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PubMed1979

Probable pituitary adenoma with adrenocorticotropin hypersecretion (corticotropinoma) secondary to Addison's disease.

A 50-yr-old woman with Addison's disease from the age of 14 yr was diagnosed as empty sella turcica in 1974 (Rev Clin Esp 139: 183, 1975). She subsequently continued with hyperpigmentation in spite of adequate hormone substitution therapy which permitted her to lead a normal life. When studied she showed an extreme elevation of plasma ACTH (1500--2000 pg/ml), and with dexamethasone (2 and 8 mg/day) continued to have levels of 900 pg/ml. With 60 mg hydrocortisone daily, effects of overdosage were observed (swelling and Cushingoid facies) associated with depigmentation. However, she continued to manifest levels of plasma ACTH of 700 pg/ml and an absence of circadian rhythm. It seems likely that this patient represents a case of pituitary ACTH secretory adenoma (corticotropinoma) secondary to the preexisting Addison's disease. The circulating levels of other pituitary hormones were normal.

Addison Disease↗
PubMedDate not supplied

Liver involvement and abnormal iron variables in undiagnosed Addison's disease.

OBJECTIVE: To describe a case of untreated Addison's disease manifesting as severe gastrointestinal symptoms, persistently increased liver enzymes, substantially increased ferritin, and hepatic iron deposition and to document changes in these variables after corticosteroid replacement. METHODS: We thoroughly reviewed the clinical history and results of laboratory tests before and after treatment in a 23-year-old man during a period of 18 months. The relevant medical literature was also reviewed. RESULTS: The study patient had frequent episodes of severe abdominal symptoms, hemodynamic instability, and electrolyte imbalance. He underwent extensive laboratory investigations and was prescribed various treatment regimens. Increased levels of serum transaminases, ferritin, and transferrin saturation led to a liver biopsy, which showed lymphocytic infiltration and increased iron deposition. Eventually, cosyntropin stimulation (250 microg) confirmed the presence of adrenal insufficiency, and these abnormalities resolved after institution of daily administration of glucocorticoids and mineralocorticoids. CONCLUSION: Addison's disease can be a cause of unexplained hypertransaminasemia and profoundly increased ferritin levels. These changes are reversible but may lead to diagnostic confusion and delay in commencement of lifesaving corticosteroid therapy.

Addison Disease↗
PubMedDate not supplied

Keratopathy associated with hypoparathyroidism and Addison's disease.

Two siblings suffering from keratopathy, one with hypoparathyroidism associated with Addison's disease and the other with Addison's disease alone, are described. The hypothesis that there was an autoimmune etiology with variant manifestations in each subject is suggested and discussed.

Addison Disease↗
PubMed1984

Evidence that patients with Addison's disease are undertreated with fludrocortisone.

Ten patients with Addison's disease, nine with undetectable plasma aldosterone, were found to be sodium and water depleted with high levels of plasma-renin activity despite receiving 0.05-0.1 mg/day of fludrocortisone and optimum doses of glucocorticoid replacement therapy. Fludrocortisone was withdrawn while patients were in hospital on a fixed sodium intake. There was an immediate natriuresis with a further increase in plasma-renin activity. When a daily dose of 0.3 mg of fludrocortisone was given all patients retained sodium and water and gained weight. There was a fall in plasma-renin activity in all patients and an associated fall in blood urea and plasma potassium, and an increase in plasma volume; oedema developed in some patients. At outpatient follow-up, the dose of fludrocortisone was adjusted according to plasma-renin activity. Most patients required 0.2 mg of fludrocortisone to maintain adequate sodium and water balance. These results suggest that patients with Addison's disease on 0.05-0.1 mg of fludrocortisone with undetectable plasma aldosterone levels are currently being undertreated with fludrocortisone. The best way of assessing sodium balance in these patients and their response to fludrocortisone is by measurement of plasma-renin activity in conjunction with 24 h urinary sodium excretion.

Addison Disease↗
PubMed2004

Addison's disease presenting in four adolescents with type 1 diabetes.

Primary adrenocortical insufficiency (Addison's disease) is a potentially fatal condition that often develops insidiously and can be easily overlooked. Although rare in the general population, it is more common in patients with type 1 diabetes mellitus (T1DM). The combination of Addison's disease with T1DM and/or autoimmune thyroid disease is known as autoimmune polyendocrine syndrome type-2 (APS-2). T1DM commonly precedes the development of adrenocortical insufficiency in most patients with APS-2. We, in this study, present four cases of Addison's disease developing in adolescents with pre-existing T1DM. Risk factors for Addison's disease in this population include a history of other organ-specific autoimmunity, particularly thyroid, and a positive family history. In addition to the 'classic' Addisonian features, the development of unexplained recurrent hypoglycemia, reduction in total insulin requirement, improvement in glycemic control, or abnormal pigmentation should arouse suspicion of adrenocortical insufficiency. Adrenal antibodies have been proposed as a screening tool for Addison's disease in the T1DM population, but doubts remain about their specificity and sensitivity. The addition of specific HLA DRB1 subtyping has been proposed to improve predictive value.

