Urinary coproporphyrin I in lead poisoning.

Many aspects of haemopoiesis in lead poisoning remain obscure. When industrial plumbism was common the haemolytic action of lead was frequently described (Aub, Fairhall, Minot, and Reznikoff, 1925), although there were atypical features. The erythrocytes were somewhat deficient in haemoglobin, and faecal urobilinogen was not increased. Lead poisoning also differs from true haemolytic anaemia in the occurrence of coproporphyrin III in the urine (Grotepass, 1932; Fischer and Duesberg, 1932; Watson, 1936). It is coproporphyrin I which is excreted in haemolytic conditions characterized by hyperplasia of the bone marrow (Watson, 1937; Dobriner and Rhoads, 1938; Grinstein, Kamen, Wikoff, and Moore, 1950). Rimington (1936) advanced the view that in enzymic synthesis of the porphyrins, in addition to type III porphyrin used in haemoglobin formation, a small amount of type I series is always produced, which, being of no value, is excreted. Urinary coproporphyrin I excretion therefore provided an index of the rate of haemopoiesis. Rimington (1938) further postulated that the coproporphyrin III excretion in lead poisoning is due to a partial blockage by lead of the entrance of iron into protoporphyrin 9, thus interfering with haernoglobin formation (Fig. 1). He discounted the haemolytic action of lead, since faecal urobilinogen was normal; but recent isotopic studies by London, Shemin, and Rittenberg (1948) on the conversion in vivo of glycine N1' to stercobilinogen have shown that the latter is a very unreliable index of the rate of degradation of circulating haemoglobin. Kench, Gillam, and Lane (1942) found that excretion of coproporphyrin III was not sufficient by itself to account for the degree of haemoglobin deficit in this disease, and suggested that lead interfered all along the line of enzymatic syntheses, causing restricted formation of porphyrin and other intermediates. R&MINcGTONS ENZYMIC HYPOrTESS.