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PubMed1981

HLA antigens in two siblings with autoimmune Addison's disease.

The diagnosis of autoimmune Addison's disease was established in two siblings by demonstration of serum antibodies against adrenal cortex antigen, elevated P-ACTH combined with a low P-cortisol, and the absence of P-cortisol response to exogenous ACTH. HLA typing in the two siblings and their parents revealed the same HLA phenotype in the two patients. This is compatible with an autosomal recessive mode of inheritance and indicates that a supposed trait for autoimmune Addison's disease may segregate with the HLA complex in the familial form of autoimmune Addison's disease.

Addison Disease↗
PubMed1977

[Idiopathic adrenal cortex dystrophy with the clinical picture of Addison's disease].

Clinical and autopsy findings are reported of three cases of Addisons disease due to idiopathic dystrophy of the adrenal cortex as seen in two women, 20 and 37 years of age respectively as well as a boy of 14 years. Idiopathic dystrophy of the adrenal cortex as a cause of Addisons disease has become aware of more and more frequently for some years. Its classification as an auto-aggression disease has been made a subject for discussion. Morphological findings and immunological investigations with three own cases confirm this conception. This disease should be reminded of with regard to the problem of clinically diagnosing it and the fatal prognosis of untreated cases.

Addison Disease↗
PubMed2002

Adrenal lymphoma and Addison's disease: report of a case.

Addison's disease due to adrenal lymphoma usually manifests as bilateral adrenal enlargement. We report a patient with Addsion's disease in whom the initial overt primary adrenal insufficiency was accompanied by an only slightly enlarged right adrenal gland. The 80-year-old man presented with nausea, anorexia, weight loss, and hyperpigmentation of the skin and buccal mucosa. Addison's disease was diagnosed based on this clinical presentation and laboratory findings of low cortisol and high adrenocorticotropin levels. Computerized tomography (CT) of the adrenal glands revealed a small right adrenal tumor. His family refused to allow percutaneous or surgical biopsy to determine the nature of the tumor. His general condition improved after steroid supplementation. However, about 1 year later, dizziness, fever, night sweats, and edema of the lower legs developed, and adrenal CT scanning revealed that the left adrenal gland had enlarged and now exceeded the size of the right one. Left adrenalectomy was performed and pathology showed a diffuse large B-cell lymphoma. Staging work-up using whole-body CT scanning suggested a stage IIIb lymphoma. Chemotherapy was given, but the disease still progressed and the patient died 4 months after diagnosis. Primary adrenal lymphoma should be considered in the differential diagnosis of Addison's disease, even if only slight enlargement of the adrenal glands is found initially.

Addison Disease↗
PubMed1994

Major histocompatibility complex class II and III in Addison's disease. MHC alleles do not predict autoantibody specificity and 21-hydroxylase gene polymorphism has no independent role in disease susceptibility.

The major autoantigens in Addison's disease have recently been shown to be members of the adrenal steroidogenic enzymes, such as 21OH. The genes encoding the 21OH enzyme are located in the class III segment of the MHC complex. Therefore, its identification as an autoantigen provides a novel link between MHC and susceptibility to this autoimmune disease. We have determined the MHC class II (DRB1, DQA1, DQB1, DPB1) and class III (TNF, HSP70, C4, 21OH) gene polymorphism in patients with Addison's disease. Also, we tested whether presence of autoantibodies against 21OH is associated with specific alleles in MHC. Our results show that patients with Addison's disease in association with APS2 or Addison's disease as an isolated form share highly similar MHC class II and class III alleles. A very strong association with HLA DRB1*0301, DQA1*0501, DQB1*0201, and DPB1*0101, as well as with the C4A + 21OHA gene deletion and TNFB*1 allele was observed. However, identical gene markers were observed also in controls matched for DRB1*0301, thus suggesting that the patient group did not carry MHC gene segments specific for Addison's disease. The presence of autoantibodies against 21OH was not found to be directly determined by the MHC alleles; rather it was associated with the clinical form of the disease.

Addison Disease↗
PubMed1993

[A case of Addison's disease caused by adrenal tuberculosis, and revealed acute hypoadrenocorticism].

