Elevated Lipase Levels Research Articles

Neonatal hyperlipidemia with pancreatitis

Lipoprotein lipase (LPL) deficiency is an autosomal recessive metabolic disorder with varying presentation in infancy and childhood, whereas clinical manifestations are rare in neonatal period. The estimated prevalence is one in a million births. A 23-day-old baby was admitted with complaints of fever, vomiting, and lethargy. Blood sample drawn appeared lipemic. Lipemia retinalis was noted on funduscopic examination. Biochemical analysis revealed abnormal lipid profile with severe hypertriglyceridemia (10,300 mg/dL) and elevated serum lipase level (517 IU/L) indicative of LPL deficiency with acute pancreatitis. LPL deficiency was suspected and was confirmed by molecular genetic testing, which revealed a novel mutation in LPL gene. Dietary management and gemfibrozil were started following which serum triglyceride level decreased and serum lipase level normalized. The patient is following up regularly for growth and development monitoring.

A case of biliary atresia with pancreaticobiliary maljunction

BackgroundThe pathogenesis of biliary atresia (BA) is still unknown. There are several reports on the etiology of BA, including pancreaticobiliary maljunction (PBM). We experienced a case of Kasai type IIIa BA with PBM, in which we found elevation of pancreatic enzymes in the gallbladder. We evaluated whether PBM is related to the pathogenesis of BA based on our findings.Case presentationThe patient was born at 40 weeks of gestation. His body weight at birth was 2850 g. At the age of 4 days, he had an acholic stool and was referred to our hospital. Abdominal ultrasonography showed that triangular cord sign was negative. The gallbladder was isolated with a diameter of 19 mm, and it contracted in response to oral feeding. His ultrasonographic findings were atypical for BA, but his jaundice did not improve. Therefore, we performed an operation at the age of 56 days. Intraoperative cholangiography showed a common bile duct and pancreatic duct and a common channel patent, while the common hepatic duct or intrahepatic duct was not visualized. Bile in the gallbladder contained colorless fluid, which showed elevated lipase level (34,100 IU/L). We performed Kasai portoenterostomy under the diagnosis of Kasai type IIIa BA with PBM. The patient’s postoperative course was uneventful, and he was discharged on day 30 after the operation. Histopathological evaluation showed that the lumens of the common bile duct and cystic duct were patent. However, the common hepatic duct was closed, and only bile ductules with diameters of less than 50 μm were isolated. Infiltration of lymphocytes was detected in the porta hepatis. No apparent inflammation was observed around the cystic duct, which was constantly exposed to pancreatic juice because of reflux through PBM.ConclusionsReflux of pancreatic juice through PBM might not be an etiological factor for BA, but might be associated with patency of the common and cystic bile ducts in Kasai type IIIa BA.

Protective effects of tropisetron on cerulein-induced acute pancreatitis in mice

Acute pancreatitis (AP) causes morbidity and mortality. The aim of the present study was to investigate the protective effect of tropisetron against AP induced by cerulein.Cerulein (50μg/kg, 5 doses) was used to induce AP in mice. Six hours after final cerulein injection, animals were decapitated. Hepatic/pancreatic enzymes in the serum, pancreatic content of malondialdehyde (MDA), pro-inflammatory cytokines and myeloperoxidase (MPO) activity were measured.Tropisetron significantly attenuated pancreatic injury markers and decreased the amount of elevated serum amylase, lipase, alanine aminotransferase (ALT), aspartate aminotransferase (AST), MPO activities and pro-inflammatory cytokines levels caused by AP in mice. Tropisetron didn’t affect the pancreatic levels of MDA.Our results suggest that tropisetron could attenuate cerulein-induced AP by combating inflammatory signaling. Further clinical studies are needed to confirm its efficacy in patients with AP.

Pneumatosis Cystoides Intestinales and Portomesenteric Venous Gas following Anticholinesterase Pesticide Poisoning

