Background and aim Idiopathic chronic pancreatitis (ICP) is said to be present when no identifiable etiology can be identified. Robust evidence suggested that the serine protease inhibitor nucleus Kazol type 1 (SPINK1) N34S mutation was frequently associated with ICP. As there is a paucity of data on genetic studies in ICP cases from the coastal eastern region of India, we performed this study with an aim to evaluate the SPINK1 genetic mutations and other associated clinical correlates in ICP cases. Material and methods Consecutive ICP cases attending the department of gastroenterology, Institute of Medical Sciences (IMS) and SUM Hospital, were enrolled and evaluated for the pertinent clinical history and undergone detailed biochemical and radiological evaluations. Two ml of venous blood in ethylenediaminetetraacetic acid (EDTA) vials were collected from each case and subjected to a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) test for genetic analysis. Result In this study, the mean age of the cases at the time of the first consultation with us and the age of the first clinical presentation were 34.52±6.44 and 28.73±5.52 years, respectively. Males outnumbered females (Male:Female - 2.12:1). Out of the total of 200 cases, 50% had no SPINK1 mutation, whereas 40% and 10% cases had SPINK1 N34S heterozygous and homozygous mutations, respectively. The mean age of clinical presentation, severe abdominal pain, exocrine and endocrine insufficiency, and parenchymal atrophy were significantly more common in mutants as compared to non-mutants (p-value <0.05). Conclusion In our region, 50% of ICP cases had the SPINK1 N34S mutation. The SPINK1 mutants had a relatively more severe variety of pancreatitis as compared to non-mutants.
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http://dx.doi.org/10.7759/cureus.14427 | DOI Listing |
Sci Rep
December 2024
Department of Endocrinology and Metabolism, Institute of Post Graduate Medical Education & Research, 244 AJC Bose Road, Kolkata, 700020, India.
Panel of known genetic mutations (SPINK1, PRSS1, PRSS2, CTRC, and CFTR) in patients with Fibrocalcific pancreatic diabetes (FCPD)compared to Type 2 Diabetes (T2DM) and healthy controls with emphasis on SPINK1 (N34S) mutations. Whole blood samples were used to detect mutations by PCR followed by Sanger sequencing. In-silico analysis of N34S performed, to explore role in pathogenesis.
View Article and Find Full Text PDFFront Pediatr
November 2024
Department of Pediatrics, Affiliated Changzhou Children's Hospital of Nantong University, Changzhou, Jiangsu, China.
J Surg Case Rep
October 2024
Department of General Surgery, Santa Casa de Misericórdia de Porto Alegre, Porto Alegre, Brazil.
Am J Hum Genet
October 2024
Univ Brest, Inserm, EFS, UMR 1078, GGB, 29200 Brest, France. Electronic address:
PLoS One
August 2024
Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America.
Background/objectives: Germline genetic testing is recommended for younger patients with idiopathic pancreatitis but there has been a lack of consensus in recommendations for those over age 35. We aimed to analyze the results of genetic testing among subjects of varying ages.
Methods: Individuals who underwent germline multigene testing for pancreatitis susceptibility genes (CASR, CFTR, CPA1, CTRC, PRSS1, SPINK1) through a large commercial laboratory between 2017 and 2022 were included.
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