甘遂和低分子量肝素联合应用治疗重症急性胰腺炎的实验研究

目的 ： 探讨甘遂和低分子量肝素联合应用对重症急性胰腺炎治疗是否有协同作用。方法 ：分析比较假手术组（A组）、重症急性胰腺炎组（B组）、重症急性胰腺炎甘遂治疗组（C组）、重症急性胰腺炎低分子量肝素治疗组（D组）、重症急性胰腺炎甘遂和低分子量肝素联合治疗组（E组）各组血清TNF-α，IL-6水平和胰腺组织的TXB2/6-keto-PGF1α比值以及组织学检查结果。结果 ：C，D，E 3个治疗组血清TNF-α，IL-6水平和胰腺组织的TXB2/6-keto-PGF1α比值在6，12，24h各时点的值较B组低（ P <0.05或 P <0.01），而C，D，E 3个治疗组在各时间点无显著差异。组织学检查结果显示，A组胰腺的形态学正常;C，D，E 3组胰腺病理学改变轻于B组。结论 ：联合应用甘遂和低分子量肝素治疗SAP有效，但尚未发现甘遂和低分子量肝素的协同作用，亦未发现不利影响。     

乌司他丁对急性坏死性胰腺炎大鼠血清MIF的影响

目的：探讨乌司他丁对急性坏死性胰腺炎（ANP）大鼠血清巨噬细胞游走抑制因子（MIF）水平的影响。方法：健康Wister大鼠52只分为3组：正常对照组（C组,12只）、ANP组（A组,20只）和乌司他丁治疗组（U组,20只）。A组大鼠经十二指肠乳头逆行注射3.5%牛黄胆酸钠诱导构建ANP模型;U组同法诱导构建ANP模型后,经门静脉给予乌司他丁40000U/kg;C组开腹仅翻动胰腺和十二指肠。各组于术后3、6、12和24h分批处死大鼠,切取胰腺组织,采集下腔静脉血。对各组不同时点大鼠胰腺组织进行胰腺组织病理学评分,并测定血清淀粉酶和血清MIF水平。结果：A组各时点胰腺组织病理学评分及血清淀粉酶、血清MIF水平明显高于C组（P〈0.01）;U组各时点胰腺组织病理学评分、血清淀粉酶和血清MIF水平均低于A组（P〈0.05或P〈0.01）,A组血清MIF水平与胰腺组织病理学评分成正相关（r=0.513,P〈0.05）。结论：MIF可能在ANP的发病中发挥重要作用;乌司他丁下调MIF水平,从而减轻胰腺病理损伤,改善重症急性胰腺炎预后。     

肿瘤坏死因子α对重症急性胰腺炎低钙血症的影响及作用机制

我们通过检测重症急性胰腺炎大鼠血清肿瘤坏死因子α（TNF—α）、血钙水平及骨、肾组织甲状旁腺激素受体（PTHR）mRNA表达，同时观察抗肿瘤坏死因子α单克隆抗体（TNF—αMCAb）治疗后对血钙、血清TNF—α水平及骨、肾组织PTHR mRNA表达的影响，并探讨TNF—α在重症急性胰腺炎低钙血症发生中的作用机制。     

尿激酶区域动脉灌注对重症急性胰腺炎大鼠胰腺微循环的影响

目的探讨尿激酶区域动脉灌注（LAI）对重症急性胰腺炎（SAP）大鼠微循环的影响.方法将1 20只大鼠随机分成4组,每组40只.A组为假手术组（S组）;B组为SAP组;C组为SAP尿激酶LAI组;D组为SAP生理盐水LAI组（对照组）.以激光多普勒检测大鼠胰腺血流量,以伊文思蓝（Evans Blue）漏出率检测胰腺微循环血管的通透性,同时观察胰腺病理变化.结果（1）胰腺血流量（PBF）：A组1 h和3 h的胰腺PBF高于其他3组,差异有显著性（均P＜0.05）;B组1 h和3h的PBF与D组差异无显著性;C组1 h和3h的PBF明显高于B组和D组（P＜0.05）.（2）EB漏出率：B,C,D组胰腺组织EB的漏出率显著高于A组（均P＜0.05）,但B,C,D组之间无统计学差异（均P＞0.05）.（3）胰腺组织病理评分：术后1,3 h时,C组评分明显高于A组（P＜0.05）,但明显低于B,D组（均P＜0.05）,B,D组之间无明显差异（P＞0.05）.结论尿激酶LAI能改善SAP大鼠胰腺微循环,但不能完全阻止SAP的病理演变.     

