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Digestive Diseases 2004

Chronic parotitis: not another SPINKosis.

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Felix Gundling
Fabian Reitmeier
Andrea Tannapfel
Alexander Schutz
Anette Weber
Jurgen Ussmuller
Volker Keim
Joachim Mossner
Niels Teich

Mo kle

Abstrè

BACKGROUND

Pancreatitis and parotitis share several etiological, pathohistological and functional similarities. It arose from recent pancreatitis research that some cases of chronic pancreatitis are associated with mutations of the serine protease inhibitor, Kazal type-1 (SPINK1). We tested the hypothesis that the pancreatitis-associated N34S mutation of SPINK1 is also a risk factor for chronic parotitis.

METHODS

Reverse-transcriptase polymerase chain reaction was used to investigate SPINK1 transcription in the parotid gland. Forty-five blocks of formalin-fixed, paraffin wax-embedded tissues with chronic parotitis of unknown cause were analyzed for the SPINK1-N34S mutation.

RESULTS

The SPINK1 gene is transcribed in the parotid gland. Two of the 45 patients (4.4%) with chronic parotitis carried the N34S mutation heterozygously. Of 82 healthy blood donors, 3 subjects (3.7%) were identified as carrying this mutation heterozygously (p = 0.83).

CONCLUSIONS

The SPINK1-N34S mutation is not associated with chronic parotitis.

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