Pancreatitis and renal disease.

Pancreatitis has been described previously following renal transplantation, but not in association with chronic renal failure. Analysis of 168 patients with renal transplants revealed five who developed pancreatitis, three of whom died. All five were on treatment with prednisone and azathioprine. Four patients were seen with definite attacks of pancreatitis and chronic, stable renal failure from a variety of causes. None had received immunosuppressive agents, prednisone nor thiazide diuretics, but two were on regular frusemide. One patient was on maintenance dialysis, which could not be related directly to the pancreatitis. In either group alcohol ingestion, cholethiathiasis, or hypercalcaemia was not a factor. This diagnosis of pancreatitis was established on clinical grounds and serum amylast levels of greater than 900 iu/1. Similar serum amylast elevation was not found ina random group of patients with chronic renal failure. Hyperlipidaemia was not present in any patient with pancreatitis. Although hypercalcaemia and primary hyperparathyroidism was not found in the transplant and non-transplant subjects, elevated serum parathormone levels have been described in uraemic patients with normocalcaemia. Hyperparathyroidism may be a factor in the development of pancreatitis in reanl failure. Pancreatitis carries a significant mortality risk in renal transplantation. The four non-transplanted patients have survived, despite recurrent attacks of pancreatitis.     

代谢综合征对急性胰腺炎患者预后的影响

目的 探讨代谢综合征对急性胰腺炎患者预后的影响。方法 回顾性分析2004年7月～2007年10月我院收治的起病时伴代谢综合征的急性胰腺炎19例（A组）和不伴代谢综合征的急性胰腺炎24例（B组），对两组腹部Balthazar CT分级评分、血CRP、血钙、血氧分压、腹痛缓解时间、禁食时间、血淀粉酶恢复时间、住院天数进行比较。结果 与B组相比，A组的Balthazar CT分级评分较高；血钙和血氧分压水平较低；A组的腹痛缓解时间、禁食时间、血淀粉酶恢复时间、住院天数明显长于B组。结论 代谢综合征与急性胰腺炎病情程度密切相关，代谢综合征可作为急性胰腺炎的预后因素。     

A case of recurrent pancreatitis due to hyperlipidemia misdiagnosed as familial Mediterranean fever

Familial Mediterranean fever (FMF) is prevalent among Arabic, Turkish, Armenian, and Jewish people and it must always be considered in the differential diagnosis of patients from these ethnic groups presenting with recurrent abdominal pain with fever. In cases of fever and recurrent abdominal pain, acute pancreatitis is an important clinical condition, which should be considered in the differential diagnosis. Serum amylase concentration in acute pancreatitis is usually more than three times the upper limit of normal. However, in recurrent pancreatitis secondary to hypertriglyceridemia, serum amylase levels, for reasons that are not well understood, may be normal or mildly elevated. Recurrent pancreatitis secondary to hypertriglyceridemia may thus pose a problem in the differential diagnosis and may lead to an erroneous diagnosis of FMF. Measurement of serum triglyceride along with amylase levels should be required for a suspected diagnosis. Computerized examination of the abdomen may need to be undertaken to exclude acute pancreatitis in the presence of hypertriglyceridemia since serum amylase levels may be normal or slightly elevated.     

Carboxylic ester hydrolase: a serum marker of acute pancreatitis

By use of an enzyme-linked immunosorbent assay we established serum reference values of carboxylic ester hydrolase, a pancreatic secretory lipolytic enzyme, and explored to see if a raised serum level is indicative of acute pancreatitis. Postoperative elevation of carboxylic ester hydrolase was observed in seven out of ten patients who underwent pancreatic surgery. Serum levels of carboxylic ester hydrolase and amylase were determined in 129 patients admitted due to abdominal emergency conditions. Amylase was elevated in 27 patients, and in 20 of these raised carboxylic ester hydrolase levels affirmed the diagnosis acute pancreatitis. In five out of the seven patients with elevated amylase alone no etiologic factor of acute pancreatitis was found. Another 11 patients had raised carboxylic ester hydrolase levels without concomitant elevation of amylase. In all these patients, a likely cause of pancreatic inflammation was identifiable. Hence, a raised carboxylic ester hydrolase level, even in presence of normal amylase, could be indicative of acute pancreatic inflammation.     