血液透析患者甲状旁腺全切除加上臂移植术后低钙血症的防治

目的 观察因继发性甲状旁腺功能亢进症（secondary hyperparathyroidism,SHPT）进行甲状旁腺全切除加上臂移植术（total parathyroidectomy with upper arm autograft,TPTX＋AT）的血液透析患者,术后使用不同钙离子浓度的透析液行透析治疗低钙血症的效果,探讨如何更有效防治术后低钙血症.方法 选择2011年3月至2013年6月在我院接受TPTX＋AT的血液透析患者29例,按照手术时间的先后顺序进行编号,随机将偶数分在A组14例,奇数分在B组15例.术前B组补钙及骨化三醇;术后2组均予补钙及骨化三醇.A组使用钙浓度1.50 mmol/L透析液,B组使用钙浓度1.75 mmol/L高钙透析液.观察术后8 h、24 h、48 h、1周、2周及4周的血钙、血磷及甲状旁腺素（intact parathyroid hormone,iPTH）的变化,记录低钙血症的临床症状,术后达到治疗目标所需要的时间及静脉补钙量.结果 术后血钙、血磷、iPTH均明显下降.术后低钙血症主要表现四肢末端发麻,全身无力,焦虑、烦躁;少数患者表现为心悸、多汗、肌肉痉挛、四肢抽搐,血压低、腹痛或腹泻.A组低钙血症发生率为 85.7%（12/14）、B组为 73.3%（11/15）.术后1周B组血钙水平[（1.95±0.18）mmol/L]明显高于A组[（1.76±0.21）mmol/L].B组术后达到治疗目标所需要的时间为[（7.56±2.25）d],少于A组[（10.54±3.12）d];而B组所需静脉补钙量[（6.86±2.13）g]少于A组[（9.28±2.81）g],差异均有统计学意义（P＜0.05）.结论 并发SHPT的血液透析患者在TPTX＋AT术后常会出现低钙血症,术前、术后足量补充钙剂和骨化三醇,术后使用高钙透析液透析能更加有效防治低钙血症.     

肾素和血管紧张素Ⅱ在急性胰腺炎大鼠病程演变中的作用

目的：探讨肾素、血管紧张素Ⅱ在急性胰腺炎病程演变中的作用。方法：42只SD大鼠分急性胰腺炎组和对照组，对照组仅作胃窦切开缝合术，血管胰腺炎组用十二指肠闭襻法复制急性胰腺炎模型，结果：（1）急性胰腺炎组随着病变的进展，血浆淀粉酶升高，病程10h时胰腺炎病理呈水肿性改变，24h时呈出血坏死性改变；病程24h胰腺组织病理学评分显高于10h（P＜0．05）。（2）急性胰腺炎组血浆肾素活性在病程10h时显高于对照组（P＜0．01），在24h时略高于10h，但差别无统计学意义（P＞0．05）。（3）急性胰腺炎组血浆血管紧张素Ⅱ水平在病程10h,24h时均显高于对照组（P＜0．05，P＜0．01），24h又显高于10h（P＜0．05）。结论：肾素、血血管紧张素Ⅱ在急性胰腺炎病变发展中起重要作用。     

