Whereas the results described and the following discussion (Michael 
Freemantle) do suggest a case of porphyrinuria other than that due to 
porphyria, we would advocate carrying out faecal porphyrin analysis 
for completeness.

Certainly, the slightly elevated PBG and normal ALA/creat ratios do 
not indicate an acute porphyria provided the urine sample was taken 
when the patient was symptomatic (probably not if she was seen in the 
OP clinic).  However, whereas PBG levels may be raised between 
attacks in AIP, this is not the case for patients with VP or HCP 
where PBG may fall to normal or be only slightly elevated post 
attack.  Follow up with a plasma and faecal sample can be useful.  
Patients with VP show a characteristic emission peak at 624nm on a 
fluorescence emission scan of the plasma and may demonstrate 
increased protoporphyrin and copro III isomer in the faeces.  
Patients with HCP show increased faecal excretion of Copro III.  
Liver disease may also affect faecal porphyrin excretion but the only 
suggestion of liver disease in this patient is a slightly elevated 
ALT.  Presumably, other LFTs were normal (does this include AST and 
Gamma GT)?  Are there any details of the drug history and is there 
any evidence of alcohol abuse which may also affect urine poprhyrin 
excretion?

Keith Allen
Tim Degg

United Leeds Teaching Hospitals


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