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At least 667 records · Page 37Linked to original sources
PubMed1985

[Adrenal tuberculosis in 13 patients with Addison's disease. CT findings].

A series of thirteen cases of adrenal tuberculosis with Addison's disease is presented. At the onset of disease, CT findings consisted of an enlargement of both glands, with peripheral enhancement after contrast medium was injected. The CT differential diagnosis among tubercular, metastatic and amyloidotic etiology was not possible. When the course of the illness was favourable, CT showed a generalized glandular atrophy with calcifications. In two fatal cases, the diagnosis could be made only at post-mortem examination.

Addison Disease↗
PubMed1998

Tuberculous Addison's disease: lack of normalization of adrenocortical function after anti-tuberculous chemotherapy.

OBJECTIVE: Tuberculosis of the adrenal glands is a common cause of Addison's disease in developing countries. We conducted a study to determine if treatment of such patients with modern anti-tuberculous chemotherapy would lead to an improvement in plasma cortisol and aldosterone levels. DESIGN: Prospective study. PATIENTS: 5 patients with Addison's disease secondary to tuberculosis. MEASUREMENTS: Basal and ACTH stimulated plasma cortisol and aldosterone levels were measured prior to instituting anti-tuberculous chemotherapy, as well as one month after its conclusion. Four patients were again studied over the next 2-5 years. RESULTS: Peak plasma cortisol levels prior to treatment were markedly reduced (range, < 14-110 mumol/l). There was no improvement one month (< 14-143 mumol/l) or 2-5 years (< 14-69 mumol/l) after completing anti-tuberculous chemotherapy. Peak plasma aldosterone at diagnosis was < 56-210 pmol/l; it was undetectable in 4 patients. No improvement was observed one month (< 56-210 pmol/l), or 2-5 years (< 56-389 pmol/l) after stopping anti-tuberculous chemotherapy. Plasma aldosterone levels at both these time points were far lower than those in control subjects (median 736 pmol/l, 560-1512 pmol/l; p < 0.01). One patient had an increase in peak aldosterone from < 56 pmol/l to 389 pmol/l, though peak cortisol actually declined in this subject (from 110 mumol/l to 69 mumol/l). CONCLUSIONS: Treatment of tuberculous Addison's disease with anti-tuberculous chemotherapy does not lead to normalization of ACTH stimulated plasma cortisol or aldosterone levels during the 2-5 year period of study. However, prolonged follow up with regular adrenal function tests is warranted in all such patients.

Addison Disease↗
PubMed1992

Steroid 21-hydroxylase is a major autoantigen involved in adult onset autoimmune Addison's disease.

An adrenal-specific protein reacting with autoantibodies in the sera of patients with adult onset Addison's disease has been purified from human adrenal glands. The protein, mol.wt. 55K, has the biochemical characteristics of steroid 21-hydroxylase and reacts on Western blots with rabbit antibodies to recombinant 21-hydroxylase. Absorption of the native human 55K adrenal protein with human adrenal autoantibodies prevented the subsequent reaction of the 55K protein with rabbit antibodies to 21-hydroxylase in Western blot analysis. In addition, human adrenal autoantibodies reacted with recombinant 21-hydroxylase expressed in yeast. These data indicate that the adrenal specific enzyme steroid 21-hydroxylase is a major autoantigen involved in adult onset autoimmune Addison's disease.

Addison Disease↗
PubMed2005

Molecular evidence of recurrent histoplasmosis with 9-year latency in a patient with Addison's disease.

We present a case of fatal histoplasmosis in a patient with Addison's disease and long-term use of corticosteroid. The patient acquired Histoplasma capsulatum in China and initially presented with a laryngeal mass. He developed fulminant pneumonia and respiratory failure 9 years later. Nucleotide sequences of internal transcribed spacer regions of rRNA genes of the H. capsulatum isolate recovered from biopsied lung tissue and of the extracted fungal DNA from the laryngeal lesion were identical, indicating the recurrent nature of infection.

Addison Disease↗
PubMed1985

Hyperthyroidism and Addison's disease in a patient with myotonic dystrophy.

A 53-year-old man had myotonic dystrophy, hyperthyroidism, and Addison's disease, an association not previously reported, to our knowledge. In the literature, at least five cases of hyperthyroidism associated with myotonic dystrophy have been described, but none also had Addison's disease. The presence of thyroid anti-microsomal antibodies and anti-adrenal antibodies suggests that the two endocrine disorders may be autoimmune. In our case, the treatment of the two endocrinopathies caused a reduction of myotonic symptoms.

Addison Disease↗
PubMed1996

[Laboratory monitoring of therapy in Addison's disease].

UNLABELLED: Views on the usefulness of monitoring of substitution therapy in Addison's disease by hormonal laboratory indicators are controversial. The authors analysed the problem therefore in a group of 20 of their own patients. It was revealed that the adequacy of substitution of the cortisol deficiency can be very readily evaluated by diurnal profiles of cortisolaemia. The values of plasma ACTH provided less information, but were not unreliable. Assessment of free urinary cortisol did not prove useful. The adequacy of substitution of aldosterone deficiency reflected sensitively the plasma renin activity. CONCLUSIONS: monitoring by hormonal indicators is useful, basic means are the diurnal profile of cortisolaemia and the plasma renin activity.

Addison Disease↗
PubMed1988

Class II MHC expression in normal adrenal cortex and cortical cells in autoimmune Addison's disease.