We reported a case of Addison's disease, caused by adrenal tuberculosis. The patient was female, seventy four years old. She complained cough and body weight loss. She complained cough from June, 1989, but her home doctor didn't take care of her symptoms. September 1989, she felt appetite loss, and easy fatigue, so her home doctor suspected her disease as pulmonary tuberculosis, so he introduced our hospital, and she admitted. When she admitted, her chest roentogenogram revealed bIII2. Sputum smear examinations were negative. Laboratory data on admission, we observed slightly eosinophilia, severe iron deficiency anemia, and accenturation of blood sedimentation rate. Immediately after admission, she complained nausea, vomiting, coldness, and powerless. On 25 days after admission, she lost her senses suddenly, and her blood pressure fell 5 days after, she fell in shock state, too. We found out her blood sugar data was 29. After blood examinations, we found out that ACTH was high, cortisole, 17-KS, 17-OHCS were low. So we thought she got acute hypoadrenocorticism. We found her abdominal CT revealed calcification in her right adrenal gland. We diagnosed her disease as Addison's disease caused by adrenal tuberculosis so we began to give prednisolone, 7.5 mg per day. After giving, her state made better. We thought her disease as Addison's disease caused by adrenal tuberculosis, revealed acute hypoadrenocorticism.

Addison Disease↗
PubMed1989

[Adrenal gland masses and Addison's disease of tuberculous origin: apropos of 2 cases].

Two cases of confirmed tuberculous Addison disease, with an increase in size of the adrenal glands are presented. One patient presented also a renal adenocarcinoma; this association is very rare given the small frequency of these diseases. Based on these two cases we emphasize the utility of puncture aspiration with a fine needle (PAFN), echography and TC Scan in the study of Addison disease.

Addison Disease↗
PubMed1988

[Idiopathic Addison's disease].

Two cases of idiopathic Addison's disease affecting heterozygous twins who died from addisonian crisis at the ages of 7 and 10 years, are described, including descriptions of histologic findings in the adrenals, thymus, hypophysis, kidneys, esophagus, upper respiratory tract, and other viscera. The authors believe that autoimmunization in children with idiopathic Addison's disease develops in the presence of congenitally defective immunity and propose that activation of the juxtaglomerular complex and hypergranulation of interstitial cells in the inner renal medulla may be used as morphologic criteria in the diagnosis of addisonian crisis.

Addison Disease↗
PubMed1999

Adrenal-cortex autoantibodies and steroid-producing cells autoantibodies in patients with Addison's disease: comparison of immunofluorescence and immunoprecipitation assays.

Autoimmune Addison's disease and premature ovarian failure are characterized by the presence of organ-specific autoantibodies. The main adrenal and gonadal autoantigens have been identified and cloned, and the relationship between the autoantibodies detected by immunofluorescence techniques and those detected by the new assays using recombinant autoantigens needed to be investigated. We studied 165 patients with Addison's disease: 143 patients had different forms of autoimmune Addison's disease (13 with idiopathic premature ovarian failure) and 22 had nonautoimmune Addison's disease. Adrenal-cortex autoantibodies and steroid-producing cell autoantibodies were measured by the immunofluorescence techniques. Autoantibodies to steroid 21-hydroxylase, 17alpha-hydroxylase, and P450 side chain cleavage enzyme were measured by immunoprecipitation assay using 35S-labeled recombinant proteins. Adrenal-cortex autoantibodies and autoantibodies to 21-hydroxylase were found in 81% of the patients with autoimmune Addison's disease. None of the patients with nonautoimmune Addison's disease had adrenal-cortex autoantibodies or autoantibodies to 21-hydroxylase. A high association between these two markers in patients with different forms of autoimmune Addison's disease and in those with short- or long-standing disease was found. Steroid-producing cells autoantibodies were found in 26% of the patients with autoimmune Addison's disease, and autoantibodies to 17alpha-hydroxylase and/or P450 side chain cleavage enzyme in 36% of the patients. Steroid-producing cells autoantibodies were found in 11/13 (85%) of patients with idiopathic premature ovarian failure associated with autoimmune Addison's disease, and autoantibodies to 17alpha-hydroxylase and/or P450 side chain cleavage were found 12/13 (92%) of patients; the only case negative for all these three markers suffered from Turner's syndrome. Provided that a high standard of immunofluorescence technique is maintained, measurement of adrenal cortex autoantibodies or steroid-producing cells autoantibodies by either immunofluorescence or immunoprecipitation assay is essentially equivalent.

