The QTc is less than 450 ms in 95% of normal males, and less than 460 ms in 95% of normal females. Romano–Ward syndrome is suggested if the QTc is longer than these cutoffs. However, as 5% of normal people also fall into this category, some suggest cutoffs of 470 and 480 ms for males and females respectively, corresponding with the 99th centiles of normal values.The major subtypes of Romano–Ward syndrome are associated with specific ECG features. LQT1 is typically associated with broad-based T-waves, whereas the T-waves in LQT2 are notched and of lower amplitude, whilst in LQT3 the T-waves are often late onset, being preceded by a long isoelectric segment.Other factors beyond the QT interval should be taken into account when making a diagnosis, some of which have been incorporated into scoring systems such as the Schwartz score. These factors include a history of characteristic abnormal heart rhythms (Torsades de Pointes), unexplained blackouts (syncope), and a family history of confirmed LQT syndrome. Other investigations that may suggest a diagnosis of the LQT1 form of Romano–Ward syndrome include paradoxical lengthening of the QT interval in response to exercise (QTc >470 ms at 2–4 minutes of recovery) or during an artificial infusion of adrenaline (lengthening of the absolute QT interval >30 ms during low dose adrenaline). Treatment
The treatment for Romano–Ward syndrome aims to reduce the risk of arrhythmias. Lifestyle measures include avoiding very strenuous or competitive exercise.
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The inheritance probabilities per birth are as follows:

If both parents are carriers:
25% (1 in 4) children will have the disorder
50% (2 in 4) children will be carriers (but unaffected)
25% (1 in 4) children will be free of MSD - unaffected child that is not a carrier
If one parent is affected and one is free of MSD:
0% (0) children will have the disorder - only one parent is affected, other parent always gives normal gene
100% (4 in 4) children will be carriers (but unaffected)
If one parent is a carrier and the other is free of MSD:
50% (2 in 4) children will be carriers (but unaffected)
50% (2 in 4) children will be free of MSD - unaffected child that is not a carrier

Diagnosis
MSD may be diagnosed when deficiency of more than one sulfatase enzyme is identified in leukocytes or fibroblasts, or by molecular genetic testing which shows pathogenic variation in both alleles of the SUMF1 gene. Treatment
As there is no cure for MSD, treatment is restricted to management of symptoms. There is much research on MSD that is currently underway. MSD Action Foundation have initiated more than 15 research projects on MSD in the last 6 years. Many of these have a translational focus. It is hoped that clinical trials for MSD will happen in the not too distant future- Alan Finglas. [Ref 17. Finglas 2020]

See also
Linear porokeratosis
List of cutaneous conditions

References

[17] View from inside: When multiple sulfatase deficiency changes everything about how you live and becomes your life
Alan Finglas,
https://doi.org/10.1002/jimd.12305
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