Pneumatosis cystoides intestinalis and portomesenteric venous gas are uncommon radiological findings, but are found commonly in cases of bowel ischemia, or as a result of various non-ischemic conditions. A 72-year-old man visited an emergency center with altered mental status 2 hours after ingestion of an unknown pesticide. On physical examination, he showed the characteristic hydrocarbon or garlic-like odor, miotic pupils with no response to light, rhinorrhea, shallow respiration, bronchorrhea, and sweating over his face, chest and abdomen. Laboratory results revealed decreased serum cholinesterase, as well as elevated amylase and lipase level. We made the clinical diagnosis of organophosphate poisoning in this patient based on the clinical features, duration of symptoms and signs, and level of serum cholinesterase. Activated charcoal, fluid, and antidotes were administered after gastric lavage. A computerized tomography scan of the abdomen with intravenous contrast showed acute pancreatitis, poor enhancement of the small bowel, pneumatosis cystoides intestinalis, portomesenteric venous gas and ascites. Emergent laparotomy could not be performed because of his poor physical condition and refusal of treatment by his family. The possible mechanisms were believed to be direct intestinal mucosal damage by pancreatic enzymes and secondary mucosal disruption due to bowel ischemia caused by shock and the use of inotropics. Physicians should be warned about the possibility of pneumatosis cystoides intestinalis and portomesenteric venous gas as a complication of pancreatitis following anticholinesterase poisoning.

Pooled safety analyses of ALK-TKI inhibitor in ALK-positive NSCLC

BackgroundThe anaplastic lymphoma kinase tyrosine kinase inhibitors (ALK-TKIs) have been administered to patients with ALK-positive non-small cell lung cancer for a long period of time and show a promising response. However, the differences in the toxicity profiles among these drugs are still unclear.MethodsWe performed a comprehensive search of the MEDLINE, EMBASE, WEB OF SCIENCE and COCHRANE databases from the drugs’ inception to May 2016 to identify clinical trials. Severe adverse events (AEs) (grade ≥ 3) based on the ALK-TKI type were analysed.ResultsSeventeen trials published between 2011 and 2016, including a total of 1826 patients, were eligible for analysis. Patients in 10 trials (n = 1000) received crizotinib, patients in 5 trials (n = 601) received ceritinib and patients in 2 trials (n = 225) received alectinib. The overall frequencies of treatment-related death and AEs due to treatment withdrawal were 0.9% (12/1365) and 5.5% (85/1543), respectively. Moreover, the frequency of severe AEs in patients treated with ceritinib was significantly higher than patients treated with crizotinib or alectinib, especially for hepatotoxicity, fatigue and some of gastrointestinal symptoms. Additionally, significant difference in the elevated lipase and amylase levels (grade ≥ 3) were detected between ceritinib and crizotinib/alectinib, whereas neutropenia was less frequent.ConclusionsALK-TKIs were safe for ALK-positive patients. Moreover, statistically significant differences in some severe AEs among ceritinib, crizotinib and alectinib were detected in present study.

English

INTRODUCTION : Acute pancreatitis is one of the important causes of acute abdomen. The aim of the study is to analyse the etiologies, the varying clinical presentations and prognosis of acute pancreatitis and to validate the clinical, biochemical and radiological signs in diagnosing acute pancreatitis. METHODS : Total of sixty patients include both male and female of adult age group admitted in the emergency ward at Tirunelveli medical college hospital with the symptoms of acute pancreatitis and evaluation confirmed the presence of the illness, between February 2015 to August 2016. Severity assessment was based on clinical, biochemical and radiological findings. RESULTS : In this study of 60 patients, most of the patients were alcoholic (90%). Abdomen pain (100%) and abdomen distension (42%) were the most common complaints. From this study, we can conclude that most of the attacks of acute pancreatitis were milder forms. In one patient the CT abdomen showed normal pancreas associated with elevated serum amylase and lipase levels. Grades A and B accounted for more than 75% of the patients. Both CT grading and Ranson’s number are correlating directly with the severity of the disease. Total mortality was 8 out of 60 patients. All had Ranson’s score of 2 and 3. CONCLUSION : Serum amylase and lipase has only role in diagnosis of acute pancreatitis. Ranson’s scoring and CT scan play a very important role in both diagnosis and assessment of severity of the disease.

