Serological Investigations on Addison's Disease

Andrada, J A

doi:10.1001/jama.1968.03150070073012

Cited by 14 publications

(3 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Over 65 per cent of patients with idiopathic AD have adrenal antibodies 5,14,16,28–34 . The antibody titers are similar in the older and younger patients; however, younger patients have a slightly higher incidence of antibodies than older patients with idiopathic AD 16,32,33 .…”

Section: Discussionmentioning

confidence: 96%

Adrenal Insufficiency (Addison's Disease) in the Elderly

Moss

England

Kowal

1985

J American Geriatrics Society

View full text Add to dashboard Cite

He was greatly anacmiated, his eyes were p c d y ; he complained of extreme languor and fiiintness; liis pulse . . . exquisitely soft and coinpressi1)lc; the iinpiilse of the heart was feeble . . . without pain, tlie stoniach w a s both urgent and distressing. . . . there were observed, chiefly on the face, neck and a r m , patches of a rather deep chestnut-brown colour . . .A patient inquiry and most careful examination fhiled to elicit any information, or to detect any lesions, sufficient to afford even a plausible explanation of the patient's siiigiilar condition. ' -Thoincis Addison's description of ci initldle-aged m i n with tirberciiloiis cidrennl iiisrifficieiicg (1855)'Addison's disease (AD) is a rare disorder that can be easily misdiagnosed in t h e elderly. hf any of t h e manifestations of AD occur frequently in the elderly such a s asthenia, anorexia, lethargy, gastrointestinal symptoms, confusion, weight loss, postural 11 y p o t e 11 s io n , p re re 11 a1 azo t e in ia, 11 y poll a t re 111 i a, and hyperlcalemia with renal insufficiency. The clinician should consider A D in an elderly patient if several of these findings are present, especially if they coexist with hypoglycemia, hyperpigmentation, Iiypotension, o r normotension in a previously hypertensive patient. Prompt treatment of AD is effective, whereas undiagnosed AD is uniformly fatal. We present a case of A D in a septagenurian and, review its incidence, etiology, clinical features, diagnosis, i1ntl therapy in t h e elderly.A 70-year-old black man liad 1)eeii in his usual good health until about eight months prior to admission, when he liad iioticed increasing fatigue, generalized weakness, and anorexia. Over tlie eight-month period, he lost ap-

show abstract

Section: Discussionmentioning

confidence: 96%

Adrenal Insufficiency (Addison's Disease) in the Elderly

Moss

England

Kowal

1985

J American Geriatrics Society

View full text Add to dashboard Cite

show abstract

“…These antibodies can be easily demonstrated by immunofluorescence. However, in APECED, but not in the other forms of AD, the autoantibodies are precipitating, and this phenomenon can be demonstrated by Ouchterlony’s immunodiffusion (Andrada et al, 1968; Krohn et al, 1974; Heinonen et al, 1976). In immunodiffusion with APECED serum against adrenal homogenate three precipitating lines were observed, and one of these were shown to represent a mitochondrial antigen while the two others were microsomal.…”

Section: Addison’s Diseasementioning

confidence: 99%

APECED: is this a model for failure of T cell and B cell tolerance?

Kluger¹,

Ranki²,

Krohn³

2012

Front. Immun.

View full text Add to dashboard Cite

In APECED, the key abnormality is in the T cell defect that may lead to tissue destruction chiefly in endocrine organs. Besides, APECED is characterized by high-titer antibodies against a wide variety of cytokines that could partly be responsible for the clinical symptoms during APECED, mainly chronic mucocutaneous candidiasis, and linked to antibodies against Th17 cells effector molecules, IL-17 and IL-22. On the other hand, the same antibodies, together with antibodies against type I interferons may prevent the patients from other immunological diseases, such as psoriasis and systemic lupus erythematous. The same effector Th17 cells, present in the lymphocytic infiltrate of target organs of APECED, could be responsible for the tissue destruction. Here again, the antibodies against the corresponding effector molecules, anti-IL-17 and anti-IL-22 could be protective. The occurrence of several effector mechanisms (CD4+ Th17 cell and CD8+ CTL and the effector cytokines IL-17 and IL-22), and simultaneous existence of regulatory mechanisms (CD4+ Treg and antibodies neutralizing the effect of the effector cytokines) may explain the polymorphism of APECED. Almost all the patients develop the characteristic manifestations of the complex, but temporal course and severity of the symptoms vary considerably, even among siblings. The autoantibody profile does not correlate with the clinical picture. One could speculate that a secondary homeostatic balance between the harmful effector mechanisms, and the favorable regulatory mechanisms, finally define both the extent and severity of the clinical condition in the AIRE defective individuals. The proposed hypothesis that in APECED, in addition to strong tissue destructive mechanisms, a controlling regulatory mechanism does exist, allow us to conclude that APECED could be treated, and even cured, with immunological manipulation.

show abstract

“…1, the adrenocortical function of asymptomatic, AA-positive individuals is often impaired. Attempts to improve the predictive value of the test using other methods such as tanned cell hemagglutination, complement fixation, gel diffusion precipitation, or enzyme-linked immunosorbent assay (ELISA) have not yielded consistent results [4,41]. Deficiency of basal serum aldosterone and cortisol concentrations arise only after most of the endocrine cortex has atrophied [25].…”

Section: Proposed Natural History Of Addison's Diseasementioning

confidence: 99%