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Results for “ADDISON'S DISEASE”

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At least 685 records · Page 38Linked to original sources
PubMed1977

[The ossification of the ear cartilage in Addison's disease].

Stiffening and tenderness of the helix of the ear, with radiologically demonstrable calcific deposits, has been reported in various conditions such as frostbite, and also in Addison's disease. To a total of 14 clinical observations with only 4 well documented cases, a first autopsy report of the disorder in a case of tuberculosus Addison's disease is added. It is shown that the elastic cartilage of the pinna, of the epiglottis and of the trachea undergoes ossification without preceding dystrophic or metastatic calcification. The ossification has been observed only in males with longstanding Addison's disease treated exclusively with mineralocorticoids over a long period. The possible pathogenetic mechanisms are discussed. An important factor seems to be the long-standing glucocorticoid deficiency.

Addison Disease↗
PubMed1990

Thyrotoxicosis in a patient with Addison's disease.

We report the case of a patient who suffered recurrent episodes of hypoadrenal crisis, despite conventional replacement therapy for Addison's disease. She was found to have hyperthyroidism and after this was treated, she had no further relapse. Thyrotoxicosis should be considered when patients taking replacement therapy for Addison's disease present in hypoadrenal crisis.

Addison Disease↗
PubMed1995

Autopsy findings of Addison's disease caused by systemic cytomegalovirus infection in a patient with acquired immunodeficiency syndrome.

We previously reported a case of Addison's disease associated with acquired immunodeficiency syndrome (AIDS) (Endocr J, 41:13, 1994). A 46-year-old man with hemophilia B and AIDS was diagnosed as Addison's disease. The positive cytomegalovirus (CMV) antigen in urine suggested that CMV adrenalitis may have caused the adrenal insufficiency. Despite treatment with ganciclovir, the patient died one year later. Autopsy findings revealed that the typical inclusions of CMV were seen in the lung, adrenal glands (both cortex and medulla) and small intestine. Here, we describe the subsequent clinical course and postmortem findings of this case.

AIDS-Related Opportunistic Infections↗
PubMed1979

Decreased blood pressure in response to an angiotensin II antagonist in Addison's disease.

The synthetic angiotensin II antagonist, 1-sarcosine, 8-isoleucine angiotensin II was infused in two patients with untreated Addison's disease. Blood pressure decreased following infusion of this angiotensin II antagonist. Re-infusion of the antagonist after cortisol replacement therapy for one month caused a slight increase in blood pressure. Addison's disease is one of the conditions in which the renin-angiotensin system is involved in the maintenance of blood pressure.

Addison Disease↗
PubMed1984

Ia-positive T lymphocytes in recently diagnosed idiopathic Addison's disease.

The Ia (DR, immune-associated) antigen is absent on normal circulating T lymphocytes, but present on activated T lymphocytes. Utilizing monoclonal antibody L243, the expression of this glycoprotein on circulating T lymphocytes was studied in five patients with recent-onset idiopathic Addison's disease, one patient with recent-onset adrenal hemorrhage, and nine patients with long-standing adrenal insufficiency (five with idiopathic Addison's disease and four after bilateral adrenalectomy for Cushing's disease). The patient with adrenal hemorrhage and the nine patients with long-standing adrenal insufficiency had percentages of circulating Ia-positive T cells within the normal range. All five patients with recent-onset idiopathic Addison's disease had an elevated percentage of circulating Ia-positive T cells (7 to 29 percent). The expression of Ia antigen on T cells in recent-onset idiopathic Addison's disease probably reflects immunologic activation, which may be of pathophysiologic importance.

Addison Disease↗
PubMed1998

A study of the epitopes on steroid 21-hydroxylase recognized by autoantibodies in patients with or without Addison's disease.

Steroid 21-hydroxylase (21-OH) autoantibodies are found in patients with autoimmune Addison's disease (AAD), either isolated or associated with autoimmune polyglandular syndrome (APS) type I and II and in adrenal-cortex autoantibody (ACA)-positive patients without AAD. In order to assess any differences in the 21-OH autoantibodies in these different patient groups, we have studied their reactivity with different epitopes on 21-OH using full length and modified 35S-labelled 21-OH proteins produced in an in vitro transcription/translation system. There were no major differences in the pattern of autoantibody reactivity with the different modified 21-OH proteins in patients with isolated AAD or with APS types I and II, and in 21-OH autoantibody-positive patients with clinical AAD, subclinical AAD and those maintaining a normal adrenal function. Our studies also indicate that the main epitopes for 21-OH autoantibodies in patients with different forms of autoimmune adrenal disease are located in the C-terminal end and in a central region of 21-OH.

Addison Disease↗
PubMed1992

[Anal incontinence in patients with Addison's disease: a gluco- and mineralocorticoid independent sphincter malfunction?].

