Prevention
It is possible to prevent the onset of prepatellar bursitis, or prevent the symptoms from worsening, by avoiding trauma to the knee or frequent kneeling.: p. 610  Protective knee pads can also help prevent prepatellar bursitis for those whose professions require frequent kneeling and for athletes who play contact sports, such as American football, basketball, and wrestling. Treatment
Non-septic prepatellar bursitis can be treated with rest, the application of ice to the affected area, and anti-inflammatory drugs, particularly ibuprofen. Elevation of the affected leg during rest may also expedite the recovery process. Severe cases may require fine-needle aspiration of the bursa fluid, sometimes coupled with cortisone injections. However, some studies have shown that steroid injections may not be an effective treatment option. After the bursitis has been treated, rehabilitative exercise may help improve joint mechanics and reduce chronic pain.: p. 2320 Opinions vary as to which treatment options are most effective for septic prepatellar bursitis.: p. 360  McAfee and Smith recommend a course of oral antibiotics, usually oxacillin sodium or cephradine, and assert that surgery and drainage are unnecessary.: p. 609  Wilson-MacDonald argues that oral antibiotics are "inadequate", and recommends intravenous antibiotics for managing the infection. Some authors suggest surgical irrigation of the bursa by means of a subcutaneous tube.: p. 360  Others suggest that bursectomy may be necessary for intractable cases; the operation is an outpatient procedure that can be performed in less than half an hour.: p.
Peroxisomal disorders represent a class of medical conditions caused by defects in peroxisome functions. This may be due to defects in single enzymes important for peroxisome function or in peroxins, proteins encoded by PEX genes that are critical for normal peroxisome assembly and biogenesis. Peroxisome biogenesis disorders
Peroxisome biogenesis disorders (PBDs) include the Zellweger syndrome spectrum (PBD-ZSD) and rhizomelic chondrodysplasia punctata type 1 (RCDP1). PBD-ZSD represents a continuum of disorders including infantile Refsum disease, neonatal adrenoleukodystrophy, and Zellweger syndrome. Collectively, PBDs are autosomal recessive developmental brain disorders that also result in skeletal and craniofacial dysmorphism, liver dysfunction, progressive sensorineural hearing loss, and retinopathy.PBD-ZSD is most commonly caused by mutations in the PEX1, PEX6, PEX10, PEX12, and PEX26 genes. This results in the over-accumulation of very long chain fatty acids and branched chain fatty acids, such as phytanic acid. In addition, PBD-ZSD patients show deficient levels of plasmalogens, ether-phospholipids necessary for normal brain and lung function.RCDP1 is caused by mutations in the PEX7 gene, which encodes the PTS2 receptor. RCDP1 patients can develop large tissue stores of branched chain fatty acids, such as phytanic acid, and show reduced levels of plasmalogens. Enzyme and transporter defects
Peroxisomal disorders also include:

References
External links

Peroxisomal+disorders at the US National Library of Medicine Medical Subject Headings (MeSH)