Entry - #611369 - LETHAL CONGENITAL CONTRACTURE SYNDROME 3; LCCS3 - OMIM - (MIRROR)
# 611369

LETHAL CONGENITAL CONTRACTURE SYNDROME 3; LCCS3


Alternative titles; symbols

MULTIPLE CONTRACTURE SYNDROME, ISRAELI BEDOUIN TYPE B


Phenotype-Gene Relationships

Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
Gene/Locus Gene/Locus
MIM number
19p13.3 Lethal congenital contractural syndrome 3 611369 AR 3 PIP5K1C 606102
Clinical Synopsis
 
Phenotypic Series
 

INHERITANCE
- Autosomal recessive
GROWTH
Other
- Small or borderline to adequate size for gestational age
RESPIRATORY
- Respiratory insufficiency at birth, lethal
SKELETAL
Limbs
- Severe multiple joint contractures
MUSCLE, SOFT TISSUES
- Severe muscle wasting and atrophy, primarily in the legs
MISCELLANEOUS
- Death due to respiratory insufficiency within minutes to hours after birth
MOLECULAR BASIS
- Caused by mutation in the gamma type 1 phosphatidylinositol 4-phosphate 5-kinase gene (PIP5K1C, 606102.0001)

TEXT

A number sign (#) is used with this entry because of evidence that lethal congenital contracture syndrome-3 (LCCS3) can be caused by homozygous mutation in the PIP5K1C gene (606102) on chromosome 19p13.


Description

Lethal congenital contracture syndrome-3 (LCCS3) is a severe autosomal recessive form of arthrogryposis characterized by multiple joint contractures with muscle wasting and atrophy (Narkis et al., 2007).

For a general phenotypic description and a discussion of genetic heterogeneity of LCCS, see LCCS1 (253310).


Clinical Features

Narkis et al. (2007) described a novel type of autosomal recessive lethal congenital contracture syndrome (LCCS) that, like LCCS2 (607598), was identified in an Israeli Bedouin kindred. The phenotype was similar to that of LCCS2 but lacked the distended bladder (neurogenic bladder defect). Affected individuals were born with severe multiple joint contractures with severe muscle wasting and atrophy, mainly in the legs. Death occurred minutes to hours after birth due to respiratory insufficiency. The phenotype can be distinguished from that of LCCS1 (253310) by the absence of hydrops, fractures, and multiple pterygia.


Inheritance

The transmission pattern of LCCS3 in the family reported by Narkis et al. (2007) was consistent with autosomal recessive inheritance.


Mapping

Using homozygosity mapping, Narkis et al. (2007) mapped the LCCS3 phenotype to a 3.4-Mb region on chromosome 19p13.


Molecular Genetics

In affected members of a large 5-generation Israeli Bedouin kindred with LCCS, and in an affected individual from an unrelated family, Narkis et al. (2007) found homozygosity for the same missense mutation in the PIP5K1C gene (D253N; 606102.0001). The mutation affects a conserved residue and abolishes PIP5K1C kinase activity.


REFERENCES

  1. Narkis, G., Ofir, R., Landau, D., Manor, E., Volokita, M., Hershkowitz, R., Elbedour, K., Birk. O. S. Lethal contractural syndrome type 3 (LCCS3) is caused by a mutation in PIP5K1C, which encodes PIPKI-gamma of the phophatidylinsitol (sic) pathway. Am. J. Hum. Genet. 81: 530-539, 2007. [PubMed: 17701898, images, related citations] [Full Text]


Contributors:
Marla J. F. O'Neill - updated : 11/7/2012
Creation Date:
Victor A. McKusick : 8/23/2007
alopez : 08/29/2024
alopez : 08/29/2024
carol : 11/21/2012
carol : 11/7/2012
alopez : 8/23/2007

# 611369

LETHAL CONGENITAL CONTRACTURE SYNDROME 3; LCCS3


Alternative titles; symbols

MULTIPLE CONTRACTURE SYNDROME, ISRAELI BEDOUIN TYPE B


SNOMEDCT: 715420005;   ORPHA: 137783;   DO: 0060653;  


Phenotype-Gene Relationships

Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
Gene/Locus Gene/Locus
MIM number
19p13.3 Lethal congenital contractural syndrome 3 611369 Autosomal recessive 3 PIP5K1C 606102

TEXT

A number sign (#) is used with this entry because of evidence that lethal congenital contracture syndrome-3 (LCCS3) can be caused by homozygous mutation in the PIP5K1C gene (606102) on chromosome 19p13.


Description

Lethal congenital contracture syndrome-3 (LCCS3) is a severe autosomal recessive form of arthrogryposis characterized by multiple joint contractures with muscle wasting and atrophy (Narkis et al., 2007).

For a general phenotypic description and a discussion of genetic heterogeneity of LCCS, see LCCS1 (253310).


Clinical Features

Narkis et al. (2007) described a novel type of autosomal recessive lethal congenital contracture syndrome (LCCS) that, like LCCS2 (607598), was identified in an Israeli Bedouin kindred. The phenotype was similar to that of LCCS2 but lacked the distended bladder (neurogenic bladder defect). Affected individuals were born with severe multiple joint contractures with severe muscle wasting and atrophy, mainly in the legs. Death occurred minutes to hours after birth due to respiratory insufficiency. The phenotype can be distinguished from that of LCCS1 (253310) by the absence of hydrops, fractures, and multiple pterygia.


Inheritance

The transmission pattern of LCCS3 in the family reported by Narkis et al. (2007) was consistent with autosomal recessive inheritance.


Mapping

Using homozygosity mapping, Narkis et al. (2007) mapped the LCCS3 phenotype to a 3.4-Mb region on chromosome 19p13.


Molecular Genetics

In affected members of a large 5-generation Israeli Bedouin kindred with LCCS, and in an affected individual from an unrelated family, Narkis et al. (2007) found homozygosity for the same missense mutation in the PIP5K1C gene (D253N; 606102.0001). The mutation affects a conserved residue and abolishes PIP5K1C kinase activity.


REFERENCES

  1. Narkis, G., Ofir, R., Landau, D., Manor, E., Volokita, M., Hershkowitz, R., Elbedour, K., Birk. O. S. Lethal contractural syndrome type 3 (LCCS3) is caused by a mutation in PIP5K1C, which encodes PIPKI-gamma of the phophatidylinsitol (sic) pathway. Am. J. Hum. Genet. 81: 530-539, 2007. [PubMed: 17701898] [Full Text: https://doi.org/10.1086/520771]


Contributors:
Marla J. F. O'Neill - updated : 11/7/2012

Creation Date:
Victor A. McKusick : 8/23/2007

Edit History:
alopez : 08/29/2024
alopez : 08/29/2024
carol : 11/21/2012
carol : 11/7/2012
alopez : 8/23/2007