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Thymoma, Pure Red Cell Aplasia, Pernicious Anaemia and Candidiasis: a Defect in Immunohomeostasis
Author(s) -
RobinsBrowne R. M.,
Green R.,
And J. Katz,
Becker D.
Publication year - 1977
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1977.tb05749.x
Subject(s) - pernicious anaemia , intrinsic factor , atrophic gastritis , thymoma , medicine , pure red cell aplasia , red cell , antibody , achlorhydria , lymphocyte , gastroenterology , immunology , endocrinology , vitamin b12 , bone marrow , gastritis , stomach
S ummary . A patient is reported who presented with anaemia and oral candidiasis. Investigation revealed a spindle cell thymoma, and a serum inhibitor of haem synthesis associated with pure red cell aplasia. He was also shown to have the Addisonian pernicious anaemia defect, diagnosed on the basis of a depressed serum level of vitamin B 12 , 57 Co‐cyanocobalamin absorption studies, the presence of intrinsic factor blocking antibodies and atrophic gastritis with an elevated serum gastrin level. A serum inhibitor of candida‐induced lymphocyte transformation, which may have accounted for the chronicity of the candidiasis, was also demonstrated. Following thyniectomy, whereas the antibodies to intrinsic factor and gastric mucosa, and the serum inhibitor of candida‐induced lymphocyte blastogenesis persisted, the inhibitor of haem synthesis disappeared. Moreover, red cell autoagglutinins, associated with a mildly shortened red cell life span, were detected for the first time. Although the patient's anaemia improved following thymectorny, mild megaloblastic changes were noted in the bone marrow. Parenteral vitamin B 12 therapy reversed these changes and a normal level of haemoglobin has subsequently been maintained. The candidiasis, however, has persisted. It is suggested that the defect in immunohomeostasis in the patient may have resulted from an abnormality or deficiency of specific suppressor T‐lymphocytes.