem evoked potential studies were carried out before and after myelography. Due to the analysis of amplitudes and latencies of auditory brain stem measurements, significant functional disorders of the hearing organ and the auditory pathway could be demonstrated. In most of the patients these functional disorders were found to be subclinical, whereas 12 patients showed alterations extending from a subjectively slight hearing loss to an audiometrically objectified acute hearing loss depending on its intensity in each case. The reasons of these functional disorders could not be clarified. An open cochlear aqueduct through which perilymph enters the subarachnoidal space leading to a secondary endolymphatic hydrops can be considered as the cause in cases where manifest symptoms develop. The changes in brain stem audiometry can be additionally explained by changes in osmolality of the inner ear fluids which may lead to the development of an endolymphatic hydrops.     

The effect of octreotide on the prevention of acute pancreatitis and hyperamylasemia after diagnostic and therapeutic ERCP

BACKGROUND/AIMS: Acute pancreatitis is a serious complication of diagnostic and therapeutic Endoscopic Retrograde Cholangiopancreatography (ERCP). In addition, serum pancreatic enzymes increase without symptoms in about 40-50% of patients undergoing these endoscopic procedures. In order to evaluate the efficacy of octreotide in the prevention of these complications, we performed this randomised, prospective study. METHODOLOGY: We studied 73 patients (31 males, 42 females), mean age 63.3 +/- 12.9 years (range 28-87 yrs). The patients were randomly allocated into two groups (A and B). Group A (37 patients) was given 0.1 mg of octreotide subcutaneously 30 min before and 8 and 16 hours after the procedure, and group B (36 patients) was given a placebo. Serum amylase was measured 30 min before and 3 and 6 hrs after ERCP. All patients were subjected to ultrasonography for signs of pancreatic inflammation. There was no statistically significant difference between the two groups concerning age, sex and indication for ERCP. Endoscopic sphincterotomy (ES) was performed in 14 patients of group A and 10 patients of group B. RESULTS: There were 4 cases of acute pancreatitis in each group and the mean serum amylase at 3 and 6 hrs was comparable (494/676 and 429/582 IU/L, respectively). In comparing patients who were subjected to either diagnostic or therapeutic ERCP, there was no statistically significant difference concerning episodes of acute pancreatitis and the level of serum amylase. CONCLUSION: Octreotide does not seem to prevent acute pancreatitis and hyperamylasaemia after diagnostic and therapeutic ERCP.     

Phenformin-associated pancreatitis

Although phenformin has been previously reported to be associated with acute pancreatitis, little emphasis of this association has been made in the literature. We report the case of a 70-year-old diabetic man who developed acute hemorrhagic pancreatitis and severe lactic acidosis while taking phenformin. The patient was not taking any other medications, nor did he have any of the known metabolic conditions associated with pancreatitis. We review the four previously published cases of patients who developed acute pancreatitis while taking phenformin. Three of those patients also developed lactic acidosis, a well-known complication of phenformin therapy. Although phenformin has been reported to increase the serum amylase activity and to alter the content of the pancreatic secretions in response to various stimuli, the manner in which the drug might cause acute pancreatitis remains completely unknown.