Comparatively, with arthritis mutilans in rheumatoid arthritis, bone marrow edema often involves the subchondral bone layer, while the condition as a subtype of psoriatic arthritis includes a greater extent of marrow edema, expanding to diaphysis. Treatment
Medication
The bone edema in arthritis mutilans can be treated with TNF inhibitors in the short term: a 2007 study found that the bone edema associated with psoriatic arthritis (of which arthritis mutilans is a subtype) responded to TNF inhibitors with "dramatic" improvement, but the study was not determinative of whether TNF inhibitors would prevent new bone formation, bone fusion, or osteolysis (bone resorption). Surgical
Although a 2011 research article stated that disagreements between hand surgeons and rheumatologists remain regarding the indications, timing and effectiveness of rheumatoid hand surgery, arthritis mutilans may be successfully treated by iliac-bone graft and arthrodesis of the interphalangeal joints and the metacarpophalangeal joint in each finger. Outcomes
Arthritis mutilans parent condition psoriatic arthritis leaves people with a mortality risk 60% higher than the general population, with premature death causes mirroring those of the general population, cardiovascular issues being most common. Life expectancy for people with psoriatic arthritis is estimated to be reduced by approximately 3 years. References


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Those with the Setleis syndrome may be missing eyelashes on both the upper and lower lids or may have multiple rows of lashes on the upper lids but none on the lower lids.A possible association with intra abdominal cancer has been reported but to date this has not been confirmed in other studies. Genetics
Type II appears to be due to mutations in the transcription factor TWIST2 on chromosome 2.Type IV is due to mutations in the Cyp26c1 gene. Pathology
Under the temporal lesions the skeletal muscle is almost in direct continuity with the epidermis. Diagnosis
Classification
There are at least four types of FFDD:
Type I: autosomal dominant FFDD
Type II: autosomal recessive FFDD
Type III: FFDD with other facial features : Setleis syndrome
Type IV: facial lesions resembling aplasia cutis in a preauricular distribution along the line of fusion of the maxillary and mandibular prominences. Autosomal recessive. Treatment
History
The syndrome was first described by Brauer in 1929 in a large five generation family (38 members). The affected progenitor (Johann Jokeb Van Bargen) was a man who had migrated to Germany from Holland in the 16th century. As many as 155 family members were thought to have been affected. References


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