Abstract
The mechanism of the disturbed metabolism of the respiratory pigments in pernicious anemia has been a matter of controversy. 1-4 Theoretically, qualitative and quantitative disturbance may occur at any stage in the construction and destruction of the hemoglobin molecule, but it is not clear whether the increased bile-pigment production and excretion is consequent to a quantitatively increased destruction of hemoglobin similar to that of hemolytic jaundice, or whether it is due to a partial or total pathologic metabolism of the precursors of hemoglobin.
Porphyrin and urobilin excretion in a case of pernicious anemia have been investigated quantitatively. It has been reported that an increased coproporphyrin I excretion in both the urine and feces is present during relapse, and that lower values are present during remissions. 5 , 6 , 7 However, because of the lack of adequate methods the reported data are inconclusive. Watson 8 reported adequate data on feces, but omitted determinations of the porphyrin in the urine.
Case History. A 61-year-old white male entered with anemia of 4 years' duration. Inadequate treatment with liver extract had been employed and the disease had progressed. Physical examination showed a subicteric tint of the skin, emaciation, and some atrophy of the papillae of the tongue. Examination of the blood on admission showed 900,000 R.B.C., hemoglobin 23%, mean corpuscular volume 1.13, color index 1.21, icterus index, 7, and W.B.C. 3,250. The blood smear and the histologic picture of the bone marrow were characteristic of pernicious anemia. Gastric analysis failed to reveal free hydrochloric acid, even after histamine. Details of treatment, and hematologic response are briefly summarized in Chart I. The patient received an injection of 5.0 cc. of liver extract (Lederle & Co. concentrate) and 10.0 cc. of liver extract (Eli Lilly & Co.) intramuscularly on the 16th and 17th days of observation respectively.
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