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Pancreatitis

MedGen UID:
14586
Concept ID:
C0030305
Disease or Syndrome
Synonyms: Pancreatic inflammation
SNOMED CT: Pancreatitis (75694006); Inflammation of pancreas (75694006)
 
HPO: HP:0001733

Definition

INFLAMMATION of the PANCREAS. Pancreatitis is classified as acute unless there are computed tomographic or endoscopic retrograde cholangiopancreatographic findings of CHRONIC PANCREATITIS (International Symposium on Acute Pancreatitis, Atlanta, 1992). The two most common forms of acute pancreatitis are ALCOHOLIC PANCREATITIS and gallstone pancreatitis. [from MeSH]

Conditions with this feature

Cholecystitis
MedGen UID:
920
Concept ID:
C0008325
Disease or Syndrome
In general, gallbladder disease (GBD) is one of the major digestive diseases. GBD prevalence is particularly high in some minority populations in the United States, including Native and Mexican Americans. Gallstones composed of cholesterol (cholelithiasis) are the common manifestations of GBD in western countries, including the United States. Most people with gallstones remain asymptomatic through their lifetimes; however, it is estimated that approximately 10 to 50% of individuals eventually develop symptoms. Significant risk factors associated with GBD are age, female sex, obesity (especially central obesity), lipids, diet, parity, type 2 diabetes (125853), medications, and Mexican American ethnicity. GBD appears to be strongly related to the metabolic syndrome (605552) and/or its major components, such as hyperinsulinism, dyslipidemia, and abdominal adiposity (Boland et al., 2002; Tsai et al., 2004). Infection, specifically by Helicobacter, has been implicated in cholelithiasis and cholecystitis (Silva et al., 2003; Maurer et al., 2005). Low phospholipid-associated cholelithiasis is a specific form of gallbladder disease characterized by young-adult onset of chronic cholestasis with intrahepatic sludge and cholesterol cholelithiasis. Affected individuals have recurrence of the disorder after cholecystectomy and show a favorable response to treatment with ursodeoxycholic acid (UDCA) (summary by Pasmant et al., 2012). Mutation in the ABCB4 gene can cause a spectrum of related diseases, including the more severe progressive familial intrahepatic cholestasis-3 (PFIC3; 602347), intrahepatic cholestasis of pregnancy-3 (ICP3; 614972), andoral contraceptive-induced cholestasis (OCIC; see 614972). Genetic Heterogeneity of Gallbladder Disease Two major susceptibility loci for symptomatic gallbladder disease have been identified on chromosome 1p in Mexican Americans (GBD2, 609918; GBD3, 609919). In addition, variations in the ABCG8 gene (605460) on chromosome 2p21 confer susceptibility to gallbladder disease (GBD4; 611465).
Glycogen storage disease, type I
MedGen UID:
6640
Concept ID:
C0017920
Disease or Syndrome
Glycogen storage disease type I (GSDI) is characterized by accumulation of glycogen and fat in the liver and kidneys, resulting in hepatomegaly and renomegaly. The two subtypes (GSDIa and GSDIb) are clinically indistinguishable. Some untreated neonates present with severe hypoglycemia; more commonly, however, untreated infants present at age three to four months with hepatomegaly, lactic acidosis, hyperuricemia, hyperlipidemia, hypertriglyceridemia, and/or hypoglycemic seizures. Affected children typically have doll-like faces with fat cheeks, relatively thin extremities, short stature, and protuberant abdomen. Xanthoma and diarrhea may be present. Impaired platelet function can lead to a bleeding tendency with frequent epistaxis. Untreated GSDIb is associated with impaired neutrophil and monocyte function as well as chronic neutropenia after the first few years of life, all of which result in recurrent bacterial infections and oral and intestinal mucosal ulcers. Long-term complications of untreated GSDI include growth retardation resulting in short stature, osteoporosis, delayed puberty, gout, renal disease, pulmonary hypertension, hepatic adenomas with potential for malignant transformation, polycystic ovaries, pancreatitis, and changes in brain function. Normal growth and puberty is expected in treated children. Most affected individuals live into adulthood.
Hyperlipoproteinemia, type I
MedGen UID:
7352
Concept ID:
C0023817
Disease or Syndrome
Familial lipoprotein lipase (LPL) deficiency usually presents in childhood and is characterized by very severe hypertriglyceridemia with episodes of abdominal pain, recurrent acute pancreatitis, eruptive cutaneous xanthomata, and hepatosplenomegaly. Clearance of chylomicrons from the plasma is impaired, causing triglycerides to accumulate in plasma and the plasma to have a milky (lactescent or lipemic) appearance. Symptoms usually resolve with restriction of total dietary fat to =20 g/day.
Maple syrup urine disease
MedGen UID:
6217
Concept ID:
C0024776
Disease or Syndrome
