Genetic counseling, prenatal testing, and preimplantation genetic diagnosis is available.In females, the cells expressing the mutated IKBKG gene due to lyonization selectively die around the time of birth, so the X-inactivation is extremely skewed.IP is caused by mutations in a gene called NEMO (NF-κB essential modulator). Diagnosis
The diagnosis of IP is established by clinical findings and occasionally by corroborative skin biopsy. Molecular genetic testing of the NEMO IKBKG gene (chromosomal locus Xq28) reveals disease-causing mutations in about 80% of probands. Such testing is available clinically. In addition, females with IP have skewed X-chromosome inactivation; testing for this can be used to support the diagnosis. Many people in the past were misdiagnosed with a second type of IP, formerly known as IP1. This has now been given its own name: Hypomelanosis of Ito (incontinentia pigmenti achromians). This has a slightly different presentation: swirls or streaks of hypopigmentation and depigmentation. It is not inherited and does not involve skin stages 1 or 2. Some 33–50% of patients have multisystem involvement—eye, skeletal, and neurological abnormalities. Its chromosomal locus is at Xp11, rather than Xq28. Treatment
There does not yet exist a specific treatment for IP. Treatment can only address the individual symptoms. History
This disorder was first reported by Swiss dermatologist Bruno Bloch in 1926 and American dermatologist Marion Sulzberger in 1928. See also
List of cutaneous conditions
List of radiographic findings associated with cutaneous conditions
List of dental abnormalities associated with cutaneous conditions

References
External links
GeneReview/NIH/UW entry on Incontinentia Pigmenti
Patients were randomized at 11 sites in the US to receive either omadacycline 100 mg intravenously once daily with an option to transition to 200 mg orally once daily or linezolid 600 mg intravenously twice daily with an option to transition to 600 mg orally twice daily. The results indicated that omadacycline is well tolerated and has the potential to be an effective treatment in patients with complicated skin and skin structure infections.In June 2013, the US Food and Drug Administration (FDA) designated the intravenous and oral formulations of omadacycline as a qualified infectious disease product in the treatment of acute bacterial skin and skin structure infections and community-acquired bacterial pneumonia.A 650-patient phase III registration study comparing omadacycline to linezolid for the treatment of acute bacterial skin and skin structure infections began in June 2015. Omadacycline met the primary efficacy endpoint of early clinical response with statistical non-inferiority (10% margin) compared to linezolid, and was generally safe and well tolerated. The most common treatment-emergent adverse events were gastrointestinal side effects (18.0% for omadacycline vs. 15.8% for linezolid).A 750-patient phase III study comparing omadacycline to moxifloxacin for the treatment of community-acquired bacterial pneumonia began in November 2015.