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Development of an Experimental Model Using Bilirubin 14C

MATTHEW MENKEN, MD; PETER V. D. BARRETT, MD; RICHARD L. SWARM, MD; NATHANIEL I. BERLIN, MD

Arch Neurol. 1966;15(1):68-73.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

KERNICTERUS as a clinical entity has been clearly associated with hyperbilirubinemia.¹ Plasma bilirubin levels exceeding 20 mg/100 cc are considered levels above which kernicterus can occur; yet, it is known that kernicterus can occur in infants at bilirubin levels considerably below 20 mg/100 cc, while much higher levels can be innocuous.² Normally, circulating bilirubin is entirely bound to albumin, and in vitro studies have shown that each mole of albumin can bind two³ or three⁴ moles of bilirubin. Odell⁵ showed that salicylates and sulfonamides may displace protein-bound bilirubin, emphasizing that the quantity of bilirubin that becomes unbound, and diffusible, may be of more importance in the production of kernicterus than the total bilirubin present in plasma. Silverman⁶ noted that premature infants treated with sulfisoxazole developed kernicterus six times more frequently than controls. It has been shown, however, that the cleavage of the bilirubin-albumin linkage . . . [Full Text PDF of this Article]

Author Affiliations
BETHESDA, MD

From the Metabolism Branch and Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Md. Dr. Swarm is presently at the Department of Pathology, School of Medicine, University of Cincinnati, Cincinnati.

Footnotes
Submitted for publication March 17, 1966; accepted April 4.

Read in part before the Southern Section, American Federation of Clinical Research, New Orleans, Jan 29, 1966.

Reprint requests to Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Md 20014 (Dr. Menken).

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