Acute Pancreatitis in Pregnancy: Maternal and Fetal Outcomes

ABSTRACT Aim and objective To evaluate the maternal and fetal outcomes in patients with acute pancreatitis. Materials and methods It is a retrospective observational study. A total of three patients were admitted with acute pancreatitis complicating pregnancy between January 2013 and June 2015 in the Department of Obstetrics and Gynaecology, M. S. Ramaiah Medical College and Hospital, Bengaluru, India, and were followed up until after delivery. Results Incidence of acute pancreatitis in our study was 1 in 1,620. Mean age was 24 years, and 33.3% were multiparous. Mean gestational age at onset was 33 weeks. One patient (33.3%) in our study had hypertriglyceridemia (870 mg/dL), and 66.7% of patients were idiopathic. The most common complaint was epigastric pain radiating to back. All patients showed leukocytosis and elevated amylase and lipase levels. Ultrasound showed [1] enlarged pancreas with decreased peripancreatic echogenicity and [2] pelvic and abdominal cavity effusions, in all the patients. All patients were managed conservatively in the intensive care unit. Mean duration of hospital stay was 7 days; 33.3% patients developed acute respiratory distress syndrome; 33.3% patients went into preterm spontaneous vaginal delivery. Cesarean section rate was 66.7%. Perinatal mortality was 33.3%. Conclusion Acute pancreatitis in pregnancy remains a challenging clinical problem to manage. The initial assessment, severity, and the initial management of the patient are of great importance in order to support the function and to prevent maternal and fetal mortality and morbidity. Clinical significance Acute pancreatitis either in its mild or its severe form causes maternal and fetal morbidity. However, these rates are declining due to early diagnosis and greater treatment options. Multidisciplinary approach leads to good maternal and fetal outcomes. How to cite this article Jyothi GS, Bhoosanoor SR, Swarup A. Acute Pancreatitis in Pregnancy: Maternal and Fetal Outcomes. J South Asian Feder Obst Gynae 2017;9(2):100-103.

Effects of insulin-induced hypoglycaemia on lipolysis rate, lipid oxidation and adipose tissue signalling in human volunteers: a randomised clinical study.

The aims of this study were to determine the role of lipolysis in hypoglycaemia and define the underlying intracellular mechanisms. Nine healthy volunteers were randomised to treatment order of three different treatments (crossover design). Treatments were: (1) saline control; (2) hyperinsulinaemic hypoglycaemia (HH; i.v. bolus of 0.1U/kg insulin); and (3) hyperinsulinaemic euglycaemia (HE; i.v. bolus of 0.1U/kg insulin and 20% glucose). Inclusion criteria were that volunteers were healthy, aged >18years, had a BMI between 19 and 26kg/m2, and provided both written and oral informed consent. Exclusion criteria were the presence of a known chronic disease (including diabetes mellitus, epilepsy, ischaemic heart disease and cardiac arrhythmias) and regular use of prescription medication. The data was collected at the medical research facilities at Aarhus University Hospital, Denmark. The primary outcome was palmitic acid flux. Participants were blinded to intervention order, but caregivers were not. Adrenaline (epinephrine) and glucagon concentrations were higher during HH than during both HE and control treatments. NEFA levels and lipid oxidation rates (determined by indirect calorimetry) returned to control levels after 105min. Palmitate flux was increased to control levels during HH (p = NS) and was more than twofold higher than during HE (overall mean difference between HH vs HE, 114 [95% CI 64, 165μmol/min]; p < 0.001). In subcutaneous adipose tissue biopsies, we found elevated levels of hormone-sensitive lipase (HSL) and perilipin-1 phosphorylation 30min after insulin injection during HH compared with both control and HE. There were no changes in the levels of adipose triglyceride lipase (ATGL), comparative gene identification-58 (CGI-58) or G0/G1 switch gene 2 (G0S2) proteins. Insulin-stimulated phosphorylation of Akt and mTOR were unaffected by hypoglycaemia. Expression of the G0S2 gene increased during HE and HH compared with control, without changes in ATGL (also known as PNPLA2) or CGI-58 (also known as ABHD5) mRNA levels. These findings suggest that NEFAs become a major fuel source during insulin-induced hypoglycaemia and that lipolysis may be an important component of the counter-regulatory response. These effects appear to be mediated by rapid stimulation of protein kinase A (PKA) and HSL, compatible with activation of the β-adrenergic catecholamine signalling pathway. ClinicalTrials.gov NCT01919788 FUNDING: : The study was funded by Aarhus University, the Novo Nordisk Foundation and the KETO Study Group/Danish Agency for Science Technology and Innovation (grant no. 0603-00479, to NM).

