Prevention of the decrease in sensitivity of an amperometric glucose sensor in undiluted human serum

patients with AIP and all four patients with VP. Because our three patients were excreting high concentrations of urine PBG at the time of fecal collection, their serum PBG was probably increased. If this is the source of fecal uroporphyrin, it probably would also be seen during acute attacks of the other acute porphyrias, as has been reported for VP (12). HCP was excluded from the differential diagnosis in all three cases by the low proportion of fecal coproporphyrin III (2) and by the proportion of coproporphyrin I exceeding coproporphyrin III for all three cases (13). VP is characterized by a fecal porphyrin trace in which protoporphyrin predominates (2) and was excluded because protoporphyrin was ,5% of the total porphyrin in all three patients. We therefore concluded that all three patients have AIP with increased fecal porphyrins and an increased fecal uroporphyrin fraction. The source of the uroporphyrin is probably the nonenzymatic condensation of PBG produced during the acute attack and excreted into the bile. Fecal uroporphyrin in patients excreting excess PBG could, therefore, be a feature of the acute attack in any of the three acute porphyrias.