The Presence of Thyrogastric Antibodies in First Degree Relatives of Type 1 Diabetic Patients Is Associated with Age and Proband Antibody Status

• Published in: The journal of clinical endocrinology and metabolism Vol. 86; no. 9; pp. 4358 - 4363
• Main Authors: De Block, Christophe E. M., De Leeuw, Ivo H., Decochez, Katelijn, Winnock, Frederic, Van Autreve, Jan, Van Campenhout, Christel M., Martin, Manou, Gorus, Frans K.
• Format: Journal Article
• Language: English
• Published: Endocrine Society 01-09-2001
• ISSN: 0021-972X; 1945-7197
• DOI: 10.1210/jcem.86.9.7833

A quarter of type 1 diabetic patients have thyrogastric
autoantibodies (thyroid peroxidase and gastric parietal cell
antibodies). Clinical, immune, and genetic risk factors help predict
antibody status. First degree relatives of these patients may also
frequently exhibit these antibodies. We assessed the prevalence of
thyrogastric antibodies and dysfunction in first degree relatives in
relation to age, gender, human leukocyte antigen-DQ type, β-cell
antibody (islet cell, glutamic acid decarboxylase-65, and tyrosine
phosphatase antibodies), and proband thyrogastric antibody status.
Sera from 272 type 1 diabetic patients (116 men and 156 women; mean
age, 27 ± 18 yr; duration, 10 ± 9 y), 397 first degree
relatives (192 men and 205 women; parents/siblings/offspring,
48/222/127; age, 22 ± 10 yr), and 100 healthy controls were
tested for islet cell antibodies and gastric parietal cell antibodies
by indirect immunofluorescence and for tyrosine phosphatase, glutamic
acid decarboxylase-65, and thyroid peroxidase antibodies by
radiobinding assays.
Glutamic acid decarboxylase-65 antibodies were present in 68% and 5%,
islet cell antibodies were present in 36% and 2.5%, tyrosine
phosphatase antibodies were present in 45% and 0.5%, thyroid
peroxidase antibodies were present in 21% and 4.5%, and gastric
parietal cell antibodies were present in 18% and 11% of diabetic
patients and relatives, respectively. The presence of thyroid
peroxidase antibodies in relatives was determined by age (β =
0.22; P = 0.0001) and proband thyroid peroxidase
antibodies status (β = -2.6; P = 0.002; odds
ratio = 11.1). Gastric parietal cell antibody positivity in
relatives was associated with age (β = 0.04;
P = 0.026). Gastric parietal cell antibody-positive
compared with gastric parietal cell antibody-negative relatives were
more likely to have gastric parietal cell antibody-positive probands
(P = 0.01; odds ratio = 3.0). β-Cell
antibody status and human leukocyte antigen-DQ type did not influence
thyrogastric antibody status in relatives. (Sub)clinical dysthyroidism
was found in 3%, iron deficiency anemia was present in 12% (26%
gastric parietal cell antibody-positive and 9% gastric parietal cell
antibody-negative subjects; P = 0.009), and
pernicious anemia was found in 0.5% (5% gastric parietal cell
antibody-positive and 0% gastric parietal cell antibody-negative
subjects; P = 0.012) of relatives. They had less
thyroid dysfunction (P < 0.0001) and pernicious
anemia (P = 0.018) than diabetic probands.
In conclusion, thyrogastric antibodies and dysfunction are more
prevalent in type 1 diabetic patients than in first degree relatives.
The presence of these antibodies in relatives is associated with age
and proband antibody status, but not with β-cell antibodies or human
leukocyte antigen-DQ type.