Cutis laxa may also be seen in association with inherited connective tissue disorders such as Ehlers–Danlos syndromes. Another syndrome associated with cutis laxa is Lenz-Majewski syndrome which is due to a mutation in the phosphatidylserine synthase 1 (PTDSS1) gene.In contrast, acquired cutis laxa often has a triggering event such as urticaria, drugs (such as penicillin) or neoplasms. Acquired cutis laxa may also be immunologically mediated, as it can involve dermal deposit of immunoglobulins and it can occur with autoimmune diseases. Acquired cutis laxa has been associated with granular immunoglobulin A deposits as well as abundant neutrophils. One hypothesis for the cause is excessive elastase release from neutrophils and macrophages. It has also been considered that mutations in elastin (ELN) and fibulin-5 (FBLN5) genes can increase susceptibility of elastic fibres to inflammatory degradation in acquired cutis laxa.Acquired cutis laxa has also been seen in conjunction with a number of conditions including: rheumatoid arthritis, systemic lupus erythematosus, celiac disease, and monoclonal gammopathies. It can also occur as a postinflammatory response after urticaria. Urticarial skin fibroblasts have shown a 2- to 3- fold increase in elastase activity in a patient with acquired cutis laxa. Diagnosis
Treatment
As of 2019, there is no treatment for cutis laxa. Procedures aimed at mitigating symptoms and identifying subsequent conditions are often advised. No pharmacological  agent has been able to stop the progression of the disease. However, cosmetic surgeries are potentially an option as cutis laxa does not generally involve vascular fragility. See also
Occipital horn syndrome
List of cutaneous conditions

References
Further reading
External links

Medscape entry on Cutis Laxa
Symptoms may be relieved by sitting down (flexing the spine) or even by walking while leaning over (flexion of the spine) a shopping cart.The ability to ride a stationary bike for a prolonged period of time differentiates neurogenic claudication from vascular claudication. Weakness is also a prominent feature of spinal claudication that is not usually present in intermittent claudication. Treatment
Blocking agents of the adrenoceptors alpha 1/alpha 2 are typically used to treat the effects of the vasoconstriction associated with vascular claudication. Cilostazol (trade name: Pletal) is FDA approved for intermittent claudication. It is contraindicated in patients with heart failure, and improvement of symptoms may not be evident for two to three weeks.Neurogenic claudication can be treated surgically with spinal decompression. Prognosis
The prognosis for patients with peripheral vascular disease due to atherosclerosis is poor; patients with intermittent claudication due to atherosclerosis are at increased risk of death from cardiovascular disease (e.g. heart attack), because the same disease that affects the legs is often present in the arteries of the heart.The prognosis for neurogenic claudication is good if the cause of it can be addressed surgically. References


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