Maple syrup urine disease (MSUD) is classified as classic or intermediate. Twelve hours after birth, untreated neonates with classic MSUD have a maple syrup odor in cerumen; by 12-24 hours, elevated plasma concentrations of branched-chain amino acids (BCAAs) (leucine, isoleucine, and valine) and allo-isoleucine, as well as a generalized disturbance of plasma amino acid concentration ratios; by age two to three days, ketonuria, irritability, and poor feeding; by age four to five days, deepening encephalopathy manifesting as lethargy, intermittent apnea, opisthotonus, and stereotyped movements such as "fencing" and "bicycling." By age seven to ten days, coma and central respiratory failure may supervene. Individuals with intermediate MSUD have partial BCKAD enzyme deficiency that only manifests intermittently or responds to dietary thiamine therapy; these individuals can experience severe metabolic intoxication and encephalopathy during sufficient catabolic stress.
Hereditary pancreatitis
MedGen UID:
116056
Concept ID:
C0238339
Disease or Syndrome
A disorder characterized by recurrent episodes of pancreatitis that start at a young age. It is caused by mutations in the PRSS1 or SPINK1 genes. Patients are at a high risk of developing pancreatic carcinoma.
Glucose-6-phosphate transport defect
MedGen UID:
78644
Concept ID:
C0268146
Disease or Syndrome
Glycogen storage disease type I (GSDI) is characterized by accumulation of glycogen and fat in the liver and kidneys, resulting in hepatomegaly and renomegaly. The two subtypes (GSDIa and GSDIb) are clinically indistinguishable. Some untreated neonates present with severe hypoglycemia; more commonly, however, untreated infants present at age three to four months with hepatomegaly, lactic acidosis, hyperuricemia, hyperlipidemia, hypertriglyceridemia, and/or hypoglycemic seizures. Affected children typically have doll-like faces with fat cheeks, relatively thin extremities, short stature, and protuberant abdomen. Xanthoma and diarrhea may be present. Impaired platelet function can lead to a bleeding tendency with frequent epistaxis. Untreated GSDIb is associated with impaired neutrophil and monocyte function as well as chronic neutropenia after the first few years of life, all of which result in recurrent bacterial infections and oral and intestinal mucosal ulcers. Long-term complications of untreated GSDI include growth retardation resulting in short stature, osteoporosis, delayed puberty, gout, renal disease, pulmonary hypertension, hepatic adenomas with potential for malignant transformation, polycystic ovaries, pancreatitis, and changes in brain function. Normal growth and puberty is expected in treated children. Most affected individuals live into adulthood.
Propionic acidemia
MedGen UID:
75694
Concept ID:
C0268579
Disease or Syndrome
The spectrum of propionic acidemia (PA) ranges from neonatal-onset to late-onset disease. Neonatal-onset PA, the most common form, is characterized by a healthy newborn with poor feeding and decreased arousal in the first few days of life, followed by progressive encephalopathy of unexplained origin. Without prompt diagnosis and management, this is followed by progressive encephalopathy manifesting as lethargy, seizures, or coma that can result in death. It is frequently accompanied by metabolic acidosis with anion gap, lactic acidosis, ketonuria, hypoglycemia, hyperammonemia, and cytopenias. Individuals with late-onset PA may remain asymptomatic and suffer a metabolic crisis under catabolic stress (e.g., illness, surgery, fasting) or may experience a more insidious onset with the development of multiorgan complications including vomiting, protein intolerance, failure to thrive, hypotonia, developmental delays or regression, movement disorders, or cardiomyopathy. Isolated cardiomyopathy can be observed on rare occasion in the absence of clinical metabolic decompensation or neurocognitive deficits. Manifestations of neonatal and late-onset PA over time can include growth impairment, intellectual disability, seizures, basal ganglia lesions, pancreatitis, and cardiomyopathy. Other rarely reported complications include optic atrophy, hearing loss, premature ovarian insufficiency, and chronic renal failure.
Lysinuric protein intolerance
MedGen UID:
75704
Concept ID:
C0268647
Disease or Syndrome
Lysinuric protein intolerance (LPI) typically presents after an infant is weaned; variable findings include recurrent vomiting and episodes of diarrhea, episodes of stupor and coma after a protein-rich meal, poor feeding, aversion to protein-rich food, failure to thrive, hepatosplenomegaly, and muscular hypotonia. Over time, findings include: poor growth; osteoporosis; involvement of the lungs (progressive interstitial changes; pulmonary alveolar proteinosis) and of kidneys (progressive glomerular and proximal tubular disease); hematologic abnormalities (normochromic or hypochromic anemia, leukopenia, thrombocytopenia, erythroblastophagocytosis at the bone marrow aspirate) and a clinical presentation resembling the hemophagocytic lymphohistiocytosis/macrophagic activation syndrome. Acute pancreatitis can also be seen.
