HEMATOPORPHYRINURIA is a rare disease, probably familial in origin, and caused by an inborn error of the hemoglobin metabolism, in the form of a reversion to an embryonic type.1 From the etiologic point of view the porphyrias have been classified as congenital, acute and chronic. The acute form has been further subdivided into acute toxic and acute idiopathic porphyria.2 As pointed out by Watson and others,3 the acute toxic and the acute idiopathic form probably represent the same condition and are indistinguishable either clinically or by laboratory procedures. It is assumed that both forms are produced by some toxic agent, which in the acute idiopathic form has not been identified, while in the acute toxic form it is usually a barbiturate or one of the members of the sulfonamide group.4 However, Eldahl5 stressed the fact that conditions such as anxiety, exhaustion and infection can also