- Meeting abstract
- Open Access
Sequential and combined treatment of prolidase deficiency leg ulcers
© Palumbo et al; licensee BioMed Central Ltd. 2010
- Published: 19 May 2010
- Skin Graft
- Recessive Gene
- Cutaneous Lesion
- Dose Corticosteroid
The Authors report a case of chronic cutaneous lesions in a patient affected by prolidase deficiency, a rare disorder inherited through an autosomal recessive gene (50 cases reported ).
Clinical signs of prolidase deficiency
Hypoplasia of the jaws
Dry crusted lesions
Dry fissured erythematous
Palms and soles
The deficiency of the enzyme prolidase is responsible for massive loss of proline in the urine which is estimated to be as high as 3 g/die. The diagnosis is ascertained by iminopeptiduria greater than 5 mmol/24h. A characteristic feature is absolute resistance to all forms of treatment including rejection of skin grafts.
In January 2009 and all lesions were covered and during follow-up the use of autologous PLT-gel for 10 weeks was proposed. From the third application clinical data showed good results and after the tenth application all the lesions were treated with advanced devices. No signs of infection were present. The patient is now going into complete remission of skin lesions.
Use of platelet gel is commonly accepted for the treatment of leg ulcers because it is rich in growth factors. Their presence could be a key to block the onset of a flogistic reaction to proline and hydroxyproline account in derma. All clinical investigations shows that after the PLT gel application there is not a rejection to homologous skin implants but an improvement in symptomatology and inability.
This article is published under license to BioMed Central Ltd.