Apolipoprotein C2 deficiency
MedGen UID:
328375
Concept ID:
C1720779
Disease or Syndrome
Hypocalciuric hypercalcemia, familial, type 1
MedGen UID:
369200
Concept ID:
C1809471
Disease or Syndrome
Familial hypocalciuric hypercalcemia (HHC) is a heritable disorder of mineral homeostasis that is transmitted as an autosomal dominant trait with a high degree of penetrance. HHC is characterized biochemically by lifelong elevation of serum calcium concentrations and is associated with inappropriately low urinary calcium excretion and a normal or mildly elevated circulating parathyroid hormone (PTH; 168450) level. Hypermagnesemia is typically present. Individuals with HHC are usually asymptomatic and the disorder is considered benign. However, chondrocalcinosis and pancreatitis occur in some adults (summary by Hannan et al., 2010). Genetic Heterogeneity of Hypocalciuric Hypercalcemia Familial hypocalciuric hypercalcemia type II (HHC2; 145981) is caused by mutation in the GNA11 gene (139313) on chromosome 19p13, and HHC3 (600740) is caused by mutation in the AP2S1 gene (602242) on chromosome 19q13.
Hypocalciuric hypercalcemia, familial, type III
MedGen UID:
322173
Concept ID:
C1833372
Disease or Syndrome
Visceral myopathy
MedGen UID:
331900
Concept ID:
C1835084
Disease or Syndrome
Familial visceral myopathy is a rare inherited form of myopathic pseudoobstruction, characterized by impaired function of enteric smooth muscle cells resulting in abnormal intestinal mobility, severe abdominal pain, malnutrition, and even death (Lehtonen et al., 2012). Visceral myopathy represents a phenotypic spectrum of disease characterized by inter- and intrafamilial variability, in which the most severely affected patients exhibit prenatal bladder enlargement, intestinal malrotation, neonatal functional gastrointestinal obstruction, and chronic dependence on total parenteral nutrition (TPN) and urinary catheterization (summary by Wangler et al., 2014). Another form of visceral myopathy with functional gastrointestinal obstruction is associated with external ophthalmoplegia (277320). Functional gastrointestinal obstruction also occurs in association with other abnormalities, such as 'prune belly' syndrome (100100) and Barrett esophagus (Mungan syndrome; 611376). Chronic intestinal pseudoobstruction can also be neuropathic in origin (see 609629).
Hypocalciuric hypercalcemia, familial, type II
MedGen UID:
374447
Concept ID:
C1840347
Disease or Syndrome
Partial lipodystrophy, congenital cataracts, and neurodegeneration syndrome
MedGen UID:
339794
Concept ID:
C1847582
Disease or Syndrome
Pancreatitis, sclerosing cholangitis, and sicca complex
MedGen UID:
340461
Concept ID:
C1850080
Disease or Syndrome
Methylmalonic aciduria due to methylmalonyl-CoA mutase deficiency
MedGen UID:
344424
Concept ID:
C1855114
Disease or Syndrome
Isolated methylmalonic acidemia/aciduria, the topic of this GeneReview, is caused by complete or partial deficiency of the enzyme methylmalonyl-CoA mutase (mut(0) enzymatic subtype or mut(–) enzymatic subtype, respectively), a defect in the transport or synthesis of its cofactor, adenosyl-cobalamin (cblA, cblB, or cblD-MMA), or deficiency of the enzyme methylmalonyl-CoA epimerase. Onset of the manifestations of isolated methylmalonic acidemia/aciduria ranges from the neonatal period to adulthood. All phenotypes are characterized by periods of relative health and intermittent metabolic decompensation, usually associated with intercurrent infections and stress. In the neonatal period the disease can present with lethargy, vomiting, hypotonia, hypothermia, respiratory distress, severe ketoacidosis, hyperammonemia, neutropenia, and thrombocytopenia and can result in death within the first four weeks of life. In the infantile/non-B12-responsive phenotype, infants are normal at birth, but develop lethargy, vomiting, dehydration, failure to thrive, hepatomegaly, hypotonia, and encephalopathy within a few weeks to months of age. An intermediate B12-responsive phenotype can occasionally be observed in neonates, but is usually observed in the first months or years of life; affected children exhibit anorexia, failure to thrive, hypotonia, and developmental delay, and sometimes have protein aversion and/or vomiting and lethargy after protein intake. Atypical and "benign"/adult methylmalonic acidemia phenotypes are associated with increased, albeit mild, urinary excretion of methylmalonate. Major secondary complications of methylmalonic acidemia include: intellectual impairment (variable); tubulointerstitial nephritis with progressive renal failure; “metabolic stroke” (acute and chronic basal ganglia injury) causing a disabling movement disorder with choreoathetosis, dystonia, and para/quadriparesis; pancreatitis; growth failure; functional immune impairment; and optic nerve atrophy.