Salmonella Colitis as an Unusual Cause of Elevated Lipase

Salmonella infections are a reported, albeit uncommon, cause of acute pancreatitis. However, Salmonella may precipitate elevated serum lipase levels without other signs or symptoms of acute pancreatitis. The following is a case of Salmonella colitis with elevated serum lipase but without clinical pancreatitis. A 50 year old male presented with a one week history of watery, bloody bowel movements, nausea and vomiting associated with fevers, chills, and abdominal pain. Imaging showed diffuse small bowel and colonic thickening consistent with infectious colitis and stool cultures were found be positive for Salmonella enterica. He was treated with a course of Ciprofloxacin. Shortly after discharge, the patient returned to the ED with nausea and vomiting unrelated to oral intake. Though he had minimal abdominal pain, a serum lipase was measured and found to be elevated to 1929 and amylase elevated to 230. The patient denied any history of drinking and an abdominal ultrasound showed no evidence of gallstone pathology. A CT Abdomen/Pelvis showed a normal pancreas without any signs of inflammation. His nausea and vomiting abated without intervention and he was able to tolerate a regular diet. While an elevated serum lipase may typically confirm the diagnosis of acute pancreatitis, elevated lipase levels may also be seen in other disorders. For instance, elevated serum lipase levels have been reported in patients with infectious colitis without clinical pancreatitis, though this is exceedingly rare. In addition, one study demonstrated that serum lipase may be elevated in Salmonella colitis, but may not have clinical significance. This most significant elevation in lipase was seen in Salmonella enterica serovar typhimurium. There are several hypotheses for the enzyme elevations, including increased intestinal inflammation with increased permeability leading to an increase in reabsorption of lipase. There is also some evidence that Salmonella species are present in the bile fluid and gallstone cultures and may directly infect the pancreas via the biliary duct. Regardless of the pathophysiology, physicians need to be aware that elevations in serum lipase and amylase may not always be clinically significant and should note these alternative causes, including Salmonella infections.

Intraductal Papillary Mucinous Neoplasm of the Minor Pancreatic Duct in Pancreas Divisum: A Case Report

Intraductal papillary mucinous neoplasms (IPMN) are potentially malignant intraductal epithelial neoplasms that are composed of mucin-producing columnar cells. The lesions show papillary proliferation, cyst formation, and may involve the main pancreatic duct, the branch ducts, or both. IPMNs have varying degrees of malignant potential based on anatomic location, with main duct lesions progressing in 38-68% of cases. Therefore, surgical removal is indicated for these types of lesions. Most patients are asymptomatic and incidental diagnosis is made with advances in imaging and endoscopic procedures. Here we report a case of a 66-year-old male with a history of pancreas divisum and family history of pancreatic cancer who presented with pancreatitis. Initial symptoms were progressively worsening mid-epigastric pain with elevated amylase and lipase levels. After initial medical treatment for his pancreatitis, further evaluation with upper endoscopy showed a patulous minor papilla with a “fish eye” appearance that excreted mucin. Endoscopic ultrasound identified a markedly dilated pancreatic duct in addition to an anatomic variation called pancreas divisum. Subsequent ERCP with SpyGlass DS pancreatoscopy revealed a papillary lesion at the junction of the head and body of the pancreas. Biopsy confirmed the diagnosis of this main duct IPMN. Pancreatic divisum is an anatomic variant which results when the embryologic dorsal and ventral pancreatic ducts fail to fuse properly. Our background research revealed only a few reported cases of IPMN and pancreas divisum occurring in tandem. It has been noted that IPMN in the setting of pancreas divisum carries a higher rate of malignancy. Surgical intervention based on the Sendai and Fukuoka consensus is appropriate for IPMNs and is indicated in main duct IPMN in the setting of pancreas divisum, since these patients have better survival with surgical removal. This case emphasizes the need to appropriately evaluate patients presenting with pancreatitis, as there is a possibility of an underlying malignant process.

