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. Author manuscript; available in PMC: 2017 Sep 8.
Published in final edited form as: Am J Med Genet A. 2016 Aug 2;170(11):2965–2974. doi: 10.1002/ajmg.a.37857

Table II. MMIHS and MSMDS: Summary of Clinical Data and Genotype of Individuals With Molecularly Confirmed Diagnosis.

Phenotype Megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS) Multisystemic smooth muscle dysfunction syndrome (MSMDS)
Gene ACTG2a MYH11b ACTA2c
Number of probands 23 1 23
Parental consanguinity + (Algerian origin)
Inheritance AD AR AD
Pathogenic variant Heterozygous—all missense Homozygous—stop codon Heterozygous—all missense (codon 179)
De novo variant 16/18d No 23/23
Familial recurrence of the phenotype 1/23e
Megacystis 21/23 + 4/23
Bladder dysfunction without 2/23 10/23
megacystis
Microcolon 16/23 +
Intestinal hypoperistalsis 21/21f + 5/23
Prune-belly 2/20g + 2/23
Mydriasis 23/23
Patent ductus arteriosus 23/23
Vascular involvement 23/23
Cerebrovascular 21/23
Aortic aneurism 14/23

AD, autosomal dominant, AR, autosomal recessive, MMIHS, megacystis-microcolon-intestinal hypoperistalsis syndrome; MSMDS, multisystemicsmooth muscle dysfunction syndrome; +, feature present; —, feature absent. A summary of phenotype, genotype, and family history data of all individuals with ACTG2-related disorder, including MMIHS and milder phenotypes, is described in the supplementary material (SM5).

d

Unknown finding in five of the 23 individuals (18 evaluated patients), 16/18, one individual inherited the variant from the father, who presented with milder disease—family 34 [Wangler et al., 2014] and parental inheritance in a family due to probable gonadal mosacism—family 1 [Tuzovic et al., 2015].

e

The recurrence of MMIHS was reported in a family with two affected siblings and normal parents—family 1 [Tuzovic et al., 2015].

f

Unknown finding in two of the 23 individuals (21 evaluated patients).

g

Unknown finding in three of the 23 individuals (20 evaluated patients).