Diabetes Mellitus and Pernicious Anemia

Munichoodappa, Choodappa Setty; Kozak, George P.

doi:10.2337/diab.19.10.719

Cited by 29 publications

(9 citation statements)

References 8 publications

(13 reference statements)

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“…Moreover, IDDM patients without clinical manifestations of organspecific autoimmune disease and their relatives have a high prevalence of thyroid microsomal, gastric parietal, and adrenal antibodies that support an autoimmune etiology for IDDM (5)(6)(7)(8)37). Moreover, IDDM patients without clinical manifestations of organspecific autoimmune disease and their relatives have a high prevalence of thyroid microsomal, gastric parietal, and adrenal antibodies that support an autoimmune etiology for IDDM (5)(6)(7)(8)37).…”

Section: Discussionmentioning

confidence: 97%

Autoantibodies to Glutamic Acid Decarboxylase in Patients with IDDM and Autoimmune Thyroid Disease

et al. 1994

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Autoantibodies to glutamic acid decarboxylase (GAD), previously reported to be the 64,000-M(r) (64K) islet cell protein, were measured by a radioimmunoassay using purified pig brain GAD in 29 insulin-dependent diabetes mellitus (IDDM) patients with autoimmune thyroid disease (AITD) and in 29 sex- and disease duration-matched IDDM patients without AITD. Islet cell antibodies (ICAs) and 64K antibodies were also determined. In IDDM patients with short-duration diabetes (< 1 year), the prevalence and levels of GAD antibodies were 100% (8 of 8) and 609 +/- 166 U (means +/- SE), respectively, in IDDM patients with AITD and 81.8% (9 of 11) and 90 +/- 51 U, respectively, in patients without AITD. In patients with long-standing IDDM (3-22 years), the prevalence and levels of GAD antibodies were 76.2% (16 of 21) and 193 +/- 66 U, respectively, in patients with AITD and 50.0% (9 of 18) and 36 +/- 14 U, respectively, in patients without AITD. For up to 6 years after the onset of IDDM, the levels of GAD antibodies in IDDM patients with AITD were significantly higher than in IDDM patients without AITD. A close and significant correlation was found between GAD antibodies and ICA or 64K antibodies in IDDM patients with AITD. Our results demonstrate that high levels of GAD antibodies were present in IDDM patients with AITD. The observed differences in GAD immunoreactivity between IDDM patients with and without AITD might help evaluate the role of GAD antibodies in IDDM.

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Section: Discussionmentioning

confidence: 97%

Autoantibodies to Glutamic Acid Decarboxylase in Patients with IDDM and Autoimmune Thyroid Disease

et al. 1994

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“…Clinically and serologically, pernicious anaemia is associated with diabetes (Root, 1931;Arepakis, Bock & Williams, 1963;Moore & Neilson, 1963;Irvine & Davies, 1963;Ungar et al, 1968;Munichoodappa & Kozak, 1970) and with auto-immune thyroiditis (Irvine, Davies & Delmore, 1962;Doniach, Roitt & Taylor, 1963;Tudhope & Wilson, 1960). Serologically, there is an association between auto-immune thyroiditis and diabetes (Petit, Landing & Guests, 1961;Landing et al, 1963;Simkins, 1968;Irvine et al, 1970) but no definite clinical relationship has been reported to substantiate these findings.…”

Section: Discussionmentioning

confidence: 99%

Diabetes mellitus and hypothyroidism

Bridgman

1971

Postgraduate Medical Journal

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Summary It would appear from the literature that hypothyroidism is rare in male diabetics. Serologically, there is an established association between autoimmune thyroiditis and diabetes mellitus. However, very little clinical evidence has been produced to confirm these findings. A series of four male insulin-dependent diabetics with hypothyroidism, including three who had latent pernicious anaemia, were studied. Their case histories and a review of the subject are presented

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“…This interest results from the occasional clinical association of diabetes and autoimmune diseases of the ad renal [13]. thyroid [14,15], and hemato poietic tissues [16], the increased frequency of antibodies to thyroid and gastric parietal cells among diabetics [17,18]. the presence of islet cell cytoplasmic and surface antibodies in the serum of recently diagnosed type I dia betics [19][20][21], the existence of HLA-linked and properdin factor B (BO genes [22][23][24][25], the suggestion that suppressor T cell generation is defective in type I diabetes [26], the evi dence of increased numbers of circulating lapositive T lymphocytes [27] and the observa tion of Gepts [28] and others of a striking lymphocytic infiltration of the pancreatic is lets (insulitis) in recently diagnosed type 1 di abetics.…”

Section: Introductionmentioning

confidence: 99%