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Retinal macroaneurysm leaking fluid at 0.0018 μl/min through a perivenous tunnel

nostaining to find evidence that the lens deposits were composed of crystals of L-ferritin (Brooks et al. 2002). Molecular genetic analysis has shown that different heterozygous mutations or deletions in the ironresponsive element (IRE) of the L-ferritin gene located on chromosome 19 are responsible for the syndrome (Girelli et al. 1995a,b). The mutations are thought to cause loss of the inhibitory feedback mechanism by increasing serum iron on the transcription of the L-ferritin gene. A heterozygous c.40A>G point mutation was found to cause the HHCS in our family. Three criteria must be fulfilled to make a clinical diagnosis of HHCS: increased serum ferritin concentrations in the absence of iron overload or other haematological abnormalities, and early-onset bilateral distinctive cataracts transmitted as an autosomal dominant trait. Apart from visual problems and cataract surgery when required, HHCS patients do not need any treatment once the correct diagnosis has been made (Girelli et al. 1995a,b). The most commonly encountered problem is a misdiagnosis of HHCS as hereditary haemochromatosis, which is then often inappropriately treated by phlebotomies that lead to iron deficiency anaemia (Girelli et al. 1995a,b). Since many physicians still diagnose iron overload by serum ferritin concentrations rather than using iron and transferrin saturation, it cannot be sufficiently emphasized that hyperferritinaemia does not always equal iron overload. Patients with unexplained hyperferritinaemia clearly need a thorough haematological evaluation, and such patients should certainly also be examined by an ophthalmologist, as the distinctive appearance of the cataract is paramount in establishing a correct diagnosis of HHCS.