Addison Disease↗
PubMedDate not supplied

[Evaluation of clinical symptoms of Addison's disease].

A total of 103 patients with Addison's disease were examined. The task was to determine the information content of the clinical symptoms of Addison's disease in their interrelationship. The theorem of the multiplication of probability of independent events and probability of the appearance of at least one event were used. On the basis of the above mathematical method it has been established that the most informative syndromes of Addison's disease are the combination of asthenia and adynamia with mass deficiency, arterial hypotension, skin pigmentation and nervous-psychic break-down. In comparing clinical and mathematical results it has been shown that a simultaneous appearance of the signs of the dyspeptic syndrome, its combinations with the pain abdominal syndrome and mass deficiency point out to a possibility of the Addisonian crisis or the onset of its development. At least one of three signs of muscular or articular involvement is predicted in each patient with Addison's disease. A table given in the paper makes it possible to determine the information content of numerous complexes of symptoms of Addison's disease.

Addison Disease↗
PubMedDate not supplied

Diagnostic and therapeutic problems in a case of adrenal tuberculosis and acute Addison's disease.

A case of adrenal tuberculosis with acute Addison's disease is presented. The case showed diagnostic and therapeutic problems, the latter concerning the untoward effects due to metabolic interferences and pharmacologic interactions among antitubercular drugs, substitutive corticosteroid therapy and hepatic metabolism. The side-effects, interactions and metabolism of drugs used during the course of disease are discussed.

Acute Disease↗
PubMed2006

Genetic evaluation of Addison's disease in the Portuguese Water Dog.

BACKGROUND: Addison's disease, also known as hypoadrenocorticism, has been reported in many individual dogs, although some breeds exhibit a greater incidence than the population as a whole. Addison's is presumed to be an autoimmune mediated hereditary defect but the mode of inheritance remains unclear. In particular, the heritability and mode of inheritance have not been defined for the Portuguese Water Dog although Addison's is known to be prevalent in the breed. RESULTS: The analyses present clear evidence that establishes Addison's disease as an inherited disorder in the Portuguese Water Dog with an estimate of heritability of 0.49 (+/- 0.16); there were no differences in risk for disease across sexes (p > 0.49). Further, the complex segregation analysis provides suggestive evidence that Addison's disease in the Portuguese Water Dog is inherited under the control of a single, autosomal recessive locus. CONCLUSION: The high heritability and mode of inheritance of Addison's disease in the Portuguese Water Dog should enable the detection of segregating markers in a genome-wide scan and the identification of a locus linked to Addison's. Though the confirmation of Addison's disease as an autosomal recessive disorder must wait until the gene is identified, breeders of these dogs may wish to keep the present findings in mind as they plan their breeding programs to select against producing affected dogs.

Addison Disease↗
PubMed1989

[Polyglandular autoimmune syndrome type II].

The polyglandular autoimmune syndrome type II, (Schmidts syndrome), is defined as coexistence of two of the diseases: Addison's disease, insulin dependent diabetes mellitus and autoimmune thyroid disease. The first endocrine deficiency state typically develops after the age of twenty and in most cases it is Addison's disease. The prevalence is approximately 5 per 100,000. The syndrome occurs within families in half of the cases. The immunological mechanism is not finally determined, but both the humoral and cellular systems seem to be involved and furthermore there is an association with the major histocompatibility complex. Whereas treatment of the components in polyglandular autoimmune syndrome is straightforward, diagnosis may be troublesome: Patients with Addison's disease may be biochemically hypothyroid the first months of corticosteroid treatment. Patients with myxedema show decreased urine excretion of 17-ketosteroids until thyroid substitution treatment is sufficient. A decreased insulin requirement or increased frequency of hypoglycaemic attacks may be the first sign of an adrenocortical hypofunction in diabetic patients. Patients with one autoimmune disease and their relatives are predisposed to (other) autoimmune diseases.