Recurrent Acute Pancreatitis Due to Hypertriglyceridemia Despite Apheresis

Hypertriglyceridemia (HTG) is the third cause of acute pancreatitis (AP) after gall stones and alcohol. HTG is estimated to cause 1-4% of AP cases. Disorders of lipoprotein metabolism are divided into primary and secondary which include diabetes and obesity. Serum triglyceride (TG) levels of 1,000 mg/dl or greater increases the risk of AP. The literature information about the treatment and follow-up of HTG pancreatitis (HTGP) is limited. We report a case of recurrent acute pancreatitis secondary to HTG that responded well to apheresis but the patient still experienced recurrent pancreatitis. A 39 year-old male with history of familial HTG with recurrent pancreatitis, diabetes and BMI of 27.08 kg/m2 presented with left upper quadrant abdominal pain radiating to the back. Review of systems was negative with no nausea, vomiting, fever or diarrhea. On presentation, he was found to have significantly elevated lipase level of 2650 U/L and TG level of 8762 mg/dL. CT abdomen showed AP (images). He underwent urgent apheresis with subsequent lowering of his TG level (table) that was associated with clinical improvement and normalization of his lipase levels. Few months after, he had recurrent AP with markedly elevated TG level that responded well to apheresis. The recognition of HTG as a cause of AP is often delayed or missed. Patients with HTGP commonly have recurrent attacks. The mechanism for HTGP is likely due to hydrolysis of TG by pancreatic lipase and release of free fatty acids that induce free radical damage. The treatment includes conventional treatment of AP, and management of serum TG levels with an initial goal of less than 500 mg/dL, maintenance of which was seen in multiple case series to expedite clinical improvement. Many small studies on HTGP management have evaluated the use of insulin, heparin or both. Multiple series have also recommended use of apheresis to reduce TG levels, but no randomized trials have compared the efficacy of apheresis with that of insulin and heparin with no definitive guidelines. Subsequent control of HTG with dietary restrictions, medications and regular apheresis have been shown to prevent future episodes of AP. The questions remain; what could have prevented our patient from having recurrence of AP, and should we consider regular apheresis in asymptomatic patients to decrease the recurrence risk? Development of a guideline in this area is dearly needed to improve patient care and reduce healthcare costs.Table 1Figure 1Figure 2

Tocilizumab-induced pancreatitis: case report and review of data from the FDA Adverse Event Reporting System

Tocilizumab (TCZ) is a humanized monoclonal antibody acting against the IL-6 receptor. It is a drug used in the treatment of rheumatoid arthritis and can be either given intravenously every 4 weeks or subcutaneously once a week. Known adverse events (AE) associated with TCZ include: infections of the upper respiratory tract, arterial hypertension, hypercholesterolaemia and hypertriglyceridaemia. Here, we present the first well-documented case of TCZ-induced acute pancreatitis (AP) and a systematic review of the literature including data from the Food and Drug Administration Adverse Event Reporting System (FAERS) database. Patient data collection was performed within the Berlin Case-Control Surveillance Study. A literature search for TCZ-induced AP was conducted. Analysis of the FAERS database concerning TCZ-associated pancreatic AE from the period of 2009 until the first quarter of 2013 was conducted. A 40-year-old man presented with a 2-day history of progressive upper abdominal pain with elevated serum lipase and triglyceride levels. Biliary pancreatitis was ruled out by abdominal sonography and CT scan. Cessation of intravenously administered TCZ resulted in improvement of the patient's condition and a decline in elevated laboratory values, suggesting a probable relationship between TCZ intake and AP. Analysis of the FAERS database retrieved 52 cases of TCZ-associated AP that accounted for 70% of all pancreatic AE in association with TCZ use. Further literature search detected three additional cases in which TCZ use was associated with AP. Physicians should be aware of the probable association between TCZ use and AP. Targeted post-authorization studies are needed to confirm and quantify the risk of TCZ-induced AP.

Origin, Presentation, and Clinical Course of Nonpancreatic Hyperlipasemia.

The diagnosis of acute pancreatitis (AP) is defined as a constellation of abnormal pancreatic enzymes, imaging, and characteristic pain. The origin and clinical significance of isolated hyperlipasemia is unclear. We prospectively evaluated patients with serum lipase level greater than 3 times the upper limit of normal (ULN) admitted to Los Angeles County Hospital from October 2014 to April 2015. Patients were identified by a daily laboratory query used to support an ongoing randomized trial of goal-directed therapy for AP (NCT 01761539). Nonpancreatic hyperlipasemia (NPHL) was defined as a serum lipase level greater than 3 times the ULN without characteristic pain or imaging. Among 221 patients with lipase level greater than 3 times the ULN, 170 met criterion for AP, and 51 did not. The leading etiologies for NPHL were decompensated cirrhosis and renal failure. Patients with NPHL were significantly older and had more comorbidities and lower serum lipase levels (360 ± 36 vs 1453 ± 135 IU/L, P < 0.001). There were no differences in length of hospitalization, intensive care unit admission, or mortality. Elevated serum lipase level has many nonpancreatic origins, with liver and renal failure being the most frequent. Distinct clinical features can help to differentiate between AP and NPHL.

Association Between the Pancreatic Enzyme Level and Organ Failure in Trauma Patients.

