Racial factors and the risk of chronic pancreatitis

Lowenfels, Albert B.; Maisonneuve, Patrick; Grover, Hemal; Gerber, Eric; Korsten, Mark A.; Antunes, Maria Teresa; Marques, A.P.; Pitchumoni, C. S.

doi:10.1016/s0002-9270(99)00007-6

Cited by 23 publications

(11 citation statements)

References 20 publications

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“…However, only a minority of alcoholics develop these diseases [1,4,5,7,8] ; this together with the requirement of several years of ethanol intake, racial factors [39] , and the difficulty of developing adequate experimental models have led to the consideration of other associated etiological factors [26] . The presence of a common etiological factor, i.e.…”

Section: Discussionmentioning

confidence: 99%

Does an association exist between chronic pancreatitis and liver cirrhosis in alcoholic subjects?

Aparisi¹,

Sabater²,

Del-Olmo³

et al. 2008

WJG

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AIM:To study the possible association between chronic pancreatitis (CP) and liver cirrhosis (LC) of alcoholic etiology, after excluding any other causes. METHODS: One hundred and forty consecutive alcoholic patients were subdivided into three groups: CP (n = 53), LC (n = 57), and asymptomatic alcoholic (n = 30). Clinical, biochemical and morphological characteristics, Child-Pugh index, indocyanine green test, and fecal pancreatic elastase-1 test were assessed. RESULTS: In patients with cirrhosis, major clinical manifestations of CP such as pancreatic pain and steatorrhea, as well as imaging alterations of CP such as calcifications, duct dilation and pseudocysts were absent; insulin-dependent diabetes was present in 5.3% of cases, and elastase-1 test was altered in only 7%, and severely altered in none. In patients with CP, clinical characteristics of cirrhosis such as ascites, encephalopathy and gastrointestinal hemorrhage were present in one case, Child-Pugh grade > A in 5.7%, and altered indocyanine green test in 1.9% cases. In asymptomatic alcoholism, there was only a non-coincident alteration of elastase-1 test and indocyanine test in 14.8% and 10%, respectively, but other characteristics of cirrhosis or CP were absent. An inverse correlation (r = -0.746) between elastase-1 test and indocyanine test was found in alcoholic patients. CONCLUSION:There is a scarce coincidence in clinical and morphological alterations among patients with CP or LC of alcoholic etiology, but an inverse correlation between pancreatic and liver function tests. These findings support that these alcoholic diseases evolve in a different manner and have different etiopathogenesis.

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Section: Discussionmentioning

confidence: 99%

Does an association exist between chronic pancreatitis and liver cirrhosis in alcoholic subjects?

Aparisi¹,

Sabater²,

Del-Olmo³

et al. 2008

WJG

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“…40 Earlier studies have shown that in comparison with White patients, Black patients are 2-3 times more likely to be hospitalised for chronic pancreatitis than alcoholic cirrhosis. 41 Thus, alcoholics in India may be more susceptible to chronic pancreatitis due to a combination of factors such as genetic makeup, racial difference in diet, type or quantity of alcohol, or smoking, etc. Although the present knowledge suggests that ACP patients are likely to have higher interactions with environmental factors in comparison with other types of chronic pancreatitis, there is a strong genetic basis for ACP patients in India.…”

Section: Discussionmentioning

confidence: 99%

Absence of PRSS1 mutations and association of SPINK1 trypsin inhibitor mutations in hereditary and non-hereditary chronic pancreatitis

Chandak

2004

Gut

101

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Background and aims: Mutations in the cationic trypsinogen (protease, serine, 1 (trypsin 1); PRSS1) gene are causally associated with recurrent acute and chronic pancreatitis. We investigated whether mutations in the PRSS1 gene are associated with hereditary and non-hereditary pancreatitis. As a modifier role has been proposed for trypsin inhibitor (serine protease inhibitor, Kazal type I; SPINK1) mutations, the role of SPINK1 mutations in these patients was also analysed. Subjects and methods: The coding regions of PRSS1 and SPINK1 genes were sequenced in 290 controls and 198 patients, of whom 120 were diagnosed as idiopathic (ICP), 41 as alcoholic (ACP), and 37 as hereditary pancreatitis (HP). Twenty four unaffected relatives of HP probands were also analysed and genotype-phenotype correlations and statistical analyses were performed. Results: No mutations in the PRSS1 gene were detected in any of the patients, including HP patients, while the N34S mutation was observed in the SPINK1 gene in the majority of HP patients (73%). Similarly, 26.8% of ACP (11 of 41) and 32.5% (39 of 120) of ICP patients also had SPINK1 mutations. The N34S mutation was observed in both homozygous and heterozygous conditions. In comparison, only 2.76% of the control population had the N34S allele (p,0.001). The P55S mutation was observed in one ICP and one ACP patient, and in three normal individuals. Genotype-phenotype correlations did not suggest any significant difference in the age of onset, severity of disease, or pancreatic endocrine insufficiency in patients with or without mutated SPINK1 and irrespective of the allelic status of N34S SPINK1. Conclusions: Irrespective of the aetiology, mutations in the PRSS1 gene are not associated with chronic pancreatitis, including HP. In contrast, the N34S mutation in the SPINK1 gene shows a significant correlation in these patients. A comparable phenotype in terms of age of onset, diabetes mellitus, and other phenotypic features in patients with or without SPINK1 mutations and N34S homozygotes and heterozygotes suggests that there may still be involvement of other genetic or environmental factors.

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“…One third of alcoholic patients with recurrent acute pancreatitis did not progress towards chronic calcifying pancreatitis during an observation period of 11.7 8 5.8 years [15] . Fourth, differences in racial susceptibility may exist since black patients are 2-3 times more likely to be hospitalized for pancreatitis than white patients [16] . These observations demonstrate a marked heterogeneity in susceptibility to chronic alcoholic pancreatitis.…”

Section: Alcohol Consumption and Pancreatitismentioning

confidence: 99%

Alcoholic Pancreatitis

Schneider

Singer²

2005

Dig Dis

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A history of excessive alcohol consumption is found in the majority of patients with chronic pancreatitis, and numerous research efforts revealed insights into the pathogenesis of alcohol-induced pancreatic damage. However, the exact mechanisms underlying the disease are not yet clarified, and the origin of alcoholic chronic pancreatitis continues to be the topic of speculation and investigation. This article provides an overview about the epidemiology of alcoholic chronic pancreatitis, the epidemiologic association of alcohol intake and pancreatitis and the clinical course of the disease. Finally, this article summarizes several hypothetical concepts that try to explain the early and late pathophysiological mechanisms of acute and chronic pancreatitis.

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Racial factors and the risk of chronic pancreatitis

Cited by 23 publications

References 20 publications

Does an association exist between chronic pancreatitis and liver cirrhosis in alcoholic subjects?

Does an association exist between chronic pancreatitis and liver cirrhosis in alcoholic subjects?

Absence of PRSS1 mutations and association of SPINK1 trypsin inhibitor mutations in hereditary and non-hereditary chronic pancreatitis

Alcoholic Pancreatitis

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