Hyperlipoproteinemia and pancreatitis

A prospective study was begun in 1969 to investigate the relationship between hyperlipoproteinemia and pancreatitis. Ten patients were observed at the Cleveland Clinic Hospital. All had discrete, recurrent, acute pancreatitis with typical pain, hyper-amylasemia and hypertriglyceridemia during the acute phase, but without biliary tract disease or alcoholism. Acute pancreatitis usually occurred when serum triglyceride levels were above 1,000 mg/100 ml. In all patients during the acute phases, chylomicronemia and prebeta lipoproteinemia were present; serum cholesterol levels were normal or slightly elevated. Lipoprotein electrophoretic patterns were similar to the type V pattern described by Fredrickson. Serum lipids became normal in five patients given low fat diets (10 to 15 g/day), and they had no further abdominal pain; three others had satisfactory, but not complete remissions on diet therapy. Two others continued to have recurrent abdominal pain.It is concluded that the most consistent feature of one kind of pancreatitis is hyperlipoproteinemia with chylomicronemia. This condition probably occurs more frequently than has been previously recognized. Because of the favorable response to a low fat diet, this kind of pancreatitis can be treated adequately and further recurrence prevented.     

The first 24 hours of acute pancreatitis. Changes in biochemical and endocrine homeostasis in patients with pancreatitis compared with those in control subjects undergoing stress for reasons other than pancreatitis

As a group, 20 patients with acute pancreatitis showed alterations in biochemical and endocrine homeostasis that differed from the metabolic reactions observed in 13 control patients undergoing stress for reasons other than pancreatitis. In patients with acute pancreatitis, hyperglycemia was associated with inappropriately low serum insulin levels (p < 0.005). Plasma glucagon concentrations were markedly increased in the patients with acute pancreatitis and exceeded control values (p < 0.0001) throughout the 24-hour study period. The lipolytic effect of the inadequate serum insulin concentrations, elevated blood cortisol levels and hyperglucagonemia produced in a rise in nonesterified fatty acid levels. Serum gastin and growth hormone measurements remained within the normal range. Plasma parathyroid hormone (PTH) and calcitonin concentrations were increased in both patient populations, although calcitonin levels in patients with pancreatitis were significantly lower than those in the control group (p < 0.001). In patients experiencing a recurrent attack of pancreatitis, plasma glucagon levels were low (p < 0.005) compared with levels in patients experiencing their first episode of acute pancreatitis. Appreciation of the metabolic derangements in acute pancreatitis that are independent of the normal metabolic changes which occur in response to stress will help to rationalize exogenous endocrine therapy and possibly the prognostic accuracy in this disease.     

Serum amylase, pancreatic stents, and pancreatitis after sphincter of Oddi manometry

BACKGROUND: Serum amylase levels 2 hours after ERCP predict postprocedure pancreatitis. The value of serum amylase measurements after sphincter of Oddi manometry (SOM) and the effect of pancreatic-duct stent placement on serum amylase are unknown. METHODS: Records were reviewed for 88 SOM patients who had serum amylase measured 2 hours after the procedure. Post-SOM pancreatitis was defined as pain with a >3-fold elevation of serum amylase on the morning after SOM. "Possible pancreatitis" was defined as pain with a <3-fold elevation of serum amylase on the morning after SOM. RESULTS: Post-SOM pancreatitis and possible pancreatitis each occurred in 13% of the study cohort. Post-SOM pancreatitis was associated with the absence of a pancreatic stent and occurred in 0% of patients without a stent who had normal 2-hour serum amylase vs. 67% with elevated 2-hour serum amylase (p < 0.01). Among patients who received a stent, pancreatitis occurred in 6%, regardless of whether the 2-hour serum amylase was elevated. Possible pancreatitis occurred mainly in patients who received stents, and it also was associated with elevation of the 2-hour serum amylase. CONCLUSIONS: Elevation of the serum amylase level 2 hours after SOM predicts post-SOM pancreatitis but only in patients who do not receive a pancreatic stent. Among patients who received a stent, elevated 2-hour serum amylase levels predict subsequent findings that may be caused by attenuated pancreatitis.     