BackgroundThe literature suggests an association of pancreatic enzymes with systemic inflammation resulting in secondary organ injury and dysfunction following trauma. Elevation in serum enzymes may not always be predictive of pancreatic disease, and can reflect extra pancreatic production.ObjectivesThis study was conducted to evaluate the rise in serum pancreatic enzyme levels with the incidence of organ failure following trauma.Patients and MethodsA retrospective review was performed on critically injured patients from December 2009 to March 2010. Patient’s clinical demographics, routine laboratory investigations along with amylase and lipase levels were also extracted from the patients' records. Patients with pancreatic or duodenal injuries were excluded from the study.ResultsFrom a total of 296 patients (mean age, 31 years), 85% were males. Blunt injury was seen in 91.6% of the cases and 8.4% had penetrating injury. One hundred and fifty-three patients had single organ failure, 96 had multiple organ failure and 47 had no organ failure. There was a significant difference in lipase levels (P = 0.04), potassium levels (P = 0.05) and hemoglobin levels (P = -0.004), among the three patient groups. There was no significant difference in amylase levels among the three patient groups. The observed independent predictors of mortality included coagulopathy (OR = 1.7), Glasgow coma scale (OR = 1.1, 4.7), pulmonary failure (OR = 0.0004), hepatic failure (OR = 0.048), renal failure (OR = 5.5), organ failure (OR =149.8), lipase levels (OR = 1.3), and infection (OR = 3.0).ConclusionsThere was a significant correlation between elevated lipase levels and the incidence of multiple organ failure. Moreover, No significant association was found between the elevated amylase levels and organ failure. However, on admission, measurement of these enzymes coupled with routine laboratory investigations can be a powerful tool in the early detection of patients progressing towards organ failure.

Perfusion-CT--Can We Predict Acute Pancreatitis Outcome within the First 24 Hours from the Onset of Symptoms?

PurposeSevere acute pancreatitis (AP) is still a significant clinical problem which is associated with a highly mortality. The aim of this study was the evaluation of prognostic value of CT regional perfusion measurement performed on the first day of onset of symptoms of AP, in assessing the risk of developing severe form of acute pancreatitis.Material and Methods79 patients with clinical symptoms and biochemical criteria indicative of acute pancreatitis (acute upper abdominal pain, elevated levels of serum amylase and lipase) underwent perfusion CT within 24 hours after onset of symptoms. The follow-up examinations were performed after 4–6 days to detect progression of the disease. Perfusion parameters were compared in 41 people who developed severe form of AP (pancreatic and/or peripancreatic tissue necrosis) with parameters in 38 consecutive patients in whom course of AP was mild. Blood flow, blood volume, mean transit time and permeability surface area product were calculated in the three anatomic pancreatic subdivisions (head, body and tail). At the same time the patient's clinical status was assessed by APACHE II score and laboratory parameters such as CRP, serum lipase and amylase, AST, ALT, GGT, ALP and bilirubin were compared.ResultsStatistical differences in the perfusion parameters between the group of patients with mild and severe AP were shown. Blood flow, blood volume and mean transit time were significantly lower and permeability surface area product was significantly higher in patients who develop severe acute pancreatitis and presence of pancreatic and/or peripancreatic necrosis due to pancreatic ischemia. There were no statistically significant differences between the two groups in terms of evaluated on admission severity of pancreatitis assessed using APACHE II score and laboratory tests.ConclusionsCT perfusion is a very useful indicator for prediction and selection patients in early stages of acute pancreatitis who are at risk of developing pancreatic and/or peripancreatic necrosis already on the first day of the onset of symptoms and can be used for treatment planning and monitoring of therapy of acute pancreatitis. Early suspicion of possible pancreatic necrosis both on the basis of scores based on clinical status and laboratory tests have low predictive value.

Another cutaneous sign of acute pancreatitis.