Addison Disease↗
PubMed1995

Immunoprecipitation assay for autoantibodies to steroid 21-hydroxylase in autoimmune adrenal diseases.

Adrenal autoantibodies characteristic of autoimmune Addison disease are directed towards steroid 21-hydroxylase (21-OH; EC 1.14.99.10). We describe a new assay to measure 21-OH autoantibodies (21-OH Abs), based on immunoprecipitation by the antibodies of 35S-labeled human 21-OH. Using this immunoprecipitation assay (IPA), we detected 21-OH Abs in 42 of 64 (66%) patients with Addison disease and in 14 of 19 (74%) patients with autoimmune polyendocrine syndromes type I and type II. No 21-OH Abs were detected by the IPA in any patients with Addison disease attributable to tuberculosis (n = 9) or adrenoleukodystrophy (n = 9) or in patients with autoimmune thyroid disease (n = 28), systemic lupus erythematosus (n = 10), myasthenia gravis (n = 10), rheumatoid arthritis (n = 10), or insulin-dependent diabetes mellitus (n = 12). None of the 26 sera from healthy normal blood donors was positive for 21-OH Abs by the assay. We found good agreement between 21-OH Abs measured by IPA and by Western blotting (r = 0.83, n = 123, P < 0.001). The inter- and intraassay CVs for IPA were well < 10% at high, medium, and low concentrations of 21-OH Abs. Overall, our studies indicate that the IPA provides a specific, sensitive, and convenient system for measuring 21-OH Abs.

Addison Disease↗
PubMed1982

Adrenoleukodystrophy: elevated C26 fatty acid in cultured skin fibroblasts and correlation with disease expression in three generations of a kindred.

Varying combination of central and peripheral nervous system disease and Addison disease were previously described in 14 members of a family. The diagnosis of adrenoleukodystrophy (ALD) was documented in affected individuals by increased content of C26:0 C26/C22 fatty acid ratios were not proportional to the neurologic syndrome, severity of disease, or duration.

Addison Disease↗
PubMedDate not supplied

Addison's disease presenting as acute chest syndrome: case report and review of literature.

BACKGROUND: Addison's disease is due to primary adrenal failure. It is an uncommon condition with equal prevalence in both males and females. The onset of symptoms is gradual and manifestation is non specific, hence diagnosis is easily missed without a high index of suspicion. METHODS: The medical records of a patient who presented with acute chest pain to the cardiac unit of the University of Port Harcourt Teaching Hospital were reviewed. A review of the literature using manual library and Medline search on Addison's disease was also done. RESULT: A 48 years old male presented in our medical outpatient department with a three day history of sudden onset of severe precordial chest pain that started while playing football which was associated with nausea, vomiting and difficulty in breathing. After initial clinical evaluation a diagnosis of acute myocardial infarction and cardiac failure with a suspicion of background Addison's disease was made. Serial electrocardiography done over a two week period did not show evidence of myocardial infarction, but the patient had elevated serum ACTH and very low serum cortisol levels. An abdominal CT scan done two weeks after admission showed absence of the Adrenal glands bilaterally, confirming Addison's disease. He received treatment for cardiac failure, analgesics, prednisolone and a mineralocorticoid to which he responded satisfactorily and has remained healthy. He also received a six months course of antituberculous treatment empirically. CONCLUSION: Addison's disease is an uncommon endocrine disorder which can present insidiously in a non specific manner. Diagnosis requires a high index of suspicion.

Acute Disease↗
PubMed1980

A pituitary tumour with possible ACTH and TSH hypersecretion in a patient with Addison's disease and primary hypothyroidism.

A patient with Addison's disease, who was inadequately substituted with corticosteroids for twenty-five years, developed a pituitary tumour. The diagnosis of autoimmune thryroiditis with asymptomatic hypothyroidism was also made. ACTH and TSH plasma values were abnormally elevated. The ACTH secretion was suppressed by cortisone administered perorally. It seems possible that the pituitary enlargement is due to prolonged insufficient adrenocortical replacement therapy. The differential diagnosis and possible pathogenetic factors are discussed.

