Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ADDISON'S DISEASE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 631 records · Page 35Linked to original sources
PubMed1977

Addison's disease with renal microangiopathy and renal failure (a new syndrome).

A syndrome comprising Addison's disease, renal microangiopathy and renal failure is described in two patients. The renal lesions manifested despite corticosteroid replacement therapy and were characterized by glomerular damage and thrombo-microangiopathic changes in afferent arterioles and intralobular arteries. Both patients died as a result of their renal disease.

Addison Disease↗
PubMed2002

Mutational analysis of the autoimmune regulator (AIRE) gene in sporadic autoimmune Addison's disease can reveal patients with unidentified autoimmune polyendocrine syndrome type I.

OBJECTIVE: To investigate whether patients with Addison's disease and polyendocrine syndromes have undiagnosed autoimmune polyendocrine syndrome type I (APS I). MATERIALS AND METHODS: Forty patients with clinical manifestations resembling APS I and with autoantibodies typical of this condition were screened for Norwegian autoimmune regulator (AIRE) gene mutations. RESULTS: A 30-year old man who had developed Addison' s disease at the age of 12, but had no other components of APS I, was homozygous for the 1094-1106 deletion mutation in exon 8 of the AIRE gene, the most common mutation found in Norway. CONCLUSIONS: APS I patients with milder and atypical phenotypes are difficult to diagnose on clinical grounds. Autoantibody analysis and mutational analysis of AIRE may therefore be helpful modalities for identifying these individuals.

Addison Disease↗
PubMedDate not supplied

Spontaneous intracerebral hemorrhage revealing Addison's disease.

We report a case of spontaneous intracerebral hemorrhage occurring in a young woman and revealing Addison's disease. This autoimmune primary adrenocortical insufficiency was associated with premature ovarian failure. Exhaustive research for nonhypertensive causes of intracerebral hemorrhage was negative. Initial coagulation studies disclosed severe hypofibrinogenemia and prolonged prothrombin time related to vitamin K-dependent coagulation factor deficit. Clotting abnormalities cleared at 4 months under treatment with hydrocortisone. Glucocorticoids are potent regulators of fibrinogen biosynthesis, increasing fibrinogen secretion. We conclude that primary adrenocortical insufficiency induced this hemorrhagic diathesis leading to spontaneous intracerebral hemorrhage. This latter has never been reported in Addison's disease. Primary adrenocortical insufficiency should be considered as a rare potential cause of nonhypertensive intracerebral hemorrhage.

Addison Disease↗
PubMed1991

[Adrenomyeloneuropathy as a cause of Addison's disease].

A 25-year old male, with a 3-year history of spastic paraparesis and a disturbance of bladder emptying, developed Addison's disease (plasma ACTH 1250 pg/ml, depressed cortisol values with loss of diurnal rhythm, potassium 6.8 mmol/l, sodium 123 mmol/l) associated with a urinary tract infection. The suspected diagnosis of adrenomyeloneuropathy was confirmed by the finding of raised plasma long-chain fatty acid concentrations. The patient was immediately given 0.4 mg fludrocortisone as a bolus, followed by 0.1 mg daily maintenance therapy, the urinary tract infection having already been successfully treated. Substitution therapy with hydrocortisone was also initiated (starting dose 30-20-10 mg daily, maintainance dose 20-10-5 mg daily). As a result, the electrolyte concentrations returned to normal and the neurological features improved. A family study was undertaken to determine whether the adrenomyeloneuropathy was an X-linked recessive form. Both the symptom-free mother (carrier) and the 19-year-old brother, who had suffered from Addison's disease since the third year of life, had raised plasma long-chain fatty acid concentrations. Both brothers were started on a diet low in long-chain fatty acids. Estimation of long-chain fatty acids is indicated in boys or young adult males with peripheral neuropathy or Addison's disease of uncertain aetiology.

Addison Disease↗
PubMed1994

[A case of Addison's disease which became worse during interferon therapy: insulin secretion under hyposmolarity].

We report a patient with Addison's disease whose clinical features became worse during interferon therapy for chronically active hepatitis C. A 47-year-old male was admitted because somnolence developed during a 4 week treatment with interferon-alpha-2a (IFN: 900 x 104U/day). Serum Na level was 113mEq/l and plasma osmolarity was lowered to 238mOsm/kg on admission. Plasma ACTH level was high, while serum cortisol, urinary 17-OHCS and 17-KS excretion were far below the normal levels. On admission, serum prolactin, insulin levels and urinary CPR excretion increased. Normalization of serum Na level by NaCl administration attenuated hyperinsulinemia associated with the reduction of increased CPR excretion. It was supposed that IFN administration might increase cortisol consumption and worsen hypoadrenocortinism in a patient with Addison's disease. In addition, the present case raised the possibility that hyposmolarity may induce a hyperinsulinemic state in humans.

Addison Disease↗
PubMed1996

[Addison's disease in pregnancy: a report of six cases].

OBJECTIVE: To review six cases of pregnancy with Addison's disease at Obstetrics and Gynecology Hospital, Shanghai Medical University from 1949 to 1994. METHOD: This is a clinical retrospective analysis. Five of the 6 patients were treated with hormone replacement therapy, and the remaining one received no hormone treatment due to lack of symptoms during pregnancy and neglect of previous adrenal surgery by obstetricians. RESULTS: The patient received no treatment occurred Addisonian crisis and died soon after delivery. The other five patients had smooth course of delivery and postpartum period. CONCLUSIONS: Hormone replacement therapy is important for patients with Addison's disease in pregnancy especially for acute decompensation of adrenal function. Pregnant women with history of adrenal surgery should be monitored carefully even without any symptoms and hormone treatment is necessary. Vaginal delivery is encouraged unless there is obstetric indication.

Addison Disease↗