Elevated levels of interleukin-1 beta (IL-1 beta) and IL-6 in serum and increased production of IL-1 beta mRNA in lymph nodes of patients with polyneuropathy, organomegaly, endocrinopathy, M protein, and skin changes (POEMS) syndrome

To evaluate a possible implication of cytokines in the pathogenesis of polyneuropathy, organomegaly, endocrinopathy, M protein, and skin changes (POEMS) syndrome, we studied five consecutive patients with this condition, of which four had sclerotic bone lesions and four had multicentric Castleman's disease. Interleukin-1 beta (IL-1 beta) and IL- 6 serum levels were determined in these patients (13 serum samples) and in patients with multiple myeloma (5) and Waldenstrom's macroglobulinemia (5). In situ hybridization of the relevant mRNAs was performed on lymph node specimens of two patients with POEMS syndrome who had Castleman's disease. Elevated serum levels of IL-1 beta (13/13 samples), and IL-6 (7/13 samples) were found in patients with POEMS syndrome. In the other patients, serum IL-1 beta was undetectable or slightly increased and IL-6 was elevated in a single patient with Waldenstrom's macroglobulinemia. Abundant IL-1 beta mRNA-producing cells were present in interfollicular spaces in the two tested patients, while IL-6 mRNA-producing cells were rare. We conclude that IL-1 beta and IL-6 serum levels may be chronically elevated in patients with POEMS syndrome, and that lymph node may be one site of IL-1 beta overproduction. These results are in keeping with the hypothesis that cytokines mediate systemic manifestations of POEMS syndrome.     

Decrease in serum antiphospholipid antibody levels upon development of nephrotic syndrome in patients with systemic lupus erythematosus: relationship to urinary loss of IgG and other factors.

PURPOSE: Having observed a decrease in antiphospholipid antibodies (aPL) upon the development of nephrotic syndrome, as well as a negative association between nephrotic syndrome and secondary antiphospholipid syndrome, in patients with systemic lupus erythematosus (SLE), we sought to determine if this could be due to urinary loss of aPL and/or other factors. SUBJECTS AND METHODS: IgG and IgM aPL as well as other autoantibodies were studied by enzyme-linked immunosorbent assay with cardiolipin as antigen in serum and urine from six patients with SLE who had elevated serum aPL levels and developed nephrotic syndrome (cases). For controls, we studied: (1) three SLE patients with nephrotic syndrome but low aPL levels; (2) three patients with non-SLE nephrotic syndrome; (3) three SLE patients with high-titer aPL but no proteinuria; and (4) 10 healthy volunteers. RESULTS: We found urinary IgG, but no IgM, aPL in all cases and in one control from Group 2. Serum IgG aPL had gradually decreased after the development of nephrotic syndrome and had become normal. IgM aPL had also decreased in the four patients who had elevated levels, having reached normal levels at the time of the study in two. There was an apparent correlation between serum and urine IgG aPL levels but not between urinary IgG aPL and total proteinuria. By Farr's method, we found no urinary anti-DNA despite high serum titers in three cases. The two cases and one of the controls in Group 1 who had serum antibodies to extractable antigens also had these antibodies in the urine. CONCLUSION: Urinary loss of IgG aPL during nephrotic syndrome does not completely explain the reduction in serum aPL, since IgM also decreases. There could also be decreased synthesis and/or increased catabolism of immunoglobulins.     

Serum lipase levels in chronic alcoholics.

Using an elevated serum amylase level to diagnose acute pancreatitis in an alcoholic patient with abdominal pain may not be appropriate, because hyperamylesemia is common in asymptomatic alcoholics without acute pancreatitis. To determine whether serum lipase also suffers from the same drawback, we undertook a prospective study involving 202 asymptomatic alcoholics admitted to the detoxification unit of our hospital. Sixty-six of the 202 patients had serum lipase levels above the normal range (0-213 U/L). Of these 66, 55 (83%) had levels that were one to two times normal, while 11 patients had levels ranging between two and three times normal. No patient exceeded three times the normal level. This background information is important in the interpretation of serum lipase levels in alcoholic patients with abdominal pain.     

The sphincter of Oddi and acute pancreatitis--revisited

BackgroundOne of the rare causes of recurrent acute pancreatitis is sphincter of Oddi dysfunction. This condition is objectively diagnosed by manometry of the sphincter of Oddi. An abnormally elevated sphincter of Oddi basal pressure has been shown to predict patients who have a successful outcome after transduodenal sphincteroplasty and pancreatic duct septoplasty.MethodsForty-nine patients presenting with recurrent pancreatitis and who had manometric stenosis of the sphincter of Oddi were treated by transduodenal division of the sphincter of Oddi. Clinical follow-up was conducted over a minimum of 2 years.ResultsIn all, 43 patients were either cured or improved. None of these patients had any further episodes of pancreatitis. Three of these patients developed recurrent symptoms and were noted to have restenosis of the sphincter of Oddi. They were treated by insertion of an endoscopic stent into the pancreatic duct.ConclusionThe results from this series of patients re-affirm the efficacy of transduodenal sphincteroplasty and septoplasty for treatment of sphincter of Oddi stenosis in patients presenting with recurrent acute pancreatitis.     