质子泵抑制剂对犬胰腺外分泌功能影响的研究

目的 探索质子泵抑制剂（proton pump inhibitor,PPI）对犬胰腺外分泌功能的影响。方法健康成年犬24只平均随机分成4组：对照组（A组）、对照给药组（B组）、胰腺炎组（C组）、胰腺炎给药组（D组）。A组和B组制备犬胰液外引流模型,C组和D组制备犬急性水肿型胰腺炎胰液外引流模型。采用5%牛磺胆酸钠（0.5 mL/kg）以1 mL/min胰管逆行注射制备急性水肿型胰腺炎模型。B组和D组建模成功后立即给予泮托拉唑（0.7 mg/kg+生理盐水50 mL,q12 h）,A组和C组给予等量的生理盐水。各组每12 h收集胰液一次,并测量胰液的分泌量,胰液中的淀粉酶、脂肪酶、总蛋白含量和pH值。胰腺组织送病理学和电镜检查。结果 B组与A组比较,胰液的分泌量,胰液中淀粉酶、脂肪酶的浓度和pH值在第1天和第2天均降低（P ＜0.05）。胰液中总蛋白的含量第1天B组和A组无明显统计学差异（P ＞0.05）,第2天B组低于A组（P ＜0.05）。D组与C组比较,胰液的分泌量,胰液中淀粉酶、脂肪酶、总蛋白的浓度和pH值无明显变化（P ＞0.05）。D组和C组在不同时间段的血淀粉酶、脂肪酶浓度无明显差别（P ＞0.05）。病理学检查未见明显的差别。电镜下可见PPI作用后胰腺腺泡细胞内酶原颗粒增多。结论 质子泵抑制剂能够明显抑制正常犬的胰腺外分泌,但对急性水肿型胰腺炎犬的胰腺外分泌功能影响不大。     

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目的 探讨甲状腺癌手术后低钙血症的发生发展规律及治疗方法。方法 对65例因甲状腺癌而做甲状腺全切除或近全切除的病人进行术后随访，动态监测血清钙，磷，镁的变化。结果 65例病人均出现不同程度的低钙血症，其中无症状低钙血症发生率为81．5％，术后不需静脉补钙治疗。有症状低钙血症的发生率为18．5％，需静脉补钙治疗，1例病人发生永久性甲状旁腺功能低下。有症状低钙血症组血清钙浓度在术后第1，2，3，5天较无症状低钙血症组血清钙浓度明显降低（P＜0．05）。有症状低钙血症组血清磷浓度在术后第2，3天较无症状低钙血症组血清磷浓度明显增高（P＜0．05）。结论 （1）有症状低钙血症发生在手术后3天之内，甲状腺癌手术后3天应常规监测血钙，血磷和血镁，血钙低于1.81mmol/L，高度警惕低钙症状出现。（2）有症状低钙血症病人经及时补充钙剂后，症状迅速改善，并往往在术后7天内消失。（3）血钙的高低与甲状旁腺的保留量，甲状旁腺素的浓度似乎无必然联系。     

川芎嗪和缬沙坦对大鼠胰腺炎治疗作用的实验研究

目的观察血栓素抑制剂川芎嗪（TMP）和血管紧张素-Ⅱ（AngⅡ）受体1特异性抑制剂缬沙坦对实验性大鼠胰腺炎模型的影响。方法通过十二指肠胆胰管逆行注射牛磺胆酸钠的方法制备大鼠胰腺炎模型,随机分为5组,模型对照组（A组）、急性胰腺炎组（B组）、川芎嗪治疗组（C组）、缬沙坦治疗组（D组）、川芎嗪加缬沙坦治疗组（E组）,在造模并应用药物6、12、24小时分别观察胰腺炎病理形态、并对腹水量、血清淀粉酶、脂肪酶、AngII和B2（TXB2）定量。结果胰腺炎模型顺利成功,E组的胰腺病理积分低于B、C、D组,而C、D组均低于B组;B组的腹水量、血清淀粉酶、脂肪酶、TXB2均明显高于C、D、E组,而血清AngⅡ量D组高于其他组,B组高于C、E组（P均小于0．05）。结论川芎嗪和缬沙坦均可单独改善大鼠胰腺炎的病理改变和实验室指标,二者合用似乎可起到协同作用。     

奥曲肽联合泮托拉唑预防内镜逆行胰胆管造影术后胰腺炎

目的：探讨内镜逆行胰胆管造影（ERCP）术后胰腺炎的预防措施。 方法：将2010年7月—2012年11月间行ERCP术后的患者100例,随机分为观察组和对照组,每组各50例患者。观察组术后给予联合应用生长抑素（奥曲肽0.1 mg/8 h皮下注射连用24 h）和质子泵抑制剂作预防治疗（泮托拉唑40 mg/d静脉滴注连用2 d）,对照组给予生理盐水静脉滴注。比较两组患者ERCP术后3,12,24 h的血清淀粉酶情况,及胰腺炎的发生情况。 结果：两组一般资料比较具有可比性;在术后3,12,24 h各时间点比较,观察组血清淀粉酶水平均明显低于对照组（均P<0.05）;观察组术后12,24 h高淀粉酶血症发生率及术后急性胰腺炎明显均低于对照组（18% vs. 42%;8% vs. 22%;2% vs. 16%）（均P<0.05）。 结论：联合应用生长抑素和质子泵抑制剂可减少ERCP术后高淀粉酶血症与胰腺炎的发生率,是一种安全且有效的ERCP术后胰腺炎预防措施。     

Role of creatine phosphokinase in predicting acute renal failure in hypocalcemic exertional heat stroke.

