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Experimental Biology and Medicine | 1949

A Modification of the Hemagglutination Test for Rheumatoid Arthritis.

George Heller; Abraham S. Jacobson; Maxwell H. Kolodny

Summary 1. The hemaggutination test for rheumatoid arthritis is modified by the selective absorption of non-specific factors. The details of this modification are described. 2. Of 39 cases with active peripheral rheumatoid arthritis with x-ray evidence of joint changes, 35 were positive by this test. 3. All cases of inactive peripheral rheumatoid arthritis, rheumatoid spondylitis without peripheral joint involvement and psoriatic arthritis tested were negative. 4. In presumptive cases of early rheumatoid arthritis without x-ray evidence of joint changes, the test was negative. 5. In 67 control cases, including a variety of non-rheumatoid arthropathies, the test was negative except in two cases of infectious hepatitis. 6. The modified test was positive in 90% of the proven cases of active peripheral rheumatoid arthritis tested; the Rose test in 61%; the streptococcus agglutination test in 58%. In all cases in which the modified test was negative, the Rose test and the streptococcus agglutination test were also negative. The authors express their thanks to Dr. R. Schuman, Miss E. C. Arrowsmith, and Mr. O. Vasquez of the Clinical Laboratory Service for technical assistance.


The American Journal of Medicine | 1956

The hemagglutination test for rheumatoid arthritis: III. Clinical evaluation of the sheep erythrocyte agglutination (S.E.A.) test and the gamma globulin (FII) tests

Abraham S. Jacobson; William H. Kammerer; Julius Wolf; Wallace V. Epstein; George Heller

Abstract Some 5,000 serologic tests involving two heterogenetically related test systems for the diagnosis of rheumatoid arthritis are analyzed. The tests were made in 1,576 patients with the following results, all referring to the first tests performed in individual patients: (1) Sixty-two per cent of 331 patients with rheumatoid arthritis had positive reactions to the S.E.A. test, and 69 per cent of 180 of these patients had positive reactions to the FII test. (2) Of those patients having rheumatoid spondylitis alone, rheumatoid spondylitis and rheumatoid arthritis, or psoriasis associated with arthritis, 10 per cent had positive reactions to the S.E.A. test and 15 per cent had positive reactions to the FII test. (3) Of all other varieties of arthritis including those with unclassified joint disease, 3 per cent had positive reactions to the S.E.A. test and 5.9 per cent had positive reactions to the FII test. (4) Of individuals with no joint complaints, 3 per cent had positive reactions to the S.E.A. test and 2 per cent had positive reactions to the FII test. There is an increase in the percentage of initially positive reactions to tests in rheumatoid arthritis with increase in stage of progression or class of incapacitation. However, the substance responsible for these positive reactions to tests may be present within twenty-four hours of the first joint complaints in rheumatoid arthritis. Male patients with rheumatoid arthritis have a somewhat higher incidence of positive reactions to S.E.A. tests in both initial and multiple determinations than females. Limitation of the diagnosis of rheumatoid arthritis to individuals with rheumatoid nodules results in 95 per cent positive reactions to the S.E.A. test and 92 per cent positive reactions to the FII test on first determinations. The serum titers of the majority of patients with rheumatoid arthritis vary within two dilution tubes for either test during the two years following the initial test. The response of these patients to any of the usual modes of therapy does not affect the reactions in these tests. The S.E.A. test has a greater tendency to convert from positive to negative or vice versa than does the FII test. Joint fluid studied concurrently with serum usually has the same or a significantly higher titer. The mechanisms of these tests and the nature of the circulating rheumatoid factor have been discussed.