Acute pancreatitis following hematopoietic stem cell transplantation: prevalence and cause of pancreatic amylasemia

To clarify the frequency and cause of acute pancreatitis following hematopoietic stem cell transplantation (SCT), we examined retrospectively 57 patients who underwent hematopoietic SCT in our institute from 1984 to 2000. Twelve (21%) of the patients showed an elevated level of serum pancreatic amylase following SCT. However, only 3 patients were clinically diagnosed as having acute pancreatitis. Among these 12 patients, 11 had undergone allogeneic transplantation. Furthermore, patients who had undergone unrelated transplantation (7/16; 44%) tended to show a higher incidence of increased amylase than those who had undergone related transplantation (4/24; 17%). Six patients were at an advanced stage of acute GVHD (grade III or IV) and all showed an elevated level of serum amylase, whereas only four patients showed an elevated serum amylase level among 34 with mild acute GVHD (grade I or II) or without GVHD. Furthermore, five out of 12 patients who showed an increased amylase level were concurrently diagnosed as having viral infection such as cytomegalovirus, adenovirus, or varicella zoster virus. We conclude that pancreatitis following SCT occurs more often than realized, and is mostly subclinical. This is closely associated with severe acute GVHD, and possibly viral infection.     

Pressure measurements from biliary and pancreatic segments of sphincter of oddi

Using a minimally compliant infusion system and a triple-lumen pressure recording catheter, we obtained endoscopic manometric measurements from both the common bile duct and pancreatic duct segments of the sphincter of Oddi (SO) in 58 patients. Fifteen patients (ages 27–69) had the diagnosis of functional abdominal pain, 19 patients (ages 30–76) had partial biliary obstruction, and 24 patients (ages 15–80) had idiopathic acute recurrent pancreatitis. Resting ductal pressure was similar in the common bile duct and pancreatic duct in all patient groups. In the group with functional pain, basal SO pressure was similar, whether obtained from the common bile duct or pancreatic duct sphincteric segment. Eight of 19 patients with partial biliary obstruction had elevated basal SO pressure. Five of these eight patients had elevated basal SO pressure confined exclusively to the common bile duct segment of the sphincter, while three patients had elevated basal SO in both segments. Conversely seven of 24 patients with acute recurrent pancreatitis had an elevated basal SO pressure, with five patients having pressure elevation only in the pancreatic duct segment while two patients had abnormal basal SO pressure in both segments. We conclude that selective cannulation of the common bile duct and/or the pancreatic duct during manometric study of the SO is necessary in order to diagnose segmental SO dysfunction responsible for partial biliary obstruction or episodes of acute recurrent pancreatitis.     

Celiac disease and recurrent pancreatitis

BACKGROUND: Celiac disease is associated with pancreatico-biliary disease. Postulated mechanisms include reduced gallbladder emptying due to impaired cholecystokinin release and pancreatitis due to malnutrition. We hypothesize that celiac disease may also be associated with pancreatico-biliary abnormalities due to duodenal inflammation and papillary stenosis. METHODS: Over a 48-month period, 169 patients referred for possible sphincter of Oddi dysfunction who underwent pancreatico-biliary manometry were tested for gliadin and endomysial antibodies. Duodenal and papillary biopsies were preformed in those patients who were positive. RESULTS: Celiac disease was diagnosed in 12 (7.1%; 3 men, 9 women). The mean age was 61 years as compared with 37 years for those patients without celiac disease. All of the celiac patients had been referred for recurrent abdominal pain and/or idiopathic pancreatitis. Ten had idiopathic recurrent pancreatitis with elevated amylase and lipase levels. Two of these patients also had mildly elevated liver function tests associated with the abdominal pain. Only 3 of 12 patients had a prior diagnosis of celiac disease. These 12 patients had manometric evidence of stenosis and histologic evidence of periampullary inflammation as well as histologic changes consistent with celiac disease. In 10 of 12 patients sphincterotomy or extension of a prior papillotomy was performed. Two patients were treated with a gluten-free diet alone. CONCLUSIONS: We describe 12 patients with papillary stenosis and celiac disease. In 9 cases the celiac disease was a new diagnosis. Celiac disease should be considered in the etiology of papillary stenosis or idiopathic recurrent pancreatitis.     

