Patrick. Jaynes. Gordon. F. Kapke. In Vitro Stability of Nomifensine in. Plasma. To the Editor: After oral administration in man, unconjugated nomifensine. (Figure.
relationship between Crohn’s disease and iron deficiency has been reported (8), which underlines the importance of determining iron in the serum of these patients. ESA has verified the interference of sulfasalazine with the Ferrochem 3050 measurements. References I. Mogayzel, W., Matson, W. R., Vitukevich, K., and Zink, E. W., Rapid analysis of serum iron and TIBC with the ESA, Inc. Ferrochem Model 3050 Serum lron/TIBC Analyzer. Abstr. 5th Ann. Meeting, FACSS, 1978, abstract no. 186. 2. Schroder, H., and Campbell, D. E. S., Absorption, metabolism, and excretion of salicylazosulphapyridine in man. (‘un. Pharmacol. Ther. 13, 539-551 (1972). 3. Das, K. M., Eastwood, M. A., McManus, .J. P. A., and Sircus, W., The role of the colon in the metabolism of salicylazosulphapyridine. Scand. J. Gastroenterol. 9, 137-141 (1974).
4. I)as, K. M., and Dubin, R., Clinical pharmacokinetics of sulphasalazine. Clin. Pharmacokinet.
5. A.ad Khan, A. K., and Truelove, S. C., Topics w Gastroentero/ogv, chapter 24, Hlackwell Scientific Publications, L(,ndon, England, 1976, p 367. 6. l)as, K. M., Eastwood, M. A., McManus, J. P. A., and Sircus, W., The metabolism of salicylazosulphapyridine in ulcerative Gut 14,631-641 (1973).
J. W., Summers, R. W., Kern, F. .Jr., et al., A trial of sulphasalazine as adjunctive therapy in Crohn’s disease. Gastroent erologv 77, 887-897 (1979). S. Child, ,J. A., Brozovic, N. H., Dyer, D. L., 7. Singleton,
et aI., The diagnosis tients with Crohn’s (1973).
of iron deficiency in padisease. Gut 14, 642-648
Patrick Jaynes Gordon F. Kapke Dept. Univ. Iowa
Pathol. of Iowa Hospitals City,
In Vitro Stability of Nomifensine in Plasma To the Editor:
After oral administration in man, unconjugated nomifensine (Figure 1) comprises 120 mg/L) and six
y’ -O.O2 ‘0.03 r’-O.75 p”O,OI
2O SERUM OILIRU8N
Fig. 2. Serum hyperbilirubinemic serum bilirubin
Ca2+ concentrations in and control infants vs. concentrations
as controls had daily total and Ca2+ determinations on each of the first seven postnatal days. The infants were matched for gestational age and Apgar scores, two factors important in neonatal hypocalcemia. Ca2+ in serum decreased linearly with increasing bilirubin in all samples tested in vitro (Figure 1). No precipitation was seen at any of the bilirubin concentrations in the presence of serum pro-
when bilirubin was added to serum, we were not able to detect a change in the residual binding capacity for bilirubin ascribable to increased calcium concentration. The residual binding capacity was unaltered even at a calcium concentration of 160 mg/L. When proteins were absent, increasing concentrations of bilirubin added to calcium in aqueous solution resulted in precipitation when the molar ratio of bilirubin to calcium exceeded 1:1. In the six infants with hyperbilirubinemia, serum hilirubin was highest (range 137 to 183 mg/L) and Ca2 lowest (range 31.6 to 41.7 mg/L) on postnatal days 3 to 6. In the six matched control infants, serum bilirubin was highest (range 90 to 112 mg/L) on days 3 to 5 and serum Ca2+ was lowest (range 36.2 to 39.0 mg/L) on days 2 to 3. The six hyperbilirubinemic infants had a significantly lower serum Ca2+ as compared to the six matched controls, 37.5 ± 0.4 (mean ± SEM) vs 39.6 ± 0.2 mg/L (paired t; p