Recruits frequently develop hypocalcemia in exertional heat stroke (ExHS) with rhabdomyolysis and acute renal failure (ARF) from intensive training. It usually indicated severe skeletal muscle damage. However, the relative risk of ARF in ExHS patients complicated with hypocalcemia was unknown. The present study was undertaken to evaluate the value of peak serum creatine phosphokinase (CPK) level in predicting ARF in ExHS patients with hypocalcemia. Sixty-eight army recruits with ExHS were hospitalized at the Tri-Service General Hospital, Taiwan: 17 with ARF and hypocalcemia (group A); 7 with ARF but without hypocalcemia (group B); 20 without ARF but with hypocalcemia (group C); and 24 without ARF or hypocalcemia (group D). In the 24 patients with ARF (groups A and B) the serum phosphate and peak CPK levels were significantly higher than in patients without ARF (groups C and D; p < 0.001), serum calcium levels were also significantly lower in the former (p < 0.001). In the 37 patients with hypocalcemia (groups A and C), the peak serum CPK levels were significantly higher than in those without hypocalcemia (groups B and D; p < 0.001). There was a higher proportion of hypocalcemic patients with peak serum CPK levels greater than 10,000 U/l among ARF compared with patients without ARF (chi 2 = 12.48, p < 0.001). In 24 patients with ARF, there was a negative correlation between serum Ca and peak CPK levels (t = 3.37, r = -0.58, p < 0.01). However, a positive correlation was found between serum creatinine and peak serum CPK levels in 37 patients with hypocalcemia (t = 2.47, r = 0.39, p < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of N-acetylcysteine on acute necrotizing pancreatitis in rats

The aim of this study was to investigate the influence of N-acetylcysteine (NAC) on acute necrotizing pancreatitis (ANP) induced by glycodeoxycholic acid in rats. The induction of ANP resulted in significant increase in mortality rate, pancreatic necrosis and serum activity of amylase, alanine aspartate transferase (ALT), interleukin-6 (IL-6), lactate dehydrogenase (LDH) in bronchoalveolar lavage (BAL) fluid, serum concentration of urea, tissue activity of myeloperoxidase (MPO) and malondialdehyde (MDA) in the pancreas and lung, and significant decrease of concentrations of calcium, blood pressure, urine output and pO(2). The use of NAC inhibited the changes in urine output, pO(2), tissue activity of MPO and MDA in pancreas and lungs, and the serum activity of IL-6, ALT, and serum concentrations of urea and calcium. NAC reduced the mortality and pancreatic damage. The use of NAC has a beneficial effect on the course of ANP in rats. It may be used in the treatment of acute pancreatitis.     

Hyperbaric Oxygen and N-Acetylcysteine Treatment in L-Arginine-Induced Acute Pancreatitis in Rats

ABSTRACT

Background: This study was designed to evaluate the combined effects of hyperbaric oxygen (HBO) and N-acetylcysteine (NAC) on acute necrotizing pancreatitis in rats. Methods: Experiments were performed in 50 male Wistar rats, which were divided into five groups (N = 10 for each group). The first group received normal saline (0.9% NaCl) intraperitoneal and served as the control group. In the second group, acute pancreatitis was induced by 3.2-g/kg body weight L-arginine intraperitoneal twice at an interval of 1 hr, which has been shown previously to produce severe necrotizing acute pancreatitis. In the third group, NAC treatment (1000 mg/kg) was given after 1 hr of the induction of acute pancreatitis twice 24 hr apart. In the fourth group, animals received HBO, 6 hr after the induction of pancreatitis twice 12 hr apart. In the fifth group, animals received together NAC as in Group 3 and HBO treatment as in Group 4. Groups 1, 2, and 3 were left under normal atmospheric pressures. Twelve hours after last treatment, the animals were killed by exsanguinations. Blood samples were studied for amylase, calcium, and lactate dehydrogenase (LDH), pancreatic histology, pancreatic tissue malondialdehyde, superoxide dismutase, and glutathione levels. Results: Acute pancreatitis is reduced by the treatment of NAC, HBO, NAC + HBO. HBO + NAC groups performed statistically the best in preventing L-arginine-induced acute necrotising pancreatitis. Conclusions: NAC especially combined with HBO, decreases oxidative stress parameters, serum amylase, calcium, and LDH levels, as well as histopathologic score.     