Cholestasis, benign recurrent intrahepatic 1
MedGen UID:
383756
Concept ID:
C1855731
ATP8B1 deficiency encompasses a phenotypic spectrum ranging from severe to intermediate to mild, based on an individual’s clinical findings and laboratory test results, including liver biopsy. Severe ATP8B1 deficiency is characterized by onset of symptoms of cholestasis (pruritus and attacks of jaundice) within the first few months of life. Secondary manifestations such as coagulopathy (due to vitamin K deficiency), malabsorption, and poor weight gain may present earlier than age three months. Without surgical intervention, cirrhosis and evolution to end-stage hepatic failure and death usually ensue before the third decade. Mild ATP8B1 deficiency is characterized by intermittent episodes of cholestasis manifest as severe pruritus and jaundice; chronic liver damage does not typically develop. In contrast to patients in whom bouts of cholestasis are induced only by particular triggers known to increase risk of cholestasis (drug exposure, shifts in hormonal milieu [including those resulting from ingestion of contraceptive drugs or from pregnancy], coexistent malignancy), some or all bouts of cholestasis in individuals with mild ATP8B1 deficiency have different or unknown triggers.
Citrullinemia type II
MedGen UID:
350276
Concept ID:
C1863844
Disease or Syndrome
Citrin deficiency can manifest in newborns or infants as neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD), in older children as failure to thrive and dyslipidemia caused by citrin deficiency (FTTDCD), and in adults as recurrent hyperammonemia with neuropsychiatric symptoms in citrullinemia type II (CTLN2). Often citrin deficiency is characterized by strong preference for protein-rich and/or lipid-rich foods and aversion to carbohydrate-rich foods. NICCD. Children younger than age one year have a history of low birth weight with growth restriction and transient intrahepatic cholestasis, hepatomegaly, diffuse fatty liver, and parenchymal cellular infiltration associated with hepatic fibrosis, variable liver dysfunction, hypoproteinemia, decreased coagulation factors, hemolytic anemia, and/or hypoglycemia. NICCD is generally not severe and symptoms often resolve by age one year with appropriate treatment, although liver transplantation has been required in rare instances. FTTDCD. Beyond age one year, many children with citrin deficiency develop a protein-rich and/or lipid-rich food preference and aversion to carbohydrate-rich foods. Clinical abnormalities may include growth restriction, hypoglycemia, pancreatitis, severe fatigue, anorexia, and impaired quality of life. Laboratory changes are dyslipidemia, increased lactate-to-pyruvate ratio, higher levels of urinary oxidative stress markers, and considerable deviation in tricarboxylic acid (TCA) cycle metabolites. One or more decades later, some individuals with NICCD or FTTDCD develop CTLN2. CTLN2. Presentation is sudden and usually between ages 20 and 50 years. Manifestations are recurrent hyperammonemia with neuropsychiatric symptoms including nocturnal delirium, aggression, irritability, hyperactivity, delusions, disorientation, restlessness, drowsiness, loss of memory, flapping tremor, convulsive seizures, and coma. Symptoms are often provoked by alcohol and sugar intake, medication, and/or surgery. Affected individuals may or may not have a prior history of NICCD or FTTDCD.
Homocystinuria due to CBS deficiency
MedGen UID:
461694
Concept ID:
C3150344
Disease or Syndrome
Homocystinuria caused by cystathionine ß-synthase (CBS) deficiency is characterized by involvement of the eye (ectopia lentis and/or severe myopia), skeletal system (excessive height, long limbs, scolioisis, and pectus excavatum), vascular system (thromboembolism), and CNS (developmental delay/intellectual disability). All four ? or only one ? of the systems can be involved; expressivity is variable for all of the clinical signs. It is not unusual for a previously asymptomatic individual to present in adult years with only a thromboembolic event that is often cerebrovascular. Two phenotypic variants are recognized, B6-responsive homocystinuria and B6-non-responsive homocystinuria. B6-responsive homocystinuria is usually milder than the non-responsive variant. Thromboembolism is the major cause of early death and morbidity. IQ in individuals with untreated homocystinuria ranges widely, from 10 to 138. In B6-responsive individuals the mean IQ is 79 versus 57 for those who are B6-non-responsive. Other features that may occur include: seizures, psychiatric problems, extrapyramidal signs (e.g., dystonia), hypopigmentation of the skin and hair, malar flush, livedo reticularis, and pancreatitis.
Retinitis pigmentosa 71
MedGen UID:
897209
Concept ID:
C4225342
Disease or Syndrome

