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Results for “ADDISON'S DISEASE”

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At least 973 records · Page 54Linked to original sources
PubMed1989

Addison's disease, malignant lymphoma and death from cerebral giant cell arteritis.

A 61-year-old woman with Addison's disease and malignant lymphoma for several years was admitted to hospital with a 2-month history of fatigue and a 7 kg weight loss. The erythrocyte sedimentation rate was 92 mm h-1 and a temporal biopsy was performed as a part of the clinical investigation. She suddenly suffered a paresis of the right arm, sudden blindness and her blood pressure fell to 100/60 mmHg. Hydrocortisone was given intravenously followed by betamethasone, and an Addison crisis as well as a giant cell arteritis (GCA) was suspected. Activity in the malignant lymphoma was also a possibility. The patient did not improve and died 8 d later. The temporal biopsy indicated GCA. The autopsy showed a pronounced intimal inflammatory reaction of the intracerebral arteries and an infarction in the left posterior hemisphere. A possible link between GCA and other autoimmune diseases is discussed.

Addison Disease↗
PubMed2004

Lack of association of human chemokine receptor gene polymorphisms CCR2-64I and CCR5-Delta32 with autoimmune Addison's disease.

The attraction of leukocytes to tissues is essential for inflammation and the initiation of the autoimmune reaction. The process is controlled by chemokines, which are chemotactic cytokines. We investigated whether human chemokine receptor gene polymorphisms, namely CCR5-Delta32 and CCR2-64I, are associated with susceptibility to autoimmune Addison's disease. Genotyping was performed in 56 patients and 127 healthy controls by a new method using pyrosequencing for CCR2-64I and by polymerase chain reaction and detecting gel for CCR5-Delta32. None of the CCR2 or CCR5 alleles was found to be associated, either positively or negatively, with disease risk. Our results indicate that the CCR2-64I and CCR5-Delta32 gene polymorphisms do not play a major role in conferring genetic risk for, and/or protection against, autoimmune Addison's disease.

Addison Disease↗
PubMed1993

[A case of primary non-Hodgkin lymphoma of the adrenal gland presenting with Addison's disease].

A 69-year-old male was admitted to our hospital complaining of skin pigmentation. Masses in bilateral adrenal glands were noted on computed tomography. An exploratory laparotomy revealed malignant lymphoma confined to the bilateral adrenal glands. Histological diagnosis was diffuse mixed-cell type, B-cell lymphoma. Laboratory tests disclosed an elevated ACTH level and decreased urinary 17KS and 170HCS secretion. Based on hypofunction of adrenal glands and skin pigmentation, the patient was diagnosed as having Addison's disease. After complete remission with combination chemotherapy, adrenal function recovered normal and pigmentation disappeared, Addison's disease is an extremely rare complication of primary malignant lymphoma of the adrenal gland.

Addison Disease↗
PubMed1996

Pituitary Corticotroph Adenoma in a Woman with Long-Standing Addison's Disease: A Histologic, immunocytochemical, Electron Microscopic, and In Situ Hybridization Study.

A 64-year-old woman with long-standing Addison's disease owing to destructive immune adrenalitis presented with hyperpigmentation and progressively increasing blood adrenocorticotrophic hormone (ACTH) levels. Magnetic resonance imaging demonstrated a pituitary microadenoma, which was removed by transsphenoidal surgery and investigated by histology, immunocytochemistry, transmission electron microscopy, and in situ hybridization (ISH). The morphologic studies revealed a basophilic, periodic acid-Schift (PAS)-positive pituitary adenoma immunoreactive for ACTH and B-endorphin and in several cells for a-subunit. By transmission electron microscopy, the tumor was a densely granulated corticotroph adenoma, which, by ISH, expressed pro-opiomelanocortin (POMC) mRNA. The lack of corticotroph hyperplasia in the nontumorous adenohypophysis was an intriguing finding. Corticotroph adenomas in patients with long-standing Addison's disease were very rarely examined by morphology. Our report includes a detailed morphologic analysis and is the first demonstration of POMC mRNA in the tumor cells using ISH. The question of whether the adenoma was related to increased secretory activity secondary to protracted hypocorticism or developed independently unrelated to deranged endocrine homeostasis remains unresolved. The lack of corticotroph hyperplasia in the nontumorous adenohypophysis favors the interpretation that hypothalamic stimulation played no major role in adenoma formation in our case.

Journal Article↗
PubMed1993

Acutely raised corticotropin levels in Addison's disease are not associated with increased plasma arginine vasopressin and corticotropin-releasing factor concentrations in peripheral plasma.

Using an intensive sampling protocol we have examined the associations of peripheral plasma arginine vasopressin (AVP) and CRF with nocturnal ACTH hypersecretion in patients with Addison's disease. Six subjects were studied during a phase of cortisol withdrawal (36 h) and after cortisol substitution, and the findings were compared to those in four normal control subjects. The pulse properties of ACTH hypersecretion at a 10-min sampling interval have also been examined in these settings, using Cluster analysis. In the period before cortisol replacement, the Addison's patients showed significantly greater ACTH peak maxima and peak increments than the control subjects [107 +/- 44 vs. 5.5 +/- 1.3 pmol/L (P = 0.009) and 57 +/- 23 pmol/L vs. 3.7 +/- 0.9 pmol/L (P < 0.05), respectively]. After cortisol replacement, a significant decrease in mean peak increment (57 +/- 24 vs. 15 +/- 5 pmol/L; P = 0.021) occurred. The mean interpulse intervals did not differ significantly between the Addison's and control subjects (59 +/- 5 vs. 59 +/- 4 min overall). Although not significant, the trend for the pulse interval to increase after oral cortisol (60 +/- 6 vs. 72 +/- 9 min) is probably a result of the extremely low levels of ACTH after oral cortisol administration, making peak detection difficult. Despite the ACTH hypersecretion in the Addison's subjects, plasma AVP levels were at no time different from those in the control subjects. Plasma CRF levels tended to be lower in the Addison's patients than in the control subjects. We conclude that in states of cortisol deficiency, such as Addison's disease, ACTH hypersecretion results from enhanced ACTH peak amplitude, without a change in the frequency of ACTH secretory pulses. The marked increase in plasma ACTH that follows acute cortisol deprivation is independent of detectable changes in peripheral plasma levels of CRF or AVP.