Sir, A 45-year-old male who was a chronic alcoholic for 20 years was admitted in a state of shock. He had complaints of abdominal pain and vomiting for 10 days duration. There was history of constipation for 3 days. On examination, patient was semiconscious. Pulse rate and blood pressure was 112/min and 80/60 mmHg, respectively. Abdominal examination showed distended abdomen. On palpation, there was guarding and rigidity. On auscultation bowel sounds were absent. There was positive grey turner's sign (ecchymosis of flanks). Another new ecchymosis noted in the right axilla and was deep blue in color [Figure 1]. Figure 1 Ecchymosis noted in the right axilla which was deep blue in colour Investigations showed leukocytosis with elevated liver and renal function test. There was elevated amylase (890 U/L) and lipase (595 U/L) levels. Computed tomography of abdomen showed pancreatic necrosis with peripancreatic fluid collection and peripancreatic fat stranding [Figure 2]. He was diagnosed as acute necrotising pancreatitis. Aspirate negative for gram stain and culture and sensitivity. Hence, patient managed with intravenous fluid, proton pump inhibitor, octerotide infusion, and inotropic support. In due course, he developed desaturation and was intubated. His condition improved with above measures. Ecchymosis in the right axilla started to fade during recovery period. After 15 days, there was a complete disappearance of ecchymosis in the right axilla. Figure 2 Computed tomography of abdomen showed pancreatic necrosis with peripancreatic fluid collection and peripancreatic fat stranding A cutaneous manifestation of pancreatitis is very rare compared to abdominal signs. There are numerous cutaneous sign mentioned in pancreatitis. They are (1) Grey Turner's sign-ecchymosis of flanks, (2) Cullen's sign-ecchymosis around the umbilicus, (3) Fox's sign-ecchymosis of thigh, and (4) Bryant's sign-bluish discoloration of scrotum.[1] Causes of Grey Turner's sign and Cullen's sign includes acute pancreatitis, hemorrhagic pancreatitis, retroperitoneal hemorrhage, blunt abdominal trauma, ruptured ectopic pregnancy, spontaneous bleeding following coagulopathy, ruptured aortic aneurysm, ruptured common bile duct, perforated duodenal ulcer, ruptured hepatocellular carcinoma, hepatic lymphoma, Percutaneous liver biopsy, and rectus sheath hematoma.[2,3] Etiology of Cullen's sign includes formation of methemalbumin in subcutaneous plane due to digested blood around the abdomen from the inflamed pancreas and the blood likely diffuse via the falciform ligament to the subcutaneous tissue around the umbilicus.[4] Etiology of Grey Turner's sign is spread of the pancreatic inflammation from the anterior pararenal space between the posterior renal fascia and subsequently to the lateral edge of the quadrates lumborum muscle.[5] Discoloration of skin in Grey Turner's sign or Cullen's sign varies from blue, purple, green, and yellow color. In our case, there was an ecchymosis found the flanks (Grey Turner's sign) and one more ecchymosis found near the axilla. Axillary ecchymosis appeared as deep blue color. Etiology of ecchymosis in our case was probably due to formation of methemalbumin due to pancreatitis. Our patient had severe necrotising pancreatitis and developed systemic inflammatory response syndrome. Once patient recovered from pancreatitis, the lesion started to fade away. This ecchymosis over the axilla can help to diagnose pancreatitis early. It can also act as an indicator for severity of pancreatitis. It can be considered as a new sign in pancreatitis. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

A Study of Changes in Liver Function, Pancreatic Enzyme Levels, and Creatine Phosphokinase Level in Cases of Acute Organophosphorus Poisoning

Organophosphorus (OP) compounds are widely used insecticides in this part of the world. Organophosphorus compounds are responsible for a majority of suicidal attempt in India due to its easy availability. To determine the effect of organophosphorus compounds on hepatobiliary, pancreas, and muscular system and association of biochemical markers of respective systems to determine the outcome. This is a single-center, observational, prospective study conducted on 150 organophosphorus (OP) poisoning patients diagnosed clinically and with circumferential evidence. After admission, relevant biochemical markers of respective systems were done with standard guidelines. In patients where abnormality was found in serum amylase and lipase levels, ultrasonography and/or contrast-enhanced computed tomography evaluation of abdominal organs was done as per clinical indication. Among 150 patients, 17 (11.33%) patients succumbed to death. A significant association was observed between lipase level and treatment outcome. The odds ratio of death among high-level lipase group was 11.54 times higher than normal lipase group. Only four patients developed isolated creatine phosphokinase elevation with features suggestive of rhabdomyolysis. Isolated hepatic enzyme derangements found in only one case, whereas 5 patients had concurrent elevated lipase level. Organophosphorus-induced pancreatitis with or without hepatitis is often overlooked in acute poisoning which may be fatal. An early intervention often reverses this dreaded complication.