Addison Disease↗
PubMed1995

Associated autoimmunity in Addison's disease.

As the last extensive series of patients with Addison's disease and coincident autoimmune phenomena were published approximately two decades ago, we studied the cause of the disease, the prevalence of autoimmune disorders and the frequency of occurrence of autoantibodies in 91 patients (31 men and 60 women, mean age 45.3-years-old, range 12-77) with Addison's disease. The cause of Addison's disease in six patients was tuberculosis (6.6%), and autoimmune adrenalitis was considered to be the cause in 83 patients (91.2%). In two patients (2.2%) other causes were responsible for Addison's disease. In 47% of the patients with autoimmune Addison's disease at least one other autoimmune disorder was present. Primary hypothyroidism had the highest prevalence (20.5%), followed by vitiligo (9.6%), non-toxic goiter (8.4%), premature menopause (7.3% of the women), Graves' disease (6%), pernicious anaemia (4.8%), Sjögren's disease (2.4%), hypoparathyroidism (1.2%), type 1 diabetes mellitus (1.2%) and coeliac disease (1.2%). The frequency of autoantibodies in the patients with autoimmune Addison's disease was: adrenal antibodies (82.7%), antibodies against microsomal antigens (58%), thyroglobulin antibodies (23.4%), parietal cell antibodies (19.8%), pancreatic islet cell antibodies (6.2%) and ovary antibodies (3.7% of the women). In comparison with other extensive series of patients with Addison's disease, we found the highest prevalence of autoimmune adrenalitis as the cause of Addison's disease, the highest prevalence of hypothyroidism and vitiligo as concomitant autoimmune disorders and the lowest prevalence of type 1 diabetes mellitus.

Addison Disease↗
PubMed2003

Sleep disturbances in patients with Addison's disease.

OBJECTIVE: The standard replacement therapy in Addison's disease does not restore normal nocturnal levels of the hormones of the hypothalamic-pituitary-adrenal axis. The aim of the study was to describe the prevalence and characteristics of sleep disturbances in patients with Addison's disease. METHODS: Sixty patients completed a self-administered sleep questionnaire and the Epworth Sleepiness Scale (ESS) questionnaire. Activity-based monitoring (actigraph recordings) and sleep diaries were obtained from eight patients. RESULTS: Thirty-four percent reported weekly sleep disturbances (difficulties falling asleep in 13%; repeated awakenings in 14%; early morning awakenings in 20%). The sleep need was 8.21 h (s.d. 1.34; range 6-14 h), and sleep onset latency was 29 min (s.d. 29, range 2-150 min). Forty percent of the patients were tired during daily activities more than once a week, but the scores of the ESS were 6.0 (s.d. 3.5), which is not higher than normal. The actigraph recordings showed higher sleep efficiency than the subjective recordings. CONCLUSION: We did not identify specific sleep disturbances which were characteristic for patients with Addison's disease. Patients with Addison's disease have increased daytime fatigue, but no more daytime sleepiness than normal.

Addison Disease↗
PubMed1988

The effect of low-dose naloxone infusion on plasma ACTH and LH in patients with Cushing's and Addison's diseases.

The ACTH, cortisol and LH responses to low dose (0.8 mg/h) naloxone 90 min infusion were investigated in seven patients with untreated Cushing's disease, six patients with Addison's disease and four control subjects. Naloxone had no effects on ACTH hypersecretion or normal ACTH levels. These data confirm that naloxone cannot provide additional diagnostic or therapeutic approaches in ACTH hypersecretion syndromes, mainly in Cushing's disease. The mean percentage LH levels did not significantly change during low dose naloxone in controls or patients with Cushing's and Addison's diseases. This suggests that increased endogenous opioid peptides in these diseases may not modify the LH responses to low dose of naloxone. However, since three of five adults with Cushing's disease had increased LH levels during naloxone, further studies may be indicated.

Addison Disease↗