A novel assay for pancreatic cellular damage: IV. Serum concentrations of pancreas-specific protein (PASP) in acute pancreatitis and other abdominal diseases.

Pancreas-specific protein (PASP) was compared with serum amylase in 95 episodes of acute pancreatitis with the diagnoses supported by elevated amylase levels. The etiology was typical for Scandinavian countries, with alcohol as the predominant factor, followed by cholelithiasis. PASP values were clearly raised in all patients, except in three cases found to have high salivary-type amylase levels, and one patient with recurrent alcohol pancreatitis. The rise of PASP levels were in general more pronounced than the corresponding amylase elevations, especially in severe pancreatitis. The elevations were generally parallel for the two analytes, but in 41% of the cases PASP levels remained elevated 2-11 days longer than the corresponding amylase levels. PASP was, however, eliminated from the circulation at a rate comparable to that of amylase. The serum range of PASP for 259 healthy subjects was 15-111 micrograms/L with 95% of the values within 16-98 micrograms/L. The upper reference level was set at 100 micrograms/L. PASP levels were also determined for 291 patients with disorders other than acute pancreatitis. Serum levels in patients with renal insufficiency (n = 12), primary biliary cirrhosis (n = 9), and diabetes mellitus (n = 17) were equal to those in healthy subjects. Eight patients of 173 with acute abdominal disorders and no evidence of pancreatitis had elevated PASP levels as well as 4 patients with prostatic carcinoma (n = 28) and 2 patients with benign prostatic hyperplasia (n = 16). PASP values were low in chronic painful pancreatitis (n = 15) and pancreatic cancer (n = 11).     

39例Klinefelter综合征患者的糖尿病发生率和临床特点

目的评价Klinefelter综合征人群中MS、IGT和DM的发生率以及临床特点。方法采用横断面研究,对长期随诊的39例Klinefelter综合征患者的代谢状态、血糖水平、性激素水平进行总结,分析此特殊人群发生DM的可能高危因素,及其与核型之间的关系。结果（1）初诊时,Klinefelter综合征人群的MS发生率为30．8％,在睾酮替代治疗后（中位时间4年）发生率增加到38．5％。（2）Klinefelter综合征人群DM发生率为20．5％（8／39）,有4例在睾酮替代治疗前已经诊断为DM,另外4例在睾酮替代治疗的随访中确诊为DM。发生DM的年龄为（27．1±4．5）岁（20～55岁）,有4例（50％）患者需要胰岛素治疗,8例中有1例伴急性胰腺炎,有2例伴高TG血症。（3）Klinefelter综合征人群IGT发生率为7．7％。（4）长期随访发现,有9例患者体重明显增加,其中有2例进展为DM。结论（1）Klinefelter综合征患者的MS和DM发生率明显升高。（2）该人群DM发病年龄轻,血糖升高明显,多数需用胰岛素控制血糖。（3）染色体异常、睾酮水平降低、体重进行性增加、急性胰腺炎、高TG血症,是该人群糖代谢异常的重要危险因素。     

Recurrent pancreatitis secondary to hypercalcemia following vitamin D poisoning

A 66-year-old patient had been admitted four times for recurrent episodes of acute pancreatitis. At each time, elevated serum calcium levels, between 13.5-14.5 mg/dl, were found. Surgical drainage of necrotic pancreatic tissue had to be done on one occasion. Extensive investigations failed to disclose any conventional hypercalcemic disease. At his latest admission, the serum calcium level was 13.4 mg/dl, and the serum amylase level was 440 IU/L (N, less than 85). This time, the serum 25-OH vitamin D levels were investigated using radioimmunology and proved to be raised to 330 micrograms/L (normal, 16-74 micrograms/L). Specific questioning of the patient revealed that he had been taking regularly excessive quantities of vitamin supplements as a self medication. After stopping vitamin intake, his serum amylase levels returned to normal, and he had no more episodes of pancreatitis. This case illustrates vitamin D intoxication as a cause of recurrent pancreatitis. Measuring serum 25-OH vitamin D levels is advocated in pancreatitis associated with hypercalcemia of unclear origin.     