It has been proposed that aberrant expression of class II major histocompatibility complex (MHC) molecules by target cells may be an initiating factor in some forms of organ specific autoimmunity. This hypothesis was tested in relation to the autoimmune form of Addison's disease by studying autopsy adrenal glands from eight patients who had died of recent onset idiopathic Addison's disease. Using an immunohistochemical technique, class II MHC expression was found in a minority of adrenal cortical cells in the zona reticularis in 25 normal and four hyperplastic glands, while in Addison's disease almost all residual cortical cells expressed class II MHC. Three tuberculous adrenals showed increased staining of cortical cells around areas of chronic inflammation. It is concluded that since adrenal cortical cells of the normal gland express class II MHC, aberrant expression of this product cannot be invoked as an initiating mechanism in autoimmune adrenalitis. The increased cortical expression of class II MHC seen in idiopathic Addison's disease and tuberculosis may be due to local release of lymphokines by inflammatory cells.

Addison Disease↗
PubMed1996

Hyper-adrenocorticotropinemia in a patient with Addison's disease after treatment with corticosteroids.

A 40-year-old man with Addison's disease due to adrenal tuberculosis retained high levels of adrenocorticotropic hormone (ACTH) after conventional hydrocortisone replacement. Plasma ACTH levels were completely suppressed by usual replacement with hydrocortisone (20 mg at 8:00 and 10 mg at 21:00) but rebounded to abnormally high levels the following morning. Administration of 2 mg or 8 mg of dexamethasone suppressed ACTH and cortisol. Magnetic resonance imaging of the brain showed a low-intensity lesion of the pituitary gland. Pituitary hyperplasia or microadenoma with preserved regulation of ACTH was considered to be the cause of the high plasma ACTH levels. The combination of hydrocortisone and dexamethasone reduced plasma ACTH levels.

Addison Disease↗
PubMed1997

Codon 17 polymorphism of the cytotoxic T lymphocyte antigen 4 gene in Hashimoto's thyroiditis and Addison's disease.

Endocrine autoimmune disorders share susceptibility and resistance factors of the human leukocyte antigen system on the short arm of chromosome 6, but other gene loci also contribute to predisposition and protection. Because the cytotoxic T lymphocyte antigen 4 (CTLA4) alanine-17 encoded by the CTLA4 gene on chromosome 2q33 confers susceptibility to Graves' disease, as well as to type 1 (insulin-dependent) diabetes mellitus, we investigated this dimorphism in the other endocrine autoimmune disorders: Hashimoto's thyroiditis and Addison's disease. We analyzed the CTLA4 exon 1 polymorphism (49 A/G) in 73 patients with Hashimoto's thyroiditis, 76 with Addison's disease, and 466 healthy controls. This dimorphism corresponds to an aminoacid exchange (Thr/Ala) in the leader peptide of the expressed protein. CTLA4 alleles were defined by PCR, single-strand conformational polymorphism analysis, and restriction fragment length polymorphism analysis using BbvI. Patients with Hashimoto's thyroiditis had significantly more Ala alleles than controls, both as homozygotes (22% vs. 15%) and heterozygotes (53% vs. 46%), and less Thr than controls as homozygotes (25% vs. 39%), P < 0.04. The phenotypic frequency for Ala was significantly higher in patients (75%), compared with controls (61%), P < 0.03. Patients with Addison's disease did not differ significantly from controls, but those carrying the suceptibility marker, human leukocyte antigen DQA1*0501, were significantly more CTLA4 Ala17 positive than controls with the same DQA1 allele (P < 0.05). In conclusion, an alanine at codon 17 of CTLA4 confers genetic susceptibility to Hashimoto's thyroiditis, whereas this applies only to the subgroup of DQA1*0501+ patients with Addison's disease.

Abatacept↗
PubMed2000

A murine model of allogeneic adrenocortical cell transplantation: perspectives for the treatment of Addison's disease in humans.

BACKGROUND: Hormone substitution for the treatment of adrenocortical insufficiency (Addison's disease) does not adequately substitute the hormone peaks required in stress situations. Therefore, allogeneic transplantation of adrenal cortex could offer an intriguing alternative. METHODS: Major histocompatibility complex (MHC) class I transgenic mice were used for the implementation of an animal model of adrenocortical cell transplantation in adrenalectomized mice. K(b)-transgenic cells and allogeneic adrenocortical cells were cocultured in mixed lymphocyte cultures to examine the alloimmune response. Lymphocytes from T-cell receptor transgenic mice and normal allogeneic mice served as responder cells. The effect of corticosteroids secreted by adrenocortical cells was antagonized by the steroid receptor antagonist mifepristone (RU486). RESULTS: In vitro coculture experiments showed that MHC class I disparate adrenocortical cells failed to activate B10.BR and T-cell receptor transgenic lymph node cells. In the presence of mifepristone this inhibitory effect was antagonized, resulting in strong lymphocyte proliferation. Activation of B10.BR lymphocytes by K(b)-disparate spleen cells was also abolished in the presence of adrenocortical cells. This effect, however, could not be reversed by mifepristone. CONCLUSIONS: In vitro, the presence of adrenocortical cells potently suppressed allogeneic immune responses. This effect was only in part due to the secretion of corticosteroids, pointing to an additional immunomodulatory property of adrenocortical cells.

Addison Disease↗