Addison Disease↗
PubMed1999

Celiac disease and autoimmune endocrinologic disorders.

Patients with insulin-dependent diabetes mellitus, autoimmune thyroid disease, Addison's disease, and alopecia areata are at increased risk of celiac disease. We investigated whether patients with more than one autoimmune endocrinologic disorder are even more susceptible to celiac disease or have celiac-type mucosal inflammation. All 62 patients found to have such multiple diseases in 1994-1996 were investigated. Small bowel biopsy was performed on all voluntary nonceliac subjects. The villous structure and density of intraepithelial lymphocytes were examined, and HLA-DQ alleles were determined. Seven (11%) patients had celiac disease: six cases were detected earlier and there was one new case; in addition, two had minor villous deterioration and five an increased density of mucosal intraepithelial gammadelta+ T-cells. HLA-DQ2 or DQ8 alleles were found in all subjects with mucosal changes. Patients with multiple autoimmune disorders clearly run an increased risk of developing celiac disease, and some of them have minor mucosal changes compatible with the early signs of the disease.

Addison Disease↗
PubMed2005

[Addison's disease: the challenge of an early diagnosis].

Addison's disease is a set of symptoms which is produced due to the destruction of the suprarenal cortex, of a mainly autoimmune origin, on account of the presence of antibodies which attack it. This destruction takes place in a generally slow manner, causing symptoms to appear in an insidious way, added to the fact that these symptoms tend to be unspecific. Therefore it is easy to understand that its diagnosis at an early stage will be very difficult and is often interpreted as another disease. It is only when the deficit is important and adrenal crisis develop that we can reach the right diagnosis in a situation where the death risk is considerably high. We presented a clinical case as an example of what has been described previously. After several months of progressively deteriorating symptoms and several visits to different medical units, the patient is diagnosed as having an adrenal crisis and is immediately admitted to the intensive care unit.

Addison Disease↗
PubMed2002

High prevalence and increasing incidence of Addison's disease in western Norway.

OBJECTIVE: Estimates of the prevalence of Addison's disease in Caucasians have varied from 39 to 117 per million. We have carried out an epidemiological study to obtain a confident point prevalence estimate in the Norwegian population for the end of 1999, and to find out whether the incidence is changing. PATIENTS AND METHODS: The patients were identified by a search through registers of 10 hospitals and consultant endocrinologists serving a population of 916 000. The completeness of the list was tested by a survey of general practitioners in one district, and by the member list of the local Addison Association in another district. RESULTS: We identified 128 patients with Addison's disease (59 men and 69 women), yielding a prevalence of 140 per million. Recorded mean incidence in the past decade was 0.62 per 100,000 per year. Fifty-one patients (40%) had concomitant endocrine diseases. The aetiology was almost exclusively idiopathic or autoimmune. CONCLUSIONS: We found a higher prevalence of Addison's disease in western Norway than has previously been reported anywhere. Our findings support the hypothesis of a rising incidence of autoimmune adrenal insufficiency.

Addison Disease↗
PubMed1994

Increased risk for type I (insulin-dependent) diabetes in relatives of patients with alopecia areata (AA).

The prevalence of various chronic diseases was compared in 517 individuals with alopecia areata, and 2,969 of their first degree relatives. As previous reports have suggested an increased incidence of diabetes in relatives of patients with alopecia areata, special attention was given to the prevalence of Type 1 and Type 2 diabetes in the patients and in their relatives. Several immunologic diseases were increased in alopecia probands and relatives. Thyroid disease, vitiligo, Addison disease, and pernicious anemia were more prevalent in probands and in their relatives than in the general population. Specifically, a high rate of thyroid disease was found in probands (14.7%) and in their first degree relatives (4.2%). Only one proband had Type 1 diabetes, yet there were 14 sibs with Type 1 diabetes. Thus, Type 1 diabetes was significantly more prevalent in the sibs (1.2%) than in either the probands with alopecia (0.2%), or the general population (0.12-0.25%) (P < 0.05)). In contrast, Type 2 diabetes was not more common in probands or in sibs than in the general population. These data suggest that alopecia areata protects against Type 1 diabetes in predisposed individuals. The high rate of thyroid disease suggests that screening probands and first degree relatives for thyroid disease should be considered.

Addison Disease↗
PubMed1982

Patients presenting with Addison's disease need not be pigmented.

Three consecutive cases of Addison's disease without increased pigmentation are described. We suggest that the absence of this important physical sign contributed to serious delays in diagnosis and markedly increased morbidity. We emphasize that, despite the usual textbook description, excess pigmentation is not necessarily a feature of Addison's disease.

Addison Disease↗