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[Chronic thyroiditis with hypothyroidism in patients with Addison's disease].

The authors describe two cases of Schmidt's syndrome (combined idiopathic Addison's disease and chronic autoimmune thyroiditis). In both cases, the damage to the thyroid gland occurred before adrenal pathology. In one case it was associated with overt hypothyrosis and in the other one with subclinical hypothyrosis. It is suggested that these diseases are caused by an autoimmune process, which is supported by demonstration in the blood of both patients of antibodies against thyroid and adrenal tissues.

Addison Disease↗
PubMed1994

[Adrenomyeloneuropathy. A frequent cause of Addison's disease].

Adrenomyeloneuropathy (AMN) is a "milder form" of adrenoleukodystrophy with a X-linked inheritance. Abnormal catabolism of the very long-chain fatty acids (VLCFA) results in Addison's disease and spastic paraparesis. The VLCFA concentration was measured in 23 of 26 patients with Addison's disease (mean age 48.5 [20-75] years) being treated at the University Hospital Marburg during May, 1991. The concentration was elevated in four of the 12 men with the disease, while it was within normal limits in the 11 women. Only two patients had paraparesis-like neurological deficits. This finding suggests that AMN is not as rare as has been supposed. It is recommended that the concentration of VLCFA be measured in all patients with Addison's disease, because an increase could have important consequences.

Addison Disease↗
PubMed1983

The pituitary gland in untreated Addison's disease. A histologic and immunocytologic study of 18 adenohypophyses.

The pituitary glands of 18 patients with untreated Addison's disease were studied by histologic and immunocytochemical methods. Adrenal destruction was caused by tuberculosis (13 cases) or autoimmune adrenalitis (five cases), and the duration of the adrenal insufficiency ranged from one to 16 years. Both diffuse and nodular hyperplasia of corticotropic cells were evident in each case, and the extent of hyperplasia correlated with the duration of disease. In five cases, nodular proliferations with morphologic features between those of hyperplasia and those of adenoma, termed tumorlets, were identified, as were two microadenomas, only one of which was available for study. In all instances, the proliferating corticotrophs stained positively with PAS and were immunoreactive for adrenocorticotropic hormone and beta-endorphin. We conclude that diffuse and nodular corticotroph hyperplasia are common in untreated Addison's disease, although frank adenoma formation seems to be rare. The latter may be related to the short duration of disease or may imply the absence of additional, unknown factors that are required for adenoma growth.

Addison Disease↗
PubMed1994

24-hour blood pressure profile in Addison's disease.

The purpose of this study was to evaluate the circadian blood pressure rhythmicity in patients with primary adrenal insufficiency. Ten newly diagnosed and untreated patients with Addison's disease, 17 addisonian patients (including the previous 10) following an adequate regimen of corticosteroid replacement therapy, and 15 healthy subjects as a control group were studied. Twenty-four-hour ambulatory blood pressure and heart rate were measured automatically every 30 min using a Takeda TM-2420 recorder. The runs test, used for detecting blood pressure diurnal rhythm, was compatible with a rhythm in 2 of 10 patients with untreated Addison's disease, in 13 of 17 patients with treated Addison's disease, and in 13 of 15 normals. Six of eight addisonian patients showing no evidence of blood pressure rhythm in the untreated state acquired circadian periodicity during therapy. An analysis of blood pressure readings by Fourier series with four harmonics showed that blood pressure mesor was lower in untreated than in treated addisonian and normal subjects (P < .05). The nocturnal fall was smaller for systolic and diastolic blood pressure in untreated than in treated addisonian and normal subjects (P < .05). Adrenocortical insufficiency is often characterized by loss of circadian blood pressure rhythm, and normal rhythm can be reestablished by replacement therapy. Lack of cortisol rhythm or persistent activation of the renin-angiotensin system and sympathetic tone may play a role in this phenomenon.

Addison Disease↗
PubMed1995

Subclinical Addison's disease: a cause of persistent abnormalities in transaminase values.

A common reason for referring patients to hepatologists is persistently abnormal serum transaminase levels with vague constitutional symptoms. In the United Kingdom, these abnormalities are most often caused by a fatty liver either related to obesity or alcohol abuse; they are less commonly caused by chronic liver disease, particularly chronic viral hepatitis, autoimmune hepatitis, or chronic biliary disease. Endocrine disease is rarely a cause of these abnormalities, although hypothyroidism and hyperthyroidism are well-recognized causes. Addison's disease has been only reported once in the literature by R. G. Olsson as a cause of increased transaminase levels associated with constitutional symptoms; it is not mentioned in textbooks on hepatology. Three patients with Addison's disease are reported here, all of whom had increased serum transaminase levels for more than 6 months before the recognition of the hypoadrenalism with resolution to normal after steroid replacement. Hepatologists should consider subclinical Addison's disease as a cause of persistently increased transaminase levels with constitutional symptoms in the absence of evidence for fatty liver as well as viral and autoimmune markers.

Addison Disease↗
PubMed2001

Autoimmunity in isolated Addison's disease and in polyglandular autoimmune diseases type 1, 2 and 4.

Sera from 300 Italian patients with Addison's disease were collected over a 30 year period. Among these patients, 82% had autoimmune disease, 13% had tuberculosis and 5% had another causal condition. In 59% of the cases, autoimmune disease was associated with the autoimmune manifestations contributing to the description of polyglandular autoimmune disease (PGAD). In PGAD type 1, the disease was associated with chronic candidiasis and/or chronic hypoparathyroidism. In PGAD type 2, the patients had autoimmune thyroid disease and/or diabetes mellitus type 1, and in PGAD type 4, they presented a combination with other autoimmune diseases excluding those previously mentioned. Finally, the autoimmune disease was apparently isolated in 41% of the cases. In addition, patients with these four forms of disease exhibited a different genetic pattern, sex distribution, and age at presentation in addition to minor frequency of autoimmune diseases. Adrenal cortex autoantibodies directed against 21-hydroxylase were common serological markers for these four main clinical forms, showing a very high frequency at clinical onset of adrenal insufficiency. In some patients, steroid-producing cell autoantibodies were also present and correlated with gonadal failure and they recognize of 17alpha-hydroxylase or P450 side chain cleavage enzymes as target antigens.

Addison Disease↗