Lives of the fellows

Philip Levine

b.10 August 1900 d.18 October 1987
MD Cornell(1923) Hon DSc Michigan(1967) FRCP(1973)

Philip Levine, who discovered the cause of rhesus haemolytic disease of the newborn, was born in Kletsk, Russia, but settled in Brooklyn with his parents, Morris Levine and his wife Faya Zirulick, whose father was a rabbi. After obtaining his BS at the City University of New York, Philip proceeded to Cornell University medical school where he graduated MD. From 1923-25 he was an intern at the Beth Moses Hospital, now the Maimonedes.

Philip Levine became an internationally known researcher in the field of immunohaematology and for 20 years was in charge of the Ortho Research Division at Raritan, New Jersey. In later years he was director emeritus of the Philip Levine Laboratories, a showpiece to his memory. His most important contribution to medicine, the discovery of the Rh factor, was a model of simplicity based on clinical observation and logical deduction.

Jaundice of the newborn has been known for hundreds of years, and was reported in twins in 1609. It was noticed later that babies with the familial form of the disease were also anaemic, and when in 1900 Karl Landsteiner discovered the ABO blood groups a mechanism became clear - there could be haemolysis because of ABO incompatibility between mother and baby. In white populations ABO haemolytic disease is usually not serious, and Philip’s great discovery came because he treasured his exceptions. He noted that some babies were jaundiced and seriously anaemic even when the parents were compatible on the ABO system. Further, mothers who needed blood near term often had a transfusion reaction when given their husband’s blood. Therefore Philip argued that there must be incompatibility of another blood group system.

In the USA, Landsteiner and Alexander Wiener had shown that rabbits injected with the blood of rhesus monkeys formed antibodies which agglutinated the red cells of human bloods carrying M antigen. When this anti-M antibody was absorbed it was found, c.1940, that the rabbit antibody still agglutinated 85% of human red cells. Since it was the monkey’s antigens which were responsible for the antibodies, Wiener [Munk's Roll, Vol.VII, p.592] called this system ‘rhesus’, and the terms ‘rhesus positive’ and ‘rhesus negative’ entered the language. On the clinical side, Wiener related his discovery chiefly to blood group reactions, but Levine immediately realized that here was the explanation for those unexpectedly jaundiced babies. The ones with ABO compatible parents had been damaged by rhesus incompatibility, the rhesus-negative mother having made antibodies against the baby’s paternally derived rhesus-postive cells.

This posed a question: ‘Why, with a birthrate in the UK of around 700,000 a year, were there not more affected babies?’ Theoretically there should have been around 60,000, but in fact there were only about a twentieth of that number. Levine in New York, and Race (q.v.) and Sanger (Mrs Race) in England produced the answer: some protection against rhesus immunisation was given by ABO incompatibility between mother and baby, a common occurrence. The mother’s naturally occurring anti-A (or anti-B in the rarer case of a B baby) destroyed the RH-positive foetal cells that had crossed into the maternal circulation. It was only in the ABO compatible pregnancies that the mother was at risk of being immunized against the rhesus antigen.

A generation later a British team found that rhesus-positive cells in the mother’s circulation could be destroyed by giving the anti-rhesus antibody, anti-D. Within 30 years rhesus disease had been both discovered and rendered preventable. In the prevention story, the USA and the UK were in competition, but Philip helped both sides equally, characteristically putting aside any thought of rivalry. Ronald Finn, in the UK, well remembers how, in the early days, Philip was ready to explain all the knotty problems with infinite patience.

The discoveries of Wiener and Levine were complementary, and both deserved the Nobel prize but, sadly, this was not to be. Though Philip was a delightful character, perhaps the Stockholm committee sensed that Wiener would not be happy with a joint award. Philip was a hard worker and in his later years wrestled with the P blood group system and its possible relation to cancer. Autoantibodies were another of his interests.

Philip Levine instituted and funded the Philip Levine lecture, presented annually on the pathogenesis of malignancy by Cornell University medical college, the Rockefeller Institute and the Memorial Sloan-Kettering Institute for Cancer Research.

It was for Levine’s work on rhesus haemolytic disease that the College elected him to the Fellowship in 1973. Philip was delighted and came specially to London to receive the award.

Philip Levine was a gentle man yet firm in his approach to science. His fascination for the unknown never waned and he had the admiration and respect of his peers. His dedication was untiring, and his genius for solving problems of incredibly complexity was unquenchable.

He married Hilda Perlmutter in 1938 and they had four children, three sons and a daughter, and five grandchildren. His wife and one son predeceased him. He was survived by their daughter and two sons.

Sir Cyril Clarke

[Lancet, 1987,2,1039-40; The Times, 21 Oct 1987; Johnson & Johnson, 2 Nov 1987; The Med.Technologist, July 1973,Vol.3,7,1; Triangle,Sandoz Journal of Med.Science, Sept 1961,3,168-70]

(Volume VIII, page 276)

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