High serum levels of secretory immunoglobulin A in chronic pancreatitis

BACKGROUND AND AIM: Elevated levels of secretory immunoglobulin A have been reported in patients with cholestatic hepatitis. Secretory immunoglobulin A is present in the biliary and pancreatic tract. Chronic pancreatitis is a disease characterized by dilatation of Wirsung's duct. The aim of the study was to evaluate secretory immunoglobulin A levels in patients suffering from chronic pancreatitis. PATIENTS AND METHODS: The study population consisted of 66 consecutive chronic pancreatitis patients (55 male, 11 female; mean age 49.6+/-10 years), 26 patients suffering from acute recurrent pancreatitis (9 males, 17 females; mean age 39.6+/-10.6 years) and 90 healthy controls, pair-matched for sex and age with the chronic pancreatitis patients. Secretory immunoglobulin A was determined by enzyme-linked immunosorbent assay, as were serum alanine transaminase and GGT. RESULTS: Secretory immunoglobulin A levels were significantly higher in chronic pancreatitis patients (35+/-23.7 mg/l) than in those acute recurrent pancreatitis group (16.1+/- 7.9) and in healthy controls (11.8+/-4.9 mg/l) (p<0.0001). Secretory immunoglobulin A was significantly higher in chronic pancreatitis patients with steatorrhoea, diabetes and calcifications and in those undergoing pancreatic surgery. Of 61 chronic pancreatitis patients, 14 (23%) had pathological GGT. When only chronic pancreatitis patients with normal GGT levels were analysed, the differences in secretory immunoglobulin A levels between groups of patients and between chronic pancreatitis subgroups remained statistically significant. CONCLUSIONS: This study demonstrates that secretory immunoglobulin A is elevated in chronic pancreatitis. Its value in the staging of patients needs to be further evaluated.     

Proteomics analysis in 28 patients with systemic IgG4-related plasmacytic syndrome

It is considered that autoimmune pancreatitis (AIP), Mikulicz’s disease (MD) and IgG4-related tubulointerstitial nephritis (TIN) comprise systemic IgG4-related plasmacytic syndrome (SIPS), of which the origin remains unknown. We analyzed these patients with focus on serological aspects to invest whether there are autoantigens in SIPS. We evaluated 28 patients with SIPS who presented at Sapporo Medical University Hospital and the collaborated institutions. They were mainly middle-aged (eight male), and consisted of 26 patients with MD and two patients with AIP. The three among 26 patients diagnosed with MD were complicated to AIP, and another three patients had IgG4-related TIN. As a control, healthy volunteers and the patients with Sjögren’s syndrome were examined. At first, we measured the levels of serum complements and circulating immune complexes in these patients. Next, immune complexes were collected from the serum of patients and healthy controls by immunoprecipitation. They were divided into immunoglobulin and the antigens by glycine–HCl solution. The divided samples including the antigens were analyzed by surface-enhanced laser desorption/ionization-time of flight-mass spectrometry (SELDI-TOF-MS). Nine patients had hypocomplementemia and 15 had elevated levels of circulating immune complexes in the group of SIPS. In the groups of healthy volunteers and SS, all showed that the levels of serum complements and circulating immune complexes were normal. SELDI-TOF-MS detected a 13.1-kDa protein from all samples of SIPS, and not in normal control and SS. It is possible that the 13.1-kDa protein is one of the autoantigens of SIPS.     

Serum interleukin-6 and interleukin-10 in patients with acute pancreatitis: clinical implications

BACKGROUND/AIMS: Cytokines are assumed to play an important role in the pathogenesis of acute pancreatitis, but little is actually known. In this study, we assessed changes in the serum levels of interleukin-6 (IL-6), a proinflammatory cytokine, and interleukin-10 (IL-10), an anti-inflammatory cytokine, in patients with acute pancreatitis. METHODOLOGY: Serum levels of IL-6 and IL-10 were measured in 47 patients with acute pancreatitis and compared with their clinical and laboratory data. Changes of the serum levels of the two cytokines were studied in relation to the severity of acute pancreatitis. In addition, the changes of these cytokines after treatment of severe acute pancreatitis were assessed. RESULTS: 1) The serum IL-6 level showed a significant correlation with markers of the severity of acute pancreatitis, suggesting that IL-6 was a useful indicator of the severity of this disease. 2) The IL-10/IL-6 ratio was significantly lower in patients with severe acute pancreatitis, suggesting that a proinflammatory response was predominant in these patients. 3) The IL-10/IL-6 ratio of the patients with severe acute pancreatitis was significantly increased after treatment, especially in patients who received continuous regional arterial infusion of a protease inhibitor and antibiotics. CONCLUSIONS: The predominant pathological state of patients with severe acute pancreatitis may be altered from the systemic inflammatory response syndrome to the compensatory anti-inflammatory response syndrome by successful treatment.