Recent clinical studies

Etiology

Jalaly NY, Moran RA, Fargahi F, Khashab MA, Kamal A, Lennon AM, Walsh C, Makary MA, Whitcomb DC, Yadav D, Cebotaru L, Singh VK
Am J Gastroenterol 2017 Aug;112(8):1320-1329. Epub 2017 Apr 25 doi: 10.1038/ajg.2017.106. PMID: 28440306
Liu T, Huang W, Szatmary P, Abrams ST, Alhamdi Y, Lin Z, Greenhalf W, Wang G, Sutton R, Toh CH
Br J Surg 2017 Aug;104(9):1215-1225. Epub 2017 Apr 24 doi: 10.1002/bjs.10538. PMID: 28436602
Majumder S, Takahashi N, Chari ST
Dig Dis Sci 2017 Jul;62(7):1762-1769. Epub 2017 Apr 1 doi: 10.1007/s10620-017-4541-y. PMID: 28365915
Machicado JD, Yadav D
Dig Dis Sci 2017 Jul;62(7):1683-1691. Epub 2017 Mar 9 doi: 10.1007/s10620-017-4510-5. PMID: 28281168Free PMC Article
da Costa DW, Dijksman LM, Bouwense SA, Schepers NJ, Besselink MG, van Santvoort HC, Boerma D, Gooszen HG, Dijkgraaf MG; Dutch Pancreatitis Study Group.
Br J Surg 2016 Nov;103(12):1695-1703. Epub 2016 Aug 12 doi: 10.1002/bjs.10222. PMID: 27517163

