Blocking type immunoglobulins in patients with nongoitrous primary hypothyroidism in area of iodine deficiency.
We have evaluated the role of circulating serum immunoglobulins (IgG) which inhibit the growth of thyroid in the etiology of thyroid atrophy in endemic cretinism. Twenty nongoitrous cretins (13 women and 7 men, age range: 9-33) were classified on the basis of clinical criteria for cretinism in China. They were born and living in an iodine deficient area, Xinjiang, northwest China. Antimicrosomal antibody titers were negative in all serum. Nine patients (seven women and two men; age range: 11-23) were biologically primary hypothyroid. Seven subjects were of a myxedematous form and two subjects were of a mixed form. We have studied thyroid-growth inhibiting immunoglobulin (TGII) activity that was measured as an inhibitory effect of 4 mg/ml IgG on TSH-induced [3H]-thymidine incorporation into the DNA of a rat thyroid follicular cell line, FRTL5 cells. Six (five women and one man) out of the nine patients with primary hypothyroidism (66.7 percent) had TGII. We also measured other growth-blocking IgG that inhibited [3H]-thymidine incorporation into DNA stimulated by insulin-like growth factor-I (IGF-I), a growth factor working through a cAMP-independent pathway. Five (three women and two men) out of nine patients (55.6 percent) with nongoitrous primary hypothyroidism had IGF-I-blocking IgG. These results indicate that TGII plays an important role in atrophy of the thyroid in spite of increased serum TSH concentrations, and IgG which inhibits thyroid growth stimulated by IGF-I also might play a role in thyroid atrophy in some endemic cretins.(ABSTRACT TRUNCATED AT 250 WORDS)
Tang
T
T
Department of Pathophysiology, Tianjin Medical College, China.
Wang
Y G
YG
Tsuboi
K
K
Irie
M
M
Ma
T
T
Ingbar
S H
SH
D000293:Adolescent; D000328:Adult; D001284:Atrophy / Q000209:etiology; D001667:Binding, Competitive; D002648:Child; D002681:China / Q000453:epidemiology; D003409:Congenital Hypothyroidism / Q000453:epidemiology / Q000209:etiology / Q000276:immunology; D004247:DNA / Q000378:metabolism; D005260:Female; D006801:Humans; D007037:Hypothyroidism / Q000453:epidemiology / Q000276:immunology* / Q000503:physiopathology; D007074:Immunoglobulin G / Q000032:analysis* / Q000502:physiology; D007334:Insulin-Like Growth Factor I / Q000502:physiology; D007455:Iodine / Q000172:deficiency*; D008297:Male; D013936:Thymidine / Q000378:metabolism; D013961:Thyroid Gland / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D013972:Thyrotropin / Q000494:pharmacology; D014316:Tritium
D007074:Immunoglobulin G; D014316:Tritium; D007334:Insulin-Like Growth Factor I; D013972:Thyrotropin; D004247:DNA; D007455:Iodine; D013936:Thymidine