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PubMedDate not supplied

[Pregnancy in Addison disease and diabetes mellitus].

Pregnancies in patients with Addison's disease and Diabetes mellitus are rarely observed. A case of pregnancy in such patient is reported. The course of pregnancy and the fetal development show, that pregnancy can be finished without great problems, if there is therapeutical full compensation of metabolic derangement by hydrocortisone and insulin. There are less complications due to Addison's disease than to Diabetes mellitus. Thus the management of delivery should be the same as in isolated Diabetes mellitus.

Addison Disease↗
PubMed2005

[Two 150 years anniversaries: Claude Bernard's internal environment and Addison disease].

In 2005 two 150 years anniversaries, which essentially influenced the development of modern medicine will be celebrated. French physiologist Claude Bernard from College de France published his work "Lectures on Experimental Physiology, applied to medicine" and British medical doctor T. Addison described insufficiency of adrenal cortex, today known as Addison disease.

Addison Disease↗
PubMed2003

Replacement therapy in Addison's disease.

Addison's disease or primary adrenal insufficiency is a rare disease, which is usually caused by autoimmune destruction of the adrenal cortex. The clinical picture is caused by deficiency of cortisol and aldosterone. These deficiencies are accompanied by adrenal androgen depletion of yet unknown significance. The current therapy is the replacement of glucocorticoids and mineralocorticoids, but the available drugs do not restore the normal diurnal variations in serum hormone levels. The clinical consequences of the grossly unphysiological replacement therapy are largely unknown. Many patients with Addison's disease on standard replacement therapy complain of fatigue, weariness, and reduced stress tolerance. One particular concern has been negative effects on both bone metabolism due to over-replacement of glucocorticoids and androgen depletion. This review discusses the evidence for the current drug and dosage recommendations. Current recommended daily starting dose for hydrocortisone and cortisone acetate are 20 and 25 mg, respectively, divided into two or preferably three doses. The mineralocorticoid depletion should be treated with fludrocortisone 0.05-2.0 mg/day [DOSAGE ERROR CORRECTED]. Replacement of dehydroepiandrosterone 20-50 mg has been advocated in adrenal failure, but the evidence for benefit is weak.

Addison Disease↗
PubMed1980

Addison disease and cerebral sclerosis in an apparently heterozygous girl: evidence for inactivation of the adrenoleukodystrophy locus.

Cerebral sclerosis and Addison disease were observed at age 14 years in a previously healthy sister of an affected boy. Clinical findings and family history established the diagnosis of X-linked adrenoleukodystrophy, which is normallly confined to males. The affected female has a normal karyotype; both X chromosomes are morphologically inconspicuous. Thus, this patient may be the first documented example of clinically manifest adrenoleukodystrophy in a heterozygote, which supports our previous conclusion that this X-linked locus is subject to inactivation.

Addison Disease↗
PubMed1995

Rothmund-Thomson syndrome and Addison disease.

We report an 18-year-old man with the unusual combination of Rothmund-Thomson syndrome (RTS) and Addison disease. He was admitted when he was 26 months old because of short stature, dehydration, metabolic acidosis, hyperpigmentation, and typical skin lesions. Because his growth remained delayed, at age 10 years he was given a trial of recombinant growth hormone. After six years of treatment no improvement in height, bone, or sexual maturation was observed. This fact may be related to a defect in connective tissue metabolism. Chromosomal analysis of peripheral blood lymphocytes revealed increased numbers of breaks and gaps. Fibroblasts cultured from affected skin did not grow. Patients with RTS are prone to developing cancer, but no malignant disease was found in our patient. Early diagnosis and treatment of both endocrinologic and malignant complications are essential for survival of patients with this rare syndrome.

Acidosis↗
PubMed1999

Encephalopathy in a patient with Addison disease.

Patients with adrenal insufficiency manifest a myriad of metabolic disorders which can inflict neurologic damage. Here we present an unusual clinical presentation and distinctive imaging features in a patient with Addison disease.

Addison Disease↗
PubMed2001

Dehydroepiandrosterone replacement in addison's disease.

Addison's disease is a rare endocrine disorder which can be life-threatening. It can also interfere with the normal development of adrenarche, resulting in the absence of pubic and axillary hair growth. We report a case of satisfactory restoration of adrenarche through DHEA administered in conjunction with the standard glucocortisone and fluorocortisone replacement.

Addison Disease↗
PubMed1985

Hyperpigmentation, vitiligo, and Addison's disease.