Anorectal motor function was evaluated in 15 female patients with Addison's disease and androgen deficiency and 15 age-matched healthy volunteers. Medical history revealed symptoms of faecal incontinence in 5 patients. The patients showed decreased maximum retention volumes (p less than 0.01) in the rectal saline infusion test. Lowered anal sphincter resting (p less than 0.01) and squeeze pressure (p less than 0.01) was demonstrated in patients with adrenocortical insufficiency. No differences between patients and controls were found in respect of perception volume, minimal distension volume for sphincter relaxation and rectal compliance by means of intrarectal balloon distension. Electromyography of the external anal sphincter was performed in 8 patients and showed no evidence for a neurogenic defect. Relevant morphological changes of the anorectum could be excluded endoscopically in 13 of the 15 patients. Therefore impaired anorectal muscular function is responsible for faecal incontinence in patients with Addison's disease and androgen deficiency. Further investigations will show, whether these findings are the consequence of lowered androgen production.

Addison Disease↗
PubMedDate not supplied

Addison's disease due to metastatic carcinoma: the value of CT scan.

A case of Addison's disease secondary to bilateral adrenal metastasis is reported. The adrenal metastasis were secondary to bronchogenic carcinoma and the diagnosis was made on the basis of the CT scan. The role of CT in the diagnosis of adrenal disease as well as the importance of including the adrenals in the chest CT scan for preoperative staging of bronchogenic carcinoma is discussed.

Addison Disease↗
PubMed1993

Tuberculous Addison's disease. Utility of CT in diagnosis and follow-up.

The computed tomographic (CT) findings in five patients with tuberculous Addison's disease were evaluated. All patients had extra-adrenal tuberculosis. Two patients had enlarged adrenal glands with calcifications at the times of diagnosis. Follow-up CT from 4 to 30 months showed a progressive decrease in the size of adrenal glands from bilateral enlargement to small calcified glands and provides a clue to the etiology of Addison's disease and proper therapy.

Addison Disease↗
PubMed1977

Addison's disease secondary to North American blastomycosis.

Reported is the fifth known case of Addison's disease due to adrenal involvement by North American blastomycosis (Blastomyces dermatitidis infection). The fact that amphotericin B therapy precipitated an addisonian crisis suggests that patients with disseminated blastomycosis should have their adrenal function and reserve evaluated before undergoing systemic chemotherapy.

Addison Disease↗
PubMed1994

Fludrocortisone induced heart failure in Addison's disease.

The first reported case of congestive cardiac failure in a child with Addison's disease secondary to fludrocortisone therapy is presented. A renal adaptation to compensate for chronic salt and water deprivation is suggested as a possible mechanism for the development of congestive cardiac failure in this patient.

Addison Disease↗
PubMed2000

Improvement in mood and fatigue after dehydroepiandrosterone replacement in Addison's disease in a randomized, double blind trial.

Dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS) are adrenal precursors of steroid biosynthesis and centrally acting neurosteroids. Glucocorticoid and mineralocorticoid deficiencies in Addison's disease require life-long hormone replacement, but the associated failure of DHEA synthesis is not corrected. We conducted a randomized, double blind study in which 39 patients with Addison's disease received either 50 mg oral DHEA daily for 12 weeks, followed by a 4-week washout period, then 12 weeks of placebo, or vice versa. After DHEA treatment, levels of DHEAS and Delta(4)-androstenedione rose from subnormal to within the adult physiological range. Total testosterone increased from subnormal to low normal with a fall in serum sex hormone-binding globulin in females, but with no change in either parameter in males. In both sexes, psychological assessment showed significant enhancement of self-esteem with a tendency for improved overall well-being. Mood and fatigue also improved significantly, with benefit being evident in the evenings. No effects on cognitive or sexual function, body composition, lipids, or bone mineral density were observed. Our results indicate that DHEA replacement corrects this steroid deficiency effectively and improves some aspects of psychological function. Beneficial effects in males, independent of circulating testosterone levels, suggest that it may act directly on the central nervous system rather than by augmenting peripheral androgen biosynthesis. These positive effects, in the absence of significant adverse events, suggest a role for DHEA replacement therapy in the treatment of Addison's disease.

Addison Disease↗
PubMed2006

Tuberculous epididymitis presenting with Addison's disease: a rare case.

This report describes a case of tuberculosis with an atypical presentation characterized by epididymitis and Addison's disease in the absence of lung involvement. A 54-year-old male who presented with acute right scrotal pain and a whitish discharge, had been diagnosed four months earlier with acute epididymitis and prescribed ciprofloxacin. The clinical diagnosis was epididymitis and Addison's disease. Hydrocortisone therapy was initiated, and bilateral epididymectomy was undertaken. Biopsy specimen showed the presence of acid-fast bacilli and antituberculous treatment was initiated. On follow-up, the patient was in good clinical condition and free of symptoms. We conclude that tuberculous epididymitis can cause serious complications and should be included in the differential diagnosis for chronic epididymitis of unknown cause that does not respond to routine treatment. A high index of suspicion is required for diagnosis.

Addison Disease↗
PubMed1969

Thyroid function in Addison's disease.

Clinical evidence of a thyroid disorder was present in 10 out of 40 patients with Addison's disease. Though the remaining 30 patients had no clinical evidence of thyroid disease, six (out of 15 tested) had thyroid microsomal antibodies and a considerably impaired response to thyrotrophin. These changes are interpreted as very early indications of developing thyroid failure. When circulating microsomal antibodies are found this seems to indicate the presence of established thyroid disease.

Addison Disease↗