This is due to an increase in the refractive power of the lens, since axial length and keratometry readings do not reveal a corneal or length basis for a myopic shift. It is usually reversible with time.A possible side effect of hyperbaric oxygen therapy is the initial or further development of cataracts, which are a increase in opacity of the lens of the eye which reduces visual acuity, and can eventually result in blindness. This is a rare event, associated with lifetime exposure to raised oxygen concentration, and may be under-reported as it develops very slowly. The cause is not fully understood, but evidence suggests that raised oxygen levels may cause accelerated deterioration of the vitreous humour due to degradation of lens crystallins by cross-linking, forming aggregates capable of scattering light. This may be an end-state development of the more commonly observed myopic shift associated with hyperbaric treatment. Mechanism
The biochemical basis for the toxicity of oxygen is the partial reduction of oxygen by one or two electrons to form reactive oxygen species, which are natural by-products of the normal metabolism of oxygen and have important roles in cell signalling. One species produced by the body, the superoxide anion (O−2), is possibly involved in iron acquisition. Higher than normal concentrations of oxygen lead to increased levels of reactive oxygen species. Oxygen is necessary for cell metabolism, and the blood supplies it to all parts of the body.
Genetics
Fibrochondrogenesis is inherited in an autosomal recessive pattern. This means that the defective gene responsible for the disorder is located on an autosome, and two copies of the gene — one copy inherited from each parent — are required in order to be born with the disorder. The parents of an individual with an autosomal recessive disorder each carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder. Currently, no specific genetic mutation has been established as the cause of fibrochondrogenesis.Omphalocele is a congenital feature where the abdominal wall has an opening, partially exposing the abdominal viscera (typically, the organs of the gastrointestinal tract). Fibrochondrogenesis is believed to be related to omphalocele
type III, suggesting a possible genetic association between the two disorders. Diagnosis
Treatment
Epidemiology
Fibrochondrogenesis is quite rare. A 1996 study from Spain determined a national minimal prevalence for the disorder at 8 cases out of 1,158,067 live births.A United Arab Emirates (UAE) University report, from early 2003, evaluated the results of a 5-year study on the occurrence of a broad range of osteochondrodysplasias. Out of 38,048 newborns in Al Ain, over the course of the study period, fibrochondrogenesis was found to be the most common of the recessive forms of osteochondrodysplasia, with a prevalence ratio of 1.05:10,000 births.While these results represented the most common occurrence within the group studied, they do not dispute the rarity of fibrochondrogenesis.