Addison's disease is an uncommon disorder whose dermatologic manifestations range from vitiligo to hyperpigmentation. The association of adrenal autoantibodies and vitiligo has made the latter a possible cutaneous marker for an autoimmune cause. The other cutaneous marker, hyperpigmentation, is now more clearly understood on the basis of a prohormone common to both adrenocorticotrophic hormone (ACTH) and melanocyte-stimulating hormone (MSH).

Addison Disease↗
PubMedDate not supplied

Addison's disease.

Addison's disease, or primary adrenal insufficiency, results in glucocorticoid and mineralocorticoid deficiency. Orthostatic hypotension, fever, and hypoglycemia characterize acute adrenal crisis, whereas chronic primary adrenal insufficiency presents with a more insidious history of malaise, anorexia, diarrhea, weight loss, joint, and back pain. The cutaneous manifestations include darkening of the skin especially in sun-exposed areas and hyperpigmentation of the palmar creases, frictional surfaces, vermilion border, recent scars, genital skin, and oral mucosa. Measurement of basal plasma cortisol is an insensitive screening test. Synthetic adrenocorticotropin 1-24 at a dose of 250 microg works well as a dynamic test. Elevated plasma levels of adrenocorticotropin and renin confirm the diagnosis. Treatment involves replacement of the deficient hormones.

Addison Disease↗
PubMed2000

Addison disease after appendicitis.

A 14-year-old boy manifested acute abdominal pain, vomiting, high temperature and diarrhea. He also underwent increasing hyponatremia and hyperkalemia after appendectomy. Further testing confirmed Addison disease. The serum adrenal antibody test was positive, and other autoimmune diseases were excluded.

Abdominal Pain↗
PubMedDate not supplied

[Addison disease during pregnancy--a diagnostic dilemma. Symptoms are similar to normal pregnancy problems].

The symptoms of primary adrenocortical insufficiency (Addison's disease) such as fatigue, anorexia, hypotension and hyperpigmentation are similar to those of normal pregnancy. Addison's disease is rare and the diagnosis can easily be overlooked during pregnancy. The concentration of corticosteroid-binding globulin (CBG) and cortisol in serum as well as urinary free cortisol increase 2-3 times during pregnancy. Therefore, the reference ranges for nonpregnant persons cannot be used during pregnancy. The diagnosis of Addison's disease in pregnancy should be based on analysis of p-ACTH which remains within the reference range in normal pregnancy until delivery. A case of Addison's disease diagnosed during pregnancy is presented and it illustrates the diagnostic difficulties. In patients taking oral estrogen containing contraceptives, serum levels of CBG and cortisol also increase 2-3 times, making s-cortisol values difficult to interpret. Also in these patients, analysis of p-ACTH is of value when suspecting Addison's disease.

Addison Disease↗
PubMed1975

Cytoenzymologic activities of some oxidroeductases and alkaline phosphatase of leucocytes in Basedow, Cushing and Addison diseases.

Leukocytes, approached by histoenzymological methods for demonstration of dihydrofolate dehydrogenase, NADH2-diaphorase, lactate dehydrogenase and alcaline phosphatase activities, provided information about the impaired metabolic balance of thyrotoxicosis, Cushing and Addison diseases. The most relevant variations were found in thyrotoxicosis, the most sensitive enzyme was dihydrofolate dehydrogenase and the less sensitive was alcaline phosphatase. The neutrophils and lymphocytes had more evident enzymic variations.

Addison Disease↗
PubMed1993

[Complications after cesarean section in untreated Addison disease].

We report on a case of a patient with unknown Addison's disease who showed a variety of complications after caesarean section (preterm labour, breech presentation, 32 wks.). The main complications were endomyometritis, altered serum electrolytes, severe hypotension and weakness. Based on clinical observations and cortisol provocation test, the patient was diagnosed with Addison's disease on day 10 after caesarean section. Substitution with corticoids was started immediately. With this medication, rapid restitution and normalisation of the pathological parameters could be achieved.

Addison Disease↗
PubMed1998

A novel presentation of Addison disease: hypoglycemia unawareness in an adolescent with insulin-dependent diabetes mellitus.

A 16-year-old boy with insulin-dependent diabetes mellitus (IDDM) and a history of marginal glycemic control had severe hypoglycemia unawareness and a marked decrease in insulin requirement. His counterregulatory hormone response at the time of hypoglycemia suggested adrenocortical and adrenomedullary dysfunction. Further testing confirmed Addison disease. The patient's hypoglycemia unawareness was reversed by glucocorticoid replacement, although the plasma epinephrine response to hypoglycemia remained undetectable.

Addison Disease↗