Diagnosis

Sharma A, Masood U, Khan B, Chawla K, Manocha D
Am J Emerg Med 2017 Sep;35(9):1387.e3-1387.e4. Epub 2017 Jul 5 doi: 10.1016/j.ajem.2017.07.014. PMID: 28689859
Jalaly NY, Moran RA, Fargahi F, Khashab MA, Kamal A, Lennon AM, Walsh C, Makary MA, Whitcomb DC, Yadav D, Cebotaru L, Singh VK
Am J Gastroenterol 2017 Aug;112(8):1320-1329. Epub 2017 Apr 25 doi: 10.1038/ajg.2017.106. PMID: 28440306
Liu T, Huang W, Szatmary P, Abrams ST, Alhamdi Y, Lin Z, Greenhalf W, Wang G, Sutton R, Toh CH
Br J Surg 2017 Aug;104(9):1215-1225. Epub 2017 Apr 24 doi: 10.1002/bjs.10538. PMID: 28436602
Roggenbuck D, Goihl A, Hanack K, Holzlöhner P, Hentschel C, Veiczi M, Schierack P, Reinhold D, Schulz HU
Clin Chem Lab Med 2017 May 1;55(6):854-864. doi: 10.1515/cclm-2016-0797. PMID: 27837595
Mikolasevic I, Orlic L, Poropat G, Jakopcic I, Stimac D, Klanac A, Carovic F, Milic S
Eur J Intern Med 2017 Mar;38:73-78. Epub 2016 Nov 5 doi: 10.1016/j.ejim.2016.10.019. PMID: 27825671

Therapy

Majumder S, Takahashi N, Chari ST
Dig Dis Sci 2017 Jul;62(7):1762-1769. Epub 2017 Apr 1 doi: 10.1007/s10620-017-4541-y. PMID: 28365915
Kim SB, Kim TN, Chung HH, Kim KH
Dig Dis Sci 2017 Mar;62(3):777-783. Epub 2016 Dec 29 doi: 10.1007/s10620-016-4428-3. PMID: 28035552
Mourad MM, Evans R, Kalidindi V, Navaratnam R, Dvorkin L, Bramhall SR
Ann R Coll Surg Engl 2017 Feb;99(2):107-112. Epub 2016 Dec 5 doi: 10.1308/rcsann.2016.0355. PMID: 27917667Free PMC Article
Sandrasegaran K, Tahir B, Barad U, Fogel E, Akisik F, Tirkes T, Sherman S
AJR Am J Roentgenol 2017 Feb;208(2):315-321. Epub 2016 Nov 8 doi: 10.2214/AJR.16.16566. PMID: 27824485Free PMC Article
da Costa DW, Dijksman LM, Bouwense SA, Schepers NJ, Besselink MG, van Santvoort HC, Boerma D, Gooszen HG, Dijkgraaf MG; Dutch Pancreatitis Study Group.
Br J Surg 2016 Nov;103(12):1695-1703. Epub 2016 Aug 12 doi: 10.1002/bjs.10222. PMID: 27517163