Origin, Presentation, and Clinical Course of Non-pancreatic Hyperlipasemia

Introduction: The diagnosis of acute pancreatitis is defined by fulfillment of 2 out of 3 criterion: serum lipase greater than three times the upper limit of normal (>3x ULN); abdominal pain consistent with acute pancreatitis; imaging consistent with acute pancreatitis. The origin and clinical significance of hyperlipasemia (3xULN) without abdominal pain or imaging abnormalities consistent with pancreatitis is unclear. Methods: We prospectively studied patients who had a serum lipase level > 3x ULN after being admitted to LA County Hospital from January 2014 to April 2015. They were identified by a daily laboratory query used to support an ongoing RCT of goal directed therapy for acute pancreatitis (NCT 01761539). Nonpancreatic hyperlipasemia was defined as patients with a serum lipase > 3x ULN but did not meet the other criterion for pancreatitis. Primary outcome was the etiology of the hyperlipasemia in this group. Secondary outcomes included comparisons between length of hospitalization, time to tolerance of enteral feeding, ICU admission and mortality between patients with pancreatitis and nonpancreatic hyperlipasemia. Baseline differences in demographic and biochemical parameters were also compared. Results: 221 patients presented with lipase > 3x ULN: 170 met criterion for acute pancreatitis and 51 did not. The leading etiologies for non-pancreatitis hyperlipasemia were decompensated cirrhosis and renal failure (Table 1). Patients with non-pancreatitis hyperlipasemia required less fluid (p < 0.001) and tolerated an oral diet after a shorter interval (p < 0.001) than those with acute pancreatitis. There was no difference in length of hospitalization, ICU admission, or mortality between the two groups. Non-pancreatitis hyperlipasemia patients were also significantly older and had more comorbidities (Charlson Index) (Table 2). In addition they presented with lower serum lipase levels (360 ± 36 vs 1453 ±135 IU/L, p < 0.001) but a higher BUN level (33.0 ± 5.5 vs 15.9 ± 1.0, p < 0.001) and creatinine (2.3 ± 0.7 vs 1.4 ± 0.4, p < 0.001).Table 1: Etiologies of Non-Pancreatitic HyperlipasemiaTable 2: Baseline Characteristics and Clinical Course of Pancreatitis versus Non-Pancreatitic HyperlipasemiaConclusion: Elevated serum lipase level has many non-pancreatic origins with liver and renal failure being most frequent. Patients with nonpancreatic hyperlipasemia generally have lower serum lipase levels and are usually older with more comorbidities than those with pancreatitis. These clinical features can help clinicians expeditiously distinguish between the two entities.Figure 1

Thinking Outside the Bowels: An Atypical Cause of Acute Abdominal Pain

Introduction: Isolated spontaneous celiac artery dissection is an extremely rare entity with its occurrence without aortic dissection even rarer. We report a case of isolated spontaneous celiac artery dissection in the absence of autoimmune disease. Case Presentation: A 48-year-old male with a past medical history of migraines presents with acute, severe, persistent epigastric pain with radiation to the left upper quadrant and left paraspinal area. Cross sectional imaging performed reveals celiac artery dissection (Figure 1) without signs of an underlying vasculitis. An extensive rheumatologic evaluation undertaken was unremarkable with the only laboratory abnormality being a mildly elevated lipase level. Given his concomitant history of headaches, a temporal artery biopsy obtained was unrevealing. Blood cultures and ECHO were unremarkable for signs of thromboembolic disease and abdominal pain did not resolve with empiric trial of systemic steroids. Interval CT angiogram 2 weeks after presentation reveals no change in dissection; at this juncture, a diagnosis of isolated spontaneous celiac artery dissection was made with anticoagulation commenced and resultant clinical and radiological improvement observed (Figure 1).Figure 1Conclusion: Isolated spontaneous celiac artery dissection is a rare phenomenon with the exact etiology and natural history to date remaining an enigma. Ideal treatment modalities still remain to be clearly defined with anticoagulation, stent placement, and surgery employed. Our case demonstrates the efficacy of medical management in such a rare condition.

Healthy Chinese with benign pancreatic hyperenzymemia

Benign pancreatic hyperenzymemia, or Gullo's syndrome, is an uncommon syndrome characterized by a long-term increase of serum pancreatic enzyme in the absence of pancreatic diseases. It is primarily discovered incidentally and occurs in either sporadic or familial form. Herein, we report the first case of benign pancreatic hyperenzymemia in Taiwan. A 57-year-old Chinese male was incidentally noted with elevated serum amylase and lipase levels during a health check-up and was diagnosed with benign pancreatic hyperenzymemia using a series of image and serological tests. Although this is the first case of benign pancreatic hyperenzymemia in Taiwan, its prevalence may be underestimated due to the diagnostic difficulties. Correct diagnosis of this disease is important to avoid costly test duplication, unfounded anxieties, and multiple consultations.