急性胰腺炎大鼠TNF-α mRNA、IL-10 mRNA表达和胰腺细胞凋亡的研究

目的 探讨大鼠急性胰腺炎早期胰腺组织中TNF－αmRNA、IL－10mRNA的表达和细胞凋亡的变化规律。方法 以牛磺胆酸钠诱导20只大鼠急性水肿性胰腺炎（AEP）模型,20只急性坏死性胰腺炎（ANP）模型,另取10只正常大鼠作为对照。术后12h各处死10只大鼠,检测血清和胰腺组织中的TNF－α和IL－10水平,分析两者在胰腺组织中的mRNA较录水平,检测胰腺细胞的凋亡率。结果 正常、AEP和ANP组的细胞凋亡率分别为2．98％、17．29％和8．39％。制模后TNF－αm和IL－10增强ANP大鼠TNF－α表达增强。结论 急性胰腺炎大鼠胰腺组织中的TNF－α和IL－10的表达与其在血清和胰腺中的浓度成正比,胰腺本身可能就是产生细胞因子的主要器官。胰腺细胞凋亡率与疾病的严重程度呈负相关,凋亡是对胰腺损伤的良好反应。     

Effects of lazaroid U-74389G on acute necrotizing pancreatitis in rats

The aim of this study was to investigate the influence of U-74389G on acute necrotizing pancreatitis (ANP) induced by glycodeoxycholic acid in rats. The induction of ANP resulted in a significant increase in mortality rate, pancreatic necrosis, and serum levels of amylase, alanine aminotransferase, interleukin-6, tumor necrosis factor alpha, and urea, in lactate dehydrogenase levels in bronchoalveolar lavage fluid, and in the activities of myeloperoxidase and malondialdehyde in pancreas and lung tissue; a significant decrease was observed in serum calcium levels, blood pressure, urine output, and pO(2). The use of U-74389G inhibited the changes in serum urea, pO(2), and tissue levels of myeloperoxidase and malondialdehyde in pancreas and lungs. Moreover, it indicated a limited effect on the course of ANP in the rats and did not reduce mortality and pancreatic damage. Therefore, it may be used in the treatment of lung injury during acute pancreatitis.     

Serum calcium metabolism in acute experimental pancreatitis

Serum calcium changes in severe pancreatitis were studied in 23 dogs. Twelve dogs underwent duodenotomy and served as controls. Pancreatitis was induced in the other 11 by autologous bile injection (1 ml/kg) into the pancreatic duct. Serum amylase, total calcium, ionized calcium, albumin, magnesium, chloride, phosphorous, parathyroid hormone (PTH), and calcitonin were measured at 0, 1/2, 1, 3, 6, 24, 48, and 72 hours after duodenotomy or bile injection. Serum amylase levels became significantly elevated in all dogs with pancreatitis at 30 minutes (p less than 0.01) and remained so throughout the entire experiment. Total calcium levels dropped significantly 30 minutes after pancreatitis was induced from 10.0 +/- 0.3 mg/dl compared with 8.8 +/- 0.4 mg/dl in control dogs (p less than 0.05) and remained statistically lower for as long as 1 hour. Ionized calcium levels were significantly lower than were those of control dogs at 1/2, 1, 3, and 6 hours (p less than 0.05). Serum magnesium and chloride levels showed no significant changes between both groups. The only significant difference in phosphorus values was at 6 hours when they were higher in dogs with pancreatitis than in controls (6.2 +/- 0.3 mg/dl versus 4.8 +/- 0.4 mg/dl; p less than 0.05). Serum albumin levels remained unchanged throughout the study except for 48 hours when they were significantly lower in animals with pancreatitis (p less than 0.02). PTH levels were significantly greater in dogs with pancreatitis than in controls at 1, 3, 6, and 24 hours (p less than 0.05). There was no significant difference in calcitonin levels between both groups. Ionized calcium is a more reliable indicator of calcium fluxes in acute experimental pancreatitis since it remains depressed longer than total serum calcium. The time course of PTH elevation indicates a reaction to hypocalcemia, and failure of PTH secretion is not the cause of hypocalcemia in pancreatitis. This study does not support elevation of calcitonin as a cause of hypocalcemia in acute pancreatitis.     

