Clinical clues to the cause of Addison's disease

Vita, Joseph A.; Silverberg, Shonni J.; Goland, Robin; Austin, John; Knowlton, Abbie I.

doi:10.1016/0002-9343(85)90339-0

Cited by 105 publications

(29 citation statements)

References 16 publications

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“…The presence of adrenal calcification on CT scanning is considered an exclusion criterion for autoimmune adrenalitis (28,29). However, in our study, ACA were found in the serum of one patient whose adrenal gland was calcified.…”

Section: Discussioncontrasting

confidence: 52%

Detection of adrenocortical autoantibodies in Addison's disease with a peroxidase-labelled protein A technique

Silva

Faiçal

Laureti

et al. 1998

Braz J Med Biol Res

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Adrenocortical autoantibodies (ACA), present in 60-80% of patients with idiopathic Addison's disease, are conventionally detected by indirect immunofluorescence (IIF) on frozen sections of adrenal glands. The large-scale use of IIF is limited in part by the need for a fluorescence microscope and the fact that histological sections cannot be stored for long periods of time. To circumvent these restrictions we developed a novel peroxidase-labelled protein A (PLPA) technique for the detection of ACA in patients with Addison's disease and compared the results with those obtained with the classical IIF assay. We studied serum samples from 90 healthy control subjects and 22 patients with Addison's disease, who had been clinically classified into two groups: idiopathic (N = 13) and granulomatous (N = 9). ACA-PLPA were detected in 10/22 (45%) patients: 9/13 (69%) with the idiopathic form and 1/9 (11%) with the granulomatous form, whereas ACA-IIF were detected in 11/22 patients (50%): 10/13 (77%) with the idiopathic form and 1/9 (11%) with the granulomatous form. Twelve of the 13 idiopathic addisonians (92%) were positive for either ACA-PLPA or ACA-IIF, but only 7 were positive by both methods. In contrast, none of 90 healthy subjects was found to be positive for ACA. Thus, our study shows that the PLPA-based technique is useful, has technical advantages over the IIF method (by not requiring the use of a fluorescence microscope and by permitting section storage for long periods of time). However, since it is only 60% concordant with the ACA-IIF method, it should be considered complementary instead of an alternative method to IIF for the detection of ACA in human sera.

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Section: Discussioncontrasting

confidence: 52%

Detection of adrenocortical autoantibodies in Addison's disease with a peroxidase-labelled protein A technique

Silva

Faiçal

Laureti

et al. 1998

Braz J Med Biol Res

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“…Diagnosis of post-tuberculosis or post-paracoccidioidomycosis AD was based on anamnestic data, purified protein derivative (PPD) test, presence of antibodies against Paracoccidioides brasiliensis and on demonstration of adrenal calcification by computerized tomography (CT) (20,21). The presence of other autoimmune diseases, as well as that of organ-specific autoantibodies, such as glutamic acid decarboxylase autoantibodies (GAD 65 Ab) or thyroid autoantibodies (thyreoperoxidase antibodies, TPOAb; thyroid microsomal antibodies, TMSA) was also investigated.…”

Section: Methodsmentioning

confidence: 99%

Autoantibodies against recombinant human steroidogenic enzymes 21-hydroxylase, side-chain cleavage and 17alpha-hydroxylase in Addison's disease and autoimmune polyendocrine syndrome type III

Silva

Kater

Dib

et al. 2000

European Journal of Endocrinology

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Objective: To evaluate the frequency of autoantibodies (Ab) against 21 hydroxylase (21OH), side-chain cleavage (SCC) and 17a-hydroxylase (17OH), in Addison's disease (AD) and autoimmune polyendocrine syndrome type III (APSIII). Design and Methods: We used radiobinding assays and in vitro translated recombinant human 35 S-21OH, 35 S-SCC or 35 S-17OH and studied serum samples from 29 AD (18 idiopathic, 11 granulomatous) and 18 APSIII (autoimmune thyroid disease plus type 1 diabetes mellitus, without AD) patients. Results were compared with those of adrenocortical autoantibodies obtained with indirect immunofluorescence (ACA-IIF). Results: ACA-IIF were detected in 15/18 (83%) idiopathic and in 1/11 (9%) granulomatous AD subjects. 21OHAb were found in 14/18 (78%) idiopathic and in the same (9%) granulomatous AD subject. A significant positive correlation was shown between ACA-IIF and 21OHAb levels (r 2 ¼ 0.56, P < 0.02). The concordance rate between the two assays was 83% (24/29) in AD patients. SCCAb were found in 5/18 (28%) idiopathic (4 of whom were also positive for 21OHAb) and in the same (9%) granulomatous AD subject. 17OHAb were found in only 2/18 (11%) idiopathic and none of the granulomatous AD patients. Two APSIII patients were positive for ACA-IIF, but only one was positive for 21OHAb and SCCAb. 17OHAb were found in another two APSIII patients. Conclusions: Measurement of 21OHAb should be the first step in immune assessment of patients with AD and individuals at risk for adrenal autoimmunity, in addition to ACA-IIF. Due to their low prevalence in AD, measurement of SCCAb and 17OHAb should be indicated only for 21OHAb negative patients and/or for those with premature ovarian failure, regardless of ACA-IIF results.

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“…It can be present in all stages of the disease. The overall prevalence of calcification in the study of Vita was 53% at the time of diagnosis and indicated long-standing tuberculosis (Vita et al, 1985). Wang described small calcification on CT scan in 22% patients with active tuberculosis (Wang et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Pseudotumoral Adrenal Tuberculosis

Azzoug¹,

Terki

Chentli³

et al. 2017

ijccr

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Tuberculosis is rare nowadays, however, it should be kept in mind in the differential diagnosis of adrenal insufficiency notably in developing countries or in immunocompromised patients. We report here a case of adrenal insufficiency secondary to tuberculosis with bilateral adrenal masses. A 45 years old man was admitted to our department for investigation of a primary adrenal failure. His past medical history was significant for pleural tuberculosis eighteen years ago. He reported several months' history of generalized weakness and unintentional weight loss. On physical examination, he presented diffuse hyperpigmentation. On hormonal assessment, there was low basal cortisol level and a high level of corticotrophin. Computed tomography scan showed bilaterally enlarged adrenal glands. The tuberculin skin test was positive. With the background of tuberculosis, adrenal insufficiency diagnosed by laboratory test and positive tuberculin skin test, bilateral enlargement of adrenal glands was considered most consistent with tuberculosis. Tuberculosis remains a classic cause of adrenal insufficiency with adrenal masses. Therefore, it needs to be considered in the differential diagnosis of adrenal insufficiency or bilateral adrenal masses.

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Clinical clues to the cause of Addison's disease

Cited by 105 publications

References 16 publications

Detection of adrenocortical autoantibodies in Addison's disease with a peroxidase-labelled protein A technique

Detection of adrenocortical autoantibodies in Addison's disease with a peroxidase-labelled protein A technique

Autoantibodies against recombinant human steroidogenic enzymes 21-hydroxylase, side-chain cleavage and 17alpha-hydroxylase in Addison's disease and autoimmune polyendocrine syndrome type III

Pseudotumoral Adrenal Tuberculosis

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