Entry - %604901 - NORTH AMERICAN INDIAN CHILDHOOD CIRRHOSIS; NAIC - OMIM - (MIRROR)
% 604901

NORTH AMERICAN INDIAN CHILDHOOD CIRRHOSIS; NAIC


Cytogenetic location: 16q22   Genomic coordinates (GRCh38) : 16:66,600,001-74,100,000


Gene-Phenotype Relationships
Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
16q22 North American Indian childhood cirrhosis 604901 2

TEXT

Clinical Features

Weber et al. (1981) described an isolated nonsyndromic form of cholestasis in Ojibway-Cree children from First Nations communities in the Abitibi region of northwestern Quebec, Canada. The disease typically presents, in a child who is otherwise well, with transient neonatal jaundice that progresses to biliary cirrhosis requiring hepatic transplantation in childhood or early adulthood. The biochemical and histopathologic features of the disease suggest involvement of the bile ducts rather than of the bile canaliculi. These include elevated gamma-glutamyltransferase and alkaline phosphatase levels and, typically, marked fibrosis around portal bile ducts. Called North American Indian childhood cirrhosis, the carrier frequency in at-risk populations was estimated to be approximately 9%. Betard et al. (2000) noted that NAIC appears to be clinically distinct from previously described nonsyndromic family cholestases (see 211600) because of its marked cholangiopathic features and severe degree of fibrosis on liver histology.


Mapping

Hypothesizing that a major founder mutation underlies most or all cases of NAIC, Betard et al. (2000) used a DNA-pooling strategy to search for an excess of shared homozygosity due to identity by descent among patients, compared with their unaffected first-degree relatives. They studied 13 patients, 16 unaffected sibs, and 22 parents from 5 families and identified a chromosome 16q segment shared by all affected individuals. Assuming a completely penetrant autosomal recessive mode of inheritance, a maximum lod score of 4.44 was observed for a recombination fraction of zero with marker D16S3067. A 5-marker haplotype spanning 4.9 cM was shared by all patients. Thus the candidate gene appeared to be located at 16q22.


Inheritance

Chagnon et al. (2002) demonstrated that NAIC has an autosomal recessive pattern of inheritance.


Molecular Genetics

In affected members of 5 families segregating NAIC, Chagnon et al. (2002) identified a homozygous missense mutation in the CIRH1A (UTP4) gene (R565W; 607456.0001). However, Lek et al. (2016) found that the ExAC database contained 222 heterozygous and 4 homozygous Latino individuals carrying the CIRH1A R565W mutation, for a population frequency of 1.92%. The 4 homozygous individuals had no history of liver disease; recontact with 2 of them revealed normal liver function at ages 56 and 53. Using the ACMG guidelines (Richards et al., 2015), Lek et al. (2016) classified this variant as benign.


REFERENCES

  1. Betard, C., Rasquin-Weber, A., Brewer, C., Drouin, E., Clark, S., Verner, A., Darmond-Zwaig, C., Fortin, J., Mercier, J., Chagnon, P., Fujiwara, T. M., Morgan, K., Richter, A., Hudson, T. J., Mitchell, G. A. Localization of a recessive gene for North American Indian childhood cirrhosis to chromosome region 16q22--and identification of a shared haplotype. Am. J. Hum. Genet. 67: 222-228, 2000. [PubMed: 10820129, images, related citations] [Full Text]

  2. Chagnon, P., Michaud, J., Mitchell, G., Mercier, J., Marion, J.-F., Drouin, E., Rasquin-Weber, A., Hudson, T. J., Richter, A. A missense mutation (R565W) in cirhin (FLJ14728) in North American Indian childhood cirrhosis. Am. J. Hum. Genet. 71: 1443-1449, 2002. [PubMed: 12417987, images, related citations] [Full Text]

  3. Lek, M., Karczewski, K. J., Minikel, E. V., Samocha, K. E., Banks, E., Fennell, T., O'Donnell-Luria, A. H., Ware, J. S., Hill, A. J., Cummings, B. B., Tukiainen, T., Birnbaum, D. P., and 68 others. Analysis of protein-coding genetic variation in 60,706 humans. Nature 536: 285-291, 2016. [PubMed: 27535533, images, related citations] [Full Text]

  4. Richards, S., Aziz, N., Bale, S., Bick, D., Das, S., Gastier-Foster, J., Grody, W. W., Hegde, M., Lyon, E., Spector, E., Voelkerding, K., Rehm, H. L. Standards and guidelines for the interpretation of sequence variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics and the Association of Molecular Pathology. Genet. Med. 17: 405-424, 2015. [PubMed: 25741868, related citations] [Full Text]

  5. Weber, A. M., Tuchweber, B., Yousef, I., Brochu, P., Turgeon, C., Gabbiani, G., Morin, C. L., Roy, C. C. Severe familial cholestasis in North American Indian children: a clinical model of microfilament dysfunction? Gastroenterology 81: 653-662, 1981. [PubMed: 6894906, related citations]


Ada Hamosh - updated : 09/01/2016
Victor A. McKusick - updated : 1/8/2003
Creation Date:
Victor A. McKusick : 7/10/2000
carol : 09/02/2016
carol : 09/02/2016
carol : 09/01/2016
carol : 09/13/2012
mgross : 1/9/2003
terry : 1/8/2003
carol : 9/12/2000

