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The biochemical criteria of an acute attack include more than a fivefold increase of urinary PBG excretion (Table 1), which can be detected by a simple Watson-Schwartz or Hoesch qualitative test.31 The results should be confirmed by a quantitative measurement of urinary PBG, since false positive results in these screening tests are possible, especially, if perchloric acid instead of amyl alcohol is used as an extract.31–33 If the urine samples are not sheltered from the light, urinalysis may become false negative.31–33 Urinary excretion of PBG is elevated in 88% of the patients with AIP in remission.34 During an acute attack PBG excretion increases commonly at least two- to fourfold from the values found in remission.34 Urinary ALA is always increased during an acute attack but remains elevated only in 61% of AIP cases in remission.34 In AIP, urinary excretion of uroporphyrins is increased, including both I and III isomers, and exceeds that of coproporphyrins I and III.34 Of note, abnormal metabolism of porphyrin and their precursors may also be detected in patients with hepatopathy or heavy metal intoxications.31,35 The clinical manifestations may even resemble AIP,36 but biochemically only a mild to moderate coproporphyrinuria is present, and porphyrin precursors are commonly only transiently elevated.35,36 If urinary ALA level exceeds that of PBG significantly, lead intoxication should be excluded.31 In AIP, plasma porphyrin emission spectrum test with excitation wave length of 405 nm shows a peak at 615–620 nm during an acute attack similar to HCP but it can be less frequently found in remission.32,34 Emission peak is due to porphyrins’ ability to absorb light at wave length around 400 nm and their emission as red fluorescence, at around 600 nm.37 Plasma emission spectrum test is used mainly to exclude symptomatic V P, since it has a unique 624–627 nm spectrum due to protein-associated plasma porphyrins.31,32,38 Of note, emission peak is commonly negative at the asymptomatic phase of VP