Addison Disease↗
PubMedDate not supplied

[Hypoparathyroidism and Addison's disease with moniliasis: report of two cases in childhood (author's transl)].

Two pediatric cases are described presenting a conjunction of Addison's disease and hypoparathyroidism. One of the two cases also exhibits moniliasis of the oral cavity (Whitaker's disease). A full report is given of the symptoms and of the laboratory analyses which have motivated the diagnosis, and of the endocrinological function tests which were intended to confirm the diagnosis. The clinical process and the therapeutic criteria adopted are subsequently reported. A discussion follows focusing on the possible causes of the coexistence of the immunological defect and of the endocrinous deficiencies which are typical of the syndrome. Pathogenetic priority is attributed to the immunological defect which induces a autoimmune lesion of the endocrinous glands concerned.

Addison Disease↗
PubMed2004

Fatal toxic epidermal necrolysis in autoimmune polyglandular syndrome type I.

Autoimmune polyglandular syndrome Type I (APS I) is a disorder defined by the presence of at least two of the following diseases: Addison's disease, hypoparathyroidism, and chronic mucocutaneous candidiasis. We present the case of a 45-yr-old woman, affected by APS I, in chronic treatment with betamethasone. She was referred to a Division of General Medicine for jaundice, ascites and peripheral edema attributed to worsening of pre-existing autoimmune chronic hepatitis. During hospitalization, the following drugs were given: Amoxicillin/Clavulanic acid and Levofloxacin for bronchopneumonia, Furosemide and Canreonate for renal impairment, Pantoprazole for gastric protection, and Itraconazole for oral candidiasis. After about a month, she developed widespread, sheet-like, epidermal detachment, with painful lesions of the conjunctiva, lips and mouth. Toxic epidermal necrolysis (TEN) was diagnosed, and the patient was transferred to a Burn Center, where she died 10 days after the first onset of cutaneous rash. Autoptic and histopathological findings (epidermal necrosis and detachment, lymphomonocytic infiltration of the dermis) confirmed the clinical diagnosis. TEN is a usually drug-induced cutaneous inflammatory disorder characterized by extensive epidermal detachment and frequent mucosal involvement. It has also been associated with immuno-mediated disorders (HIV infection, graft-vs-host disease, systemic lupus erythematosus, mixed essential cryoglobulinemia), in keeping with immuno-mediated pathogenesis. We present, to our knowledge, the first report of TEN in a patient with APS I, and suggest that some pathogenetic mechanisms of APS I are shared with TEN. We stress how such a disease can occur in an autoimmune syndrome, even during corticosteroid treatment.

Fatal Outcome↗
PubMed2003

Circulating endogenous digitalis-like factor(s) (EDLF) in man is derived from the adrenals and its secretion is ACTH-dependent.

Adrenal origin and ACTH-dependent secretion of endogenous digitalis-like factor(s) (EDLF) was investigated. Twelve normal weight normotensive subjects (normal group) and 10 patients with Addison's disease (Addison group) were subjected to prolonged ACTH stimulation with 1 mg tetracosactin-depot im. Blood sampling was at 0 and 240 min. Digitalis-like reactivity was monitored in plasma extracts (combined organic solvent solid phase method) by digoxin and ouabain radioimmunoassay (RIAD and RIAO, respectively). 3H-ouabain concentration on erythrocytes (OBS) was also determined. Na+, K+-ATPase inhibition by normal plasma extract was tested by measuring Vmax and Km of 86Rb+-transport into human erythrocytes. In the normal group basal median plasma concentrations RIAD (0.07 nmol/l) and RIAO (0.89 nmol/l) increased significantly after ACTH administration (median 0.31 and 1.83, respectively; Wilcoxon, p<0.01). In contrast, in the Addison group no plasma RIAD and RIAO reactivity was detected before or after ACTH administration with minor exceptions. The OBS remained unchanged in the Addison group at 0 and 240 min; in the normal group there was a significant decline at 240 min (Wilcoxon, p<0.05) implying increase in circulating EDLF after ACTH stimulation. In the 86Rb+-transport experiments, 2 nmol/l ouabain or 2 nmol/l plasma-extracted ouabain reactivity both significantly impaired substrate affinity equally increasing Km without affecting Vmax. In men, the adrenals may produce and secrete EDLF, whose secretion appears to be ACTH-dependent.

Adrenal Glands↗
PubMed2000

Giant adrenal myelolipoma: case report and review of the literature.

Myelolipoma is a tumor-like growth composed of mature fat tissue and bone marrow elements. It occurs in the adrenal gland or as an isolated soft tissue mass. It may be associated with endocrine disorders such as hermaphroditism, Cushing's disease, Addison's disease and obesity of unknown cause. These lesions rarely measure more than 5 cm in diameter, although giant tumors have been reported in the literature. The fifth largest surgically resected adrenal myelolipoma in the literature is reported and its clinical associations and, macroscopic and microscopic features are discussed.

Adrenal Gland Neoplasms↗