% 604901

NORTH AMERICAN INDIAN CHILDHOOD CIRRHOSIS; NAIC


SNOMEDCT: 699189004;   ORPHA: 168583;  


Cytogenetic location: 16q22   Genomic coordinates (GRCh38) : 16:66,600,001-74,100,000


Gene-Phenotype Relationships

Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
16q22 North American Indian childhood cirrhosis 604901 2

TEXT

Clinical Features

Weber et al. (1981) described an isolated nonsyndromic form of cholestasis in Ojibway-Cree children from First Nations communities in the Abitibi region of northwestern Quebec, Canada. The disease typically presents, in a child who is otherwise well, with transient neonatal jaundice that progresses to biliary cirrhosis requiring hepatic transplantation in childhood or early adulthood. The biochemical and histopathologic features of the disease suggest involvement of the bile ducts rather than of the bile canaliculi. These include elevated gamma-glutamyltransferase and alkaline phosphatase levels and, typically, marked fibrosis around portal bile ducts. Called North American Indian childhood cirrhosis, the carrier frequency in at-risk populations was estimated to be approximately 9%. Betard et al. (2000) noted that NAIC appears to be clinically distinct from previously described nonsyndromic family cholestases (see 211600) because of its marked cholangiopathic features and severe degree of fibrosis on liver histology.


Mapping

Hypothesizing that a major founder mutation underlies most or all cases of NAIC, Betard et al. (2000) used a DNA-pooling strategy to search for an excess of shared homozygosity due to identity by descent among patients, compared with their unaffected first-degree relatives. They studied 13 patients, 16 unaffected sibs, and 22 parents from 5 families and identified a chromosome 16q segment shared by all affected individuals. Assuming a completely penetrant autosomal recessive mode of inheritance, a maximum lod score of 4.44 was observed for a recombination fraction of zero with marker D16S3067. A 5-marker haplotype spanning 4.9 cM was shared by all patients. Thus the candidate gene appeared to be located at 16q22.


Inheritance

Chagnon et al. (2002) demonstrated that NAIC has an autosomal recessive pattern of inheritance.


Molecular Genetics

In affected members of 5 families segregating NAIC, Chagnon et al. (2002) identified a homozygous missense mutation in the CIRH1A (UTP4) gene (R565W; 607456.0001). However, Lek et al. (2016) found that the ExAC database contained 222 heterozygous and 4 homozygous Latino individuals carrying the CIRH1A R565W mutation, for a population frequency of 1.92%. The 4 homozygous individuals had no history of liver disease; recontact with 2 of them revealed normal liver function at ages 56 and 53. Using the ACMG guidelines (Richards et al., 2015), Lek et al. (2016) classified this variant as benign.


REFERENCES

  1. Betard, C., Rasquin-Weber, A., Brewer, C., Drouin, E., Clark, S., Verner, A., Darmond-Zwaig, C., Fortin, J., Mercier, J., Chagnon, P., Fujiwara, T. M., Morgan, K., Richter, A., Hudson, T. J., Mitchell, G. A. Localization of a recessive gene for North American Indian childhood cirrhosis to chromosome region 16q22--and identification of a shared haplotype. Am. J. Hum. Genet. 67: 222-228, 2000. [PubMed: 10820129] [Full Text: https://doi.org/10.1086/302993]

  2. Chagnon, P., Michaud, J., Mitchell, G., Mercier, J., Marion, J.-F., Drouin, E., Rasquin-Weber, A., Hudson, T. J., Richter, A. A missense mutation (R565W) in cirhin (FLJ14728) in North American Indian childhood cirrhosis. Am. J. Hum. Genet. 71: 1443-1449, 2002. [PubMed: 12417987] [Full Text: https://doi.org/10.1086/344580]

  3. Lek, M., Karczewski, K. J., Minikel, E. V., Samocha, K. E., Banks, E., Fennell, T., O'Donnell-Luria, A. H., Ware, J. S., Hill, A. J., Cummings, B. B., Tukiainen, T., Birnbaum, D. P., and 68 others. Analysis of protein-coding genetic variation in 60,706 humans. Nature 536: 285-291, 2016. [PubMed: 27535533] [Full Text: https://doi.org/10.1038/nature19057]

  4. Richards, S., Aziz, N., Bale, S., Bick, D., Das, S., Gastier-Foster, J., Grody, W. W., Hegde, M., Lyon, E., Spector, E., Voelkerding, K., Rehm, H. L. Standards and guidelines for the interpretation of sequence variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics and the Association of Molecular Pathology. Genet. Med. 17: 405-424, 2015. [PubMed: 25741868] [Full Text: https://doi.org/10.1038/gim.2015.30]

  5. Weber, A. M., Tuchweber, B., Yousef, I., Brochu, P., Turgeon, C., Gabbiani, G., Morin, C. L., Roy, C. C. Severe familial cholestasis in North American Indian children: a clinical model of microfilament dysfunction? Gastroenterology 81: 653-662, 1981. [PubMed: 6894906]


Contributors:
Ada Hamosh - updated : 09/01/2016
Victor A. McKusick - updated : 1/8/2003

Creation Date:
Victor A. McKusick : 7/10/2000

Edit History:
carol : 09/02/2016
carol : 09/02/2016
carol : 09/01/2016
carol : 09/13/2012
mgross : 1/9/2003
terry : 1/8/2003
carol : 9/12/2000