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Autoimmunity Reviews
Volume 13, Issues 4–5, April–May 2014, Pages 417–422
9th International Congress on Autoimmunity


In de reeks: Diagnostic criteria in Autoimmune diseases o.a. deze 2 artikelen:
1) Hashimoto thyroiditis: Clinical and diagnostic criteria
2) Diagnosis and classification of autoimmune parathyroid disease



1) Hashimoto thyroiditis: Clinical and diagnostic criteria
Abstract
Hashimoto thyroiditis (HT), now considered the most common autoimmune disease, was described over a century ago as a pronounced lymphoid goiter affecting predominantly women. In addition to this classic form, several other clinico-pathologic entities are now included under the term HT: fibrous variant, IgG4-related variant, juvenile form, Hashitoxicosis, and painless thyroiditis (sporadic or post-partum). All forms are characterized pathologically by the infiltration of hematopoietic mononuclear cells, mainly lymphocytes, in the interstitium among the thyroid follicles, although specific features can be recognized in each variant. Thyroid cells undergo atrophy or transform into a bolder type of follicular cell rich in mitochondria called Hürthle cell. Most HT forms ultimately evolve into hypothyroidism, although at presentation patients can be euthyroid or even hyperthyroid. The diagnosis of HT relies on the demonstration of circulating antibodies to thyroid antigens (mainly thyroperoxidase and thyroglobulin) and reduced echogenicity on thyroid sonogram in a patient with proper clinical features. The treatment remains symptomatic and based on the administration of synthetic thyroid hormones to correct the hypothyroidism as needed. Surgery is performed when the goiter is large enough to cause significant compression of the surrounding cervical structures, or when some areas of the thyroid gland mimic the features of a nodule whose cytology cannot be ascertained as benign. HT remains a complex and ever expanding disease of unknown pathogenesis that awaits prevention or novel forms of treatment.

Table 1
Clinico-pathological spectrum of Hashimoto thyroiditis
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Table 2.
Key features of the clinico-pathologic forms of Hashimoto thyroiditis
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4.2. Thyroid antibodies
Circulating antibodies to thyroperoxidase are now considered the best serological marker to establish a diagnosis of HT. They are found in about 95% of HT patients but are rare in healthy controls. In post-partum thyroiditis they also have a unique predictive role since pregnant women who have thyroperoxidase antibodies at the beginning of pregnancy are at greater risk of developing hypothyroidism in the first year after delivery, as well as long-lasting thyroid impairment. The titer of thyroperoxidase antibody correlates well with the number of autoreactive lymphocytes infiltrating the thyroid [57] and the degree of sonographic hypoechogenicity.

Antibodies to thyroglobulin, the most abundant protein of the thyroid gland, are less sensitive (positive in only 60–80% of HT patients) and less specific (positive in a greater proportion of healthy controls) than thyroperoxidase antibodies. Nevertheless, they etc. etc.


Fig. 1.
Correlation between thyroperoxidase and thyroglobulin antibodies performed in 4977 serum samples received by The Johns Hopkins Immunology Laboratory between Sep 10, 2008 and May 7, 2013.

Volledig artikel:
http://www.sciencedirect.com/science/ar ... 7214000196



2) Diagnosis and classification of autoimmune parathyroid disease
Introduction
Hypoparathyroidism (HP) is a condition characterized by the presence of hypocalcemia, hyperphosphatemia, and a relatively high urinary calcium excretion. When HP is due to the destruction of the parathyroid glands, serum PTH levels are low, while they are high when the PTH is unable to exert its effects (pseudo-HP).
2. History
Idiopathic HP was first described in 1928 by Liu [1], and Torpe [2] described a case associated with moniliasis in 1929. In 1943, Sutphin [3] reported on five cases of idiopathic HP (three of whom were siblings), and one of them was associated with both moniliasis and Addison's disease (AD). Idiopathic HP is very rare. In 1958, Bronsky [4] reviewed the literature and found 50 cases, 16% of them associated with moniliasis, 10% with AD, and 8% with conjunctivitis. In 1962, McIntyre Gass examined 75 cases from the literature and the autoptic evidence of 11 cases of idiopathic HP associated with AD. The pathological picture of the parathyroids featured atrophy and mononuclear cell infiltration. There was even a complete atrophy of the parathyroids in some cases. Adrenal histology also showed pronounced atrophy, lymphocytic infiltration and fibrosis, indicating a common pathological background and suggesting an autoimmune etiology for both the diseases [5].
In 1957, Witebsky proposed the following criteria for defining an autoimmune disease [6]: a) demonstration of serum autoantibodies; b) demonstration of lympho-plasmacellular infiltration in the target organs; c) induction of the disease in animals by immunization with autoantigens and passive disease transfer by serum or lymphocytes. Based on these criteria, idiopathic HP was suspected of having an autoimmune etiology not only because of the typical pathological features of the parathyroid glands affected [5], but also because animal models of parathyroiditis were identified following the injection of parathyroid homogenates [7], [8] and [9]. The association with other autoimmune diseases and the demonstration of a genetic predisposition further support the autoimmune nature of HP (see Section 3). As for the specific autoantibodies directed against parathyroid antigens in patients with idiopathic HP, the picture is rather complicated (see Section 7).
3. Etiologic classification
Autoimmune HP may occur in the context of different autoimmune polyendocrine syndromes (APS) or as an isolated disease (see Table 1). It can be one of the three main diseases involved in APS type 1 (APS-1), in which case it develops at a younger age, it is generally preceded by chronic mucocutaneous candidiasis (CMC) and followed by AD [10]. This syndrome is inherited as an autosomal recessive disease caused by mutations within the autoimmune regulator (AIRE) gene located on chromosome 21 (21q22). As part of this syndrome, HP seems to be characterized by the presence of autoantibodies against NACHT leucine-rich-repeat protein 5 (NALP5Abs) [11], while it is not clear whether or not antibodies to calcium-sensing receptor (CaSRAbs) can be considered as markers of the autoimmune form of HP (see Section 7 and Table 2).

HP can be associated with thyroid autoimmune diseases (TAD), and in this case the condition is classified as APS type 3, or with other autoimmune diseases, in which case the autoimmune etc. etc.

Volledig artikel:
http://www.sciencedirect.com/science/ar ... 7214000561