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4. Procedure and evidence 4.1.Pharmacotherapy 5-HT1B 1D agonists The serotonin-5-HT1B 1D receptor agonists Table 1 ; almotriptan, eletriptan, frovatriptan, naratriptan, rizatriptan, sumatriptan and zolmitriptan are specific antimigraine agents which are ineffective in tensiontype headache. All triptans have been confirmed to be effective in large placebo-controlled studies Ferrari et al., 2001, Goadsby et al., 2002 ; . For sumatriptan Tfelt-Hansen et al., 1995, The Oral Sumatriptan and Aspirin plus Metoclopramide Comparative Study Group, 1992 ; and zolmitriptan Geraud et al., 2002 ; there are comparative studies with oral acetylsalicylic acid ACE ; in combination with metoclopramide. In these comparative studies the triptans were not or only marginally more effective than acetylsalicylic acid. In about 60% of non-responders to non-steroidal anti-inflammatory drugs, triptans are effective Diamond et al., 2004 ; . Sumatriptan 6 mg s.c. was more effective than 1000 mg acetylsalicylic acid i.v., but showed more side effects Diener and for the ASASUMAMIG Study Group, 1999 ; . Ergotamine was less effective in comparative studies with sumatriptan The Multinational Oral Sumatriptan Cafergot Comparative Study Group, 1991 ; and eletriptan Diener et al., 2002 ; . Triptans unlike ergotamine tartrate act at every timepoint within an attack, i.e. they do not have to be taken immediately at the start of the attack. They do however act more effectively if they are taken earlier in a migraine attack Burstein et al., 2004, Dowson et al., 2004 ; . In order to prevent the development of a medication overuse headache an early intake can only be recommended if the attacks are not too frequent 10 headache days month ; and if the patient can clearly distinguish migraine from tension-type headache. With longer-lasting migraine attacks the migraine headaches may recur at the end of the pharmacological effect of the antimigraine agent a so-called "headache recurrence" ; . Recurrence is defined as a deterioration in headache intensity from headache free or mild headache to moderate or severe headache in a period of 2 to hours after the first effective medication intake Ferrari, 1999 ; . This problem is more prevalent with triptans than with ergotamine tartrate or acetylsalicylic acid. Recurrence of the headaches occurs in 15-40% of patients after oral intake of triptans, whereby a second application of the substance is then effective again Ferrari et al., 1994 ; . If the first application of a triptan is ineffective, it is useless to use a second dose for the same migraine attack. All triptans as well as ergotamine can lead to an increase in attack frequency and ultimately to medication overuse headache or chronic migraine if they are taken too frequently Katsarava et al., 2000, Limmroth et al., 1999 ; . Therefore triptans should not be used on more than 10 days per month. Life-threatening adverse events myocardial infarctionion, severe heart rhythm disorders, stroke ; have been observed after use of sumatriptan in a frequency of 1: 000, 000 OQuinn et al., 1999, Welch et al., 2000 ; . In almost all patients there were either clear contraindications e.g. prexisting existing coronary heart disease ; , or the migraine diagnosis was wrong. For the other triptans no data have yet been published. Since the mode of action of the different triptans is identical, a similar incidence of life-threatening adverse events can be assumed oral triptans have a lower risk than subcutaneous sumatriptan ; . For safety reasons in patients who suffer from migraine with aura, triptans should only be applied after the aura fades and when the headache starts. Furthermore, triptans are ineffective when applied during the aura phase Bates et al., 1994, Olesen et al., 2004 ; . Population-based studies, however, show no raised risk for vascular events when triptans are used compared to analgesics Hall et al., 2004, Velentgas et al., 2004.

Figure 1 Family pedigree. Family members and their age are shown. The proband is indicated by an arrow and affected family members by filled shapes. TS, transferrin saturation % SF, serum ferritin concentration mg l ; . minimal staining in hepatocytes, as detected by Perls' Prussian blue staining. No fibrosis was detected. Hepatic iron concentration was 96 mmol g dry weight normal 535 ; with a hepatic iron index of 2.1 normal , 1.1 ; . No other secondary cause for iron loading for example, thalassemia, porphyria cutanea tarda, or chronic liver disease ; was detected. Liver histology and biochemistry were suggestive of ferroportin disease. The entire coding region and splice sites of the ferroportin gene from the proband were polymerase chain reaction amplified and sequenced, as previously described.4 Other family members were subsequently evaluated. The presence of a cytosine to adenine change at nucleotide 230 of ferroportin, which results in mutation of an alanine to aspartic acid at amino acid 77 A77D ; , was identified in the proband. Subsequently, this change was also identified in the proband's father, sister, and daughter fig 1 ; . This is the same mutation which was identified in Italy by Montosi and colleagues.2 There is no known ancestral link between the family reported here and that in Italy. Thus it is likely that the A77D mutation has occurred in the two populations separately, as appears to be the case with the V162del mutation48 which has so far been reported in five geographic locations. As knowledge about ferroportin disease is uncommon in the community, unlike HFE associated haemochromatosis, it is possible that some cases of this disorder are not recognised and thus remain undiagnosed. This particular case was not diagnosed until liver biopsy was performed. The raised serum ferritin level was initially attributed to viral illness. Because transferrin saturation and HFE genotype were normal, a diagnosis of iron overload was not initially considered. In conclusion, we report the first identification of ferroportin disease caused by the A77D mutation in a region outside of Italy. This suggests that the A77D mutation may be more widespread than initially thought. This report also suggests that some cases of ferroportin disease may go undiagnosed. Ferroportin disease should thus be considered when a patient presents with a high serum ferritin, even when transferrin saturation and HFE genotype are normal.

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