Genetic susceptibility to fibrocalculous pancreatic diabetes in Bangladeshi subjects: a family study

Chowdhury, Zakaria; McDermott, Michael F.; Davey, Sanjeev; Hassan, Zurina; Sinnott, Paul J.; Hemmatpour, S; Sherwin, Stephen A.; Ali, Liaquat; Aganna, Ebun; Allotey, Rebecca; North, Bernard; Cassell, Paul G.; Khan, Abul Kalam Azad; Hitman, G. A.

doi:10.1038/sj.gene.6363814

Cited by 18 publications

(11 citation statements)

References 25 publications

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“…Other groups have also demonstrated HLA associations with FCPD, although the disease-associated alleles are not always consistent between studies (Sanjeevi et al 1999). We have also found an association between the insulin gene hypervariable region and FCPD in southern Indian but not in Bangladeshi subjects (Kambo et al 1989;Chowdhury et al 2002).…”

contrasting

confidence: 53%

“…demonstrated familial clustering of the disease . More specifically, we have demonstrated associations between FCPD and human leukocyte antigen (HLA) genotype in subjects from southern India and Bangladesh, which revealed both similarities to and differences from T1D (Kambo et al 1989;Chowdhury et al 2002). Other groups have also demonstrated HLA associations with FCPD, although the disease-associated alleles are not always consistent between studies (Sanjeevi et al 1999).…”

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confidence: 88%

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SPINK1 Is a Susceptibility Gene for Fibrocalculous Pancreatic Diabetes in Subjects from the Indian Subcontinent

Hassan

Mohan

Ali

et al. 2002

The American Journal of Human Genetics

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Fibrocalculous pancreatic diabetes (FCPD) is a secondary cause of diabetes due to chronic pancreatitis. Since the N34S variant of the SPINK1 trypsin inhibitor gene has been found to partially account for genetic susceptibility to chronic pancreatitis, we used a family-based and case-control approach in two separate ethnic groups from the Indian subcontinent, to determine whether N34S was associated with susceptibility to FCPD. Clear excess transmission of SPINK1 N34S to the probands with FCPD in 69 Bangladeshi families was observed (P<.0001; 20 transmissions and 2 nontransmissions). In the total study group (Bangladeshi and southern Indian) the N34S variant was present in 33% of 180 subjects with FCPD, 4.4% of 861 nondiabetic subjects (odds ratio 10.8; P<.0001 compared with FCPD), 3.7% of 219 subjects with type 2 diabetes, and 10.6% of 354 subjects with early-onset diabetes (aged <30 years) (P=.02 compared with the ethnically matched control group). These results suggest that the N34S variant of SPINK1 is a susceptibility gene for FCPD in the Indian subcontinent, although, by itself, it is not sufficient to cause disease.

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confidence: 53%

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confidence: 88%

SPINK1 Is a Susceptibility Gene for Fibrocalculous Pancreatic Diabetes in Subjects from the Indian Subcontinent

Hassan

Mohan

Ali

et al. 2002

The American Journal of Human Genetics

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“…Another study found a positive association with DQ9 (A*0201-B*0303) [101]. In a family-based study, using TDT analysis, an overall association between TCP and HLA-DQB1 (P=0.003) was reported, that was largely due to a positive association with HLA-DQB1*0302 and a negative association with HLA-DQB1*0202 [102]. However, these findings should be interpreted with caution.…”

Section: Major Histocompatibility Complex (Mhc) Genesmentioning

confidence: 84%

Genetic aspects of tropical calcific pancreatitis

Witt

Bhatia

2008

Rev Endocr Metab Disord

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Tropical calcific pancreatitis (TCP) is a subtype of chronic pancreatitis which is unique to tropical regions. Patients present at young age with recurrent abdominal pain, nutritional deficiencies, and insulin-requiring diabetes. For a long time, the aetiology of this disorder was poorly understood. Several environmental factors, such as malnutrition or the consumption of toxic food components such as cyanogenic glycosides, were proposed as pathogenic factors. In the last decade, a major impact on the understanding of the aetiology of TCP has come from genetic studies on hereditary and idiopathic chronic pancreatitis. Genetic alterations in at least five genetic loci are clearly associated with chronic pancreatitis in the Western world. These include alterations in genes coding for trypsinogens, the most abundant digestive enzymes (PRSS1 and PRSS2), the trypsin inhibitor (SPINK1) and the trypsin-degrading enzyme, chymotrypsinogen C (CTRC). In addition, alterations in the cystic fibrosis (CFTR) gene are associated with idiopathic pancreatitis. TCP clinically resembles non-alcoholic chronic pancreatitis of Western countries, suggesting that similar genetic defects might also be of importance in this disease entity. Indeed, alterations in at least two genes, SPINK1 and CTRC, are strongly associated with TCP. The current review focuses on the recent developments in the understanding of the genetic basis of inherited pancreatitis, with special emphasis on TCP.

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“…Another study from India showed association of FCPD with DQ9 (A*0201-B*0303) [20]. Similarly, in Bangladesh, association was noted between FCPD and HLA-DQB1 [21].…”

Section: The Cassava Hypothesismentioning

confidence: 92%

Fibrocalculous pancreatic diabetes (FCPD)

Unnikrishnan

Mohan

2014

Acta Diabetol

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Fibrocalculous pancreatic diabetes (FCPD) is an uncommon form of diabetes that occurs as a result of chronic calcific pancreatitis, in the absence of alcohol abuse. The disease is restricted to tropical regions of the world, and southern India has the highest known prevalence of FCPD. The typical patient with FCPD is a lean adolescent or young adult of either sex, presenting with history of recurrent bouts of abdominal pain and steatorrhea. Demonstration of large, discrete pancreatic calculi by plain radiographs or ultrasonography of the abdomen is diagnostic. While the exact etiology of FCPD is unknown, genetic, nutritional and inflammatory factors have been hypothesized to play a role. Diabetes in FCPD is often brittle and difficult to control; most patients require multiple doses of insulin for control of glycemia. However, in spite of high blood glucose levels, patients rarely develop ketosis. Malabsorption responds to pancreatic enzyme supplementation. Surgical removal of stones is indicated for symptomatic relief of intractable pain. While patients with FCPD develop microvascular complications as frequently as those with type 2 diabetes, macrovascular disease is uncommon. Development of pancreatic malignancy is the most dreaded complication and should be suspected in any patient who complains of weight loss, back pain or jaundice.

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Genetic susceptibility to fibrocalculous pancreatic diabetes in Bangladeshi subjects: a family study

Abstract: Fibrocalculous pancreatic diabetes (FCPD) is an uncommon cause of diabetes, seen mainly in developing countries

Cited by 18 publications

References 25 publications

SPINK1 Is a Susceptibility Gene for Fibrocalculous Pancreatic Diabetes in Subjects from the Indian Subcontinent

SPINK1 Is a Susceptibility Gene for Fibrocalculous Pancreatic Diabetes in Subjects from the Indian Subcontinent

Genetic aspects of tropical calcific pancreatitis

Fibrocalculous pancreatic diabetes (FCPD)

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