Effects of dopexamine on acute necrotising pancreatitis in rats.

OBJECTIVE: To examine the effects of dopexamine on pancreatic tissue oxygen tension (PtO2) and the extent of acinar injury in rats with acute necrotising pancreatitis DESIGN: Laboratory study. SETTING: Medical school, Turkey. ANIMALS: 68 Sprague Dawley rats. MAIN OUTCOME MEASURES: Cardiorespiratory measurements, pancreatic PtO2, effects on activity of serum amylase and concentration trypsinogen activation peptide (TAP). and histological picture. RESULTS: The four study groups (sham + saline, sham + dopexamine, acute pancreatitis and acute pancreatitis + dopexamine) were each divided into two; in 9 rats in each, pancreatic biochemistry was studied, and in the remaining 8 in each group serum biochemistry and histology were studied. The groups were comparable with regard to mean arterial pressure, heart rate, arterial blood gases, packed cell volume, and serum amylase activity. The use of dopexamine increased pancreatic PtO2 in the sham + dopexamine group without the important blood pressure changes. The induction of pancreatitis resulted in a significant reduction in pancreatic PtO2 in the pancreatitis groups. The use of dopexamine did not increase pancreatic PtO2. There were no significant differences in plasma TAP concentration and the extent of acinar cell injury in the animals in the pancreatitis groups. CONCLUSION: Treatment with dopexamine does not improve the pancreatic microcirculation or reduce the extent of acinar cell injury in acute necrotising pancreatitis and is therefore unlikely to be of benefit in patients with pancreatitis.     

Reticuloendothelial system blockade promotes progression from mild to severe acute pancreatitis in the opossum

OBJECTIVE: To examine the relation between hepatic reticuloendothelial system (RES) dysfunction and the development of acute biliary pancreatitis. In an opossum model, the authors tested the hypothesis that RES blockade can turn the mild pancreatitis seen after pancreatic duct obstruction (PDO) into the severe form. SUMMARY BACKGROUND DATA: Biliary obstruction is considered the decisive event in gallstone pancreatitis. Suppression of the RES occurs during biliary obstruction. METHODS: Eighteen opossums were placed into three groups of six animals each: group A, RES blockade with lambda-carrageenan; group B, PDO; and group C, PDO and RES blockade with carrageenan. The severity of pancreatitis was evaluated by enzyme serum levels and percentage of pancreatic tissue necrosis. RES capacity was measured by dynamic liver scintigraphy, and hepatic blood flow was documented using the hydrogen clearance technique. RESULTS: No changes in hepatic blood flow occurred in groups A to C. RES capacity was suppressed in groups A and C; in group B, RES function remained unchanged. In group A, amylase and lipase levels remained normal, 3 +/- 1.9% of pancreatic tissue were necrotic. The animals in group B developed mild edematous pancreatitis with an increase in amylase and lipase levels and 15 +/- 10% of pancreatic necrosis. In group C, amylase and lipase increased significantly and histology revealed severe necrotizing pancreatitis, with 72 +/- 11% of necrotic areas. CONCLUSIONS: Artificial RES blockade can promote the progression from mild pancreatitis as observed after PDO to the severe necrotizing form of the disease. Thus, RES dysfunction resulting from biliary obstruction might be an important cofactor in the pathogenesis of bile-induced pancreatitis.     

Osteo-articular manifestations after suppurative pancreatitis

Osseous and joint manifestations (decalcification, osteolysis, osteonecrosis; poliarthrytis; periarticular fat necrosis) are sometimes encountered in chronic pancreatitis or carcinoma, but exceptional after severe acute pancreatitis, especially infected pancreatic necrosis. Pathogenesis of calcium deficiency in acute pancreatitis is multifactorial, including extensive lipolysis and metabolic disturbances. We report on a healthy, young male, that developed decalcification and polyarthritis consecutive to a long-outcome, severe acute pancreatitis. We comment upon hypocalcemia, as a rare complication of acute pancreatitis.