The American Journal of Medicine | 1952

The effect of cortisone in Hodgkin's disease

Bernard Straus; Abraham S. Jacobson; Solomon A. Berson; Theodore C. Bernstein; Robert S. Fadem; Rosalyn S. Yalow

Abstract Ten patients with advanced Hodgkins disease were treated with cortisone for periods varying between two weeks and three months. There was considerable but transient subjective improvement in seven. Fever subsided to normal in three. Three patients became worse under therapy, all of whom died. In none was the unfavorable course attributable to the hormone. In only one instance was significant regression of nodal or parenchymal involvement seen. In another patient considerable diminution of a postauricular mass occurred under cortisone therapy twenty-five days after a course of nitrogen mustard. The role of cortisone in this situation is debatable. Studies of total body potassium with K showed a significant decrease in four of six patients which was not reflected by the plasma potassium level. Depression of thyroid activity was found in five of six patients as manifested by decrease in radioiodine uptake. Serial studies of the bone marrow regularly showed a stimulation of marrow elements by cortisone with marked increase in cellularity by the twentieth day of treatment. This was not always correlated with the findings in the peripheral blood. Little effect was noted on eosinophils, blood volume or carbohydrate metabolism as a result of cortisone. The sedimentation rate fell in five patients in whom serial observations were made. Relapses following reduction in dosage to 300 mg. weekly occurred in three patients in whom this was attempted. All three regained the previous limited improvement on restoration of 100 mg. daily dosage. Undesirable effects were edema in five and rounding of the face in eight, acne in three, weakness in three following reduction in dosage, and hypertension in two. Generalized convulsions occurred in one. Gastrointestinal bleeding from a gastric ulcer due to Hodgkins infiltration occurred in one. Another patient at autopsy eight days following cessation of cortisone therapy had perforated gastric and duodenal ulcers. He had had no symptoms referable to his gastrointestinal tract either before or after the perforation, unlike the case reported recently by Habif et al. We conclude from these observations that cortisone produces symptomatic improvement in some cases of advanced Hodgkins disease. Other than reduction of fever and sedimentation rate, objective changes are few. There is little or no effect on the neoplastic process. True remission was not achieved with this hormone in any of the ten patients treated.


Journal of Immunology | 1954

The Hemagglutination Test for Rheumatoid Arthritis II. The Influence of Human Plasma Fraction II (gamma Globulin) on the Reaction

George Heller; Abraham S. Jacobson; Maxwell H. Kolodny; William H. Kammerer


Journal of Immunology | 1955

The Hemagglutination Test for Rheumatoid Arthritis IV. Characterization of the Rheumatoid Agglutinating Factors by Analysis of Serum Fractions Prepared by Ethanol Fractionation

George Heller; Maxwell H. Kolodny; Irwin H. Lepow; Abraham S. Jacobson; Maria E. Rivera; Grace H. Marks


Journal of Immunology | 1952

The Hemagglutination Test for Rheumatoid Arthritis I. An Immunological Analysis of the Factors Involved in the Reaction

George Heller; Abraham S. Jacobson; Maxwell H. Kolodny; Roslyn L. Schuman


Journal of Immunology | 1952

The Hemagglutination Test for Rheumatoid Arthritis

George Heller; Maxwell H. Kolodny; Irwin H. Lepow; Abraham S. Jacobson; Maria E. Rivera; Grace H. Marks


Blood | 1950

GUANAZOLO IN THE THERAPY OF HODGKIN’S DISEASE

Bernard Straus; Solomon S. Berson; Theodore C. Bernstein; Abraham S. Jacobson


American Journal of Clinical Pathology | 1951

The effects of cortisone on the bone marrow in Hodgkin's disease.

Robert S. Fadem; Solomon S. Berson; Abraham S. Jacobson; Bernard Straus


American Journal of Clinical Pathology | 1949

Acute hemolytic anemia associated with elevated titer of cold agglutinins; report of case.

Ira L. Rubin; Abraham S. Jacobson; Leo M. Meyer

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George Heller

United States Department of Veterans Affairs

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Maxwell H. Kolodny

United States Department of Veterans Affairs

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Bernard Straus

United States Department of Veterans Affairs

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Irwin H. Lepow

University of Connecticut

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Robert S. Fadem

United States Department of Veterans Affairs

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Solomon S. Berson

United States Department of Veterans Affairs

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Ira L. Rubin

United States Department of Veterans Affairs

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Leo M. Meyer

United States Department of Veterans Affairs

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Rosalyn S. Yalow

United States Department of Veterans Affairs

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