Prognosis

Liu T, Huang W, Szatmary P, Abrams ST, Alhamdi Y, Lin Z, Greenhalf W, Wang G, Sutton R, Toh CH
Br J Surg 2017 Aug;104(9):1215-1225. Epub 2017 Apr 24 doi: 10.1002/bjs.10538. PMID: 28436602
Machicado JD, Yadav D
Dig Dis Sci 2017 Jul;62(7):1683-1691. Epub 2017 Mar 9 doi: 10.1007/s10620-017-4510-5. PMID: 28281168Free PMC Article
Roggenbuck D, Goihl A, Hanack K, Holzlöhner P, Hentschel C, Veiczi M, Schierack P, Reinhold D, Schulz HU
Clin Chem Lab Med 2017 May 1;55(6):854-864. doi: 10.1515/cclm-2016-0797. PMID: 27837595
Mikolasevic I, Orlic L, Poropat G, Jakopcic I, Stimac D, Klanac A, Carovic F, Milic S
Eur J Intern Med 2017 Mar;38:73-78. Epub 2016 Nov 5 doi: 10.1016/j.ejim.2016.10.019. PMID: 27825671
Vander Mijnsbrugge W, Laleman W, Van Steenbergen W, Heye S, Verslype C, Maleux G
Acta Radiol 2017 Mar;58(3):316-322. Epub 2016 Jul 19 doi: 10.1177/0284185116648502. PMID: 27178033

Clinical prediction guides

Liu T, Huang W, Szatmary P, Abrams ST, Alhamdi Y, Lin Z, Greenhalf W, Wang G, Sutton R, Toh CH
Br J Surg 2017 Aug;104(9):1215-1225. Epub 2017 Apr 24 doi: 10.1002/bjs.10538. PMID: 28436602
Machicado JD, Yadav D
Dig Dis Sci 2017 Jul;62(7):1683-1691. Epub 2017 Mar 9 doi: 10.1007/s10620-017-4510-5. PMID: 28281168Free PMC Article
Mosztbacher D, Farkas N, Solymár M, Pár G, Bajor J, Szűcs Á, Czimmer J, Márta K, Mikó A, Rumbus Z, Varjú P, Hegyi P, Párniczky A
World J Gastroenterol 2017 Feb 14;23(6):957-963. doi: 10.3748/wjg.v23.i6.957. PMID: 28246469Free PMC Article
Mikolasevic I, Orlic L, Poropat G, Jakopcic I, Stimac D, Klanac A, Carovic F, Milic S
Eur J Intern Med 2017 Mar;38:73-78. Epub 2016 Nov 5 doi: 10.1016/j.ejim.2016.10.019. PMID: 27825671
Sandrasegaran K, Tahir B, Barad U, Fogel E, Akisik F, Tirkes T, Sherman S
AJR Am J Roentgenol 2017 Feb;208(2):315-321. Epub 2016 Nov 8 doi: 10.2214/AJR.16.16566. PMID: 27824485Free PMC Article

Recent systematic reviews

Vaughn VM, Shuster D, Rogers MAM, Mann J, Conte ML, Saint S, Chopra V
Ann Intern Med 2017 Jun 20;166(12):883-892. Epub 2017 May 16 doi: 10.7326/M16-2533. PMID: 28505667
Wu BU, Batech M, Quezada M, Lew D, Fujikawa K, Kung J, Jamil LH, Chen W, Afghani E, Reicher S, Buxbaum J, Pandol SJ
Am J Gastroenterol 2017 Jul;112(7):1144-1152. Epub 2017 May 2 doi: 10.1038/ajg.2017.114. PMID: 28462914Free PMC Article
Mosztbacher D, Farkas N, Solymár M, Pár G, Bajor J, Szűcs Á, Czimmer J, Márta K, Mikó A, Rumbus Z, Varjú P, Hegyi P, Párniczky A
World J Gastroenterol 2017 Feb 14;23(6):957-963. doi: 10.3748/wjg.v23.i6.957. PMID: 28246469Free PMC Article
Mourad MM, Evans R, Kalidindi V, Navaratnam R, Dvorkin L, Bramhall SR
Ann R Coll Surg Engl 2017 Feb;99(2):107-112. Epub 2016 Dec 5 doi: 10.1308/rcsann.2016.0355. PMID: 27917667Free PMC Article
Lodewijkx PJ, Besselink MG, Witteman BJ, Schepers NJ, Gooszen HG, van Santvoort HC, Bakker OJ; Dutch Pancreatitis Study Group.
Expert Rev Gastroenterol Hepatol 2016;10(5):571-80. Epub 2016 Mar 15 doi: 10.1586/17474124.2016.1141048. PMID: 26823272

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