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Addison's disease

Addison's disease (also known as chronic adrenal insufficiency, or hypocortisolism) is a rare endocrine disorder, first described by British physician Thomas Addison. more...

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It is estimated that it affects about 1 to 2 in 100,000 people.

It occurs when the adrenal glands, seated above the kidneys, fail to produce enough of the hormone cortisol and, sometimes, the hormone aldosterone.

Addison's disease refers specifically to primary adrenal insufficiency, in which the adrenal glands themselves malfunction; secondary adrenal insufficiency occurs when the pituitary gland does not produce enough adrenocorticotropic hormone (ACTH) to adequately stimulate the adrenal glands.

Signs and symptoms

Early signs

Addison's disease progresses slowly, and symptoms may not present or be noticed until some stressful illness or situation occurs. Common symptoms are:

  • chronic fatigue that gradually worsens
  • muscle weakness
  • loss of appetite
  • weight loss
  • nausea/vomiting
  • diarrhea
  • low blood pressure that falls further when standing (orthostatic hypotension)
  • areas of hyperpigmentation (darkened skin), known as melasma suprarenale.
  • irritability
  • depression
  • craving for salt and salty foods
  • hypoglycemia (worse in children)
  • for women, menstrual periods that become irregular or cease
  • tetany (particularly after drinking milk) due to phosphate excess
  • numbness of the extremities, sometimes with paralysis, due to potassium excess

Addisonian crisis

An illness or accident can aggravate the adrenal problems and cause an Addisonian crisis in which the symptoms include:

  • brown coating on tongue and teeth due to iron loss hemolysis
  • sudden penetrating pain in the legs, lower back or abdomen
  • severe vomiting and diarrhea, resulting in dehydration
  • low blood pressure
  • loss of consciousness
  • hypoglycemia

Untreated, an Addisonian crisis can be fatal. It is a medical emergency.

Diagnosis

In suspected cases of Addison's disease, one needs to demonstrate that adrenal hormone levels are low after appropriate stimulation with synthetic pituitary hormone.

Once demonstrated, the cause of adrenal failure needs to be elucidated. The most common cause is autoimmune, and can be tested for with an assay for 21-hydroxylase antibodies. If there are no antibodies present, infectious or genetic causes should be sought. This may include imaging of the adrenal glands, tests for tuberculosis or HIV infection, and searching for metastatic cancer.

Pathophysiology

Eighty to ninety percent of cases of Addison's disease are said to be due to autoantibodies directed against adrenal cells containing 21-hydroxylase, an enzyme involved in the production of cortisol and aldosterone.

Read more at Wikipedia.org


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My Addison's disease - Personal Views
From British Medical Journal, 9/9/00 by Kathleen Hilditch

Over 40 years ago I was frail, listless, and bewildered, yet no one, including my husband and doctor, seemed to notice that I was unwell. Trying to keep the house clean and the children cared for was a great effort; they were only 7 and 5 years old.

The first sign of illness was noticed by my dentist: blue marks on my gums. When I next visited my doctor he was unconcerned. About a year later the marks appeared on my nails. I became very thirsty, craving for beer, but rarely had the money to buy any.

My hair was lank and dull, I was very thin, brown pigmentation began to spread up my arms and on my cheeks; I was depressingly unattractive. This did not help the deteriorating situation with my husband. Work took him away regularly, but he grew less and less interested in me; finally I was told of the girlfriend in London. Each weekend when he was at home I tried to seem full of energy and ensure that he had a happy time with us.

Then my periods stopped. The doctor laughed. "We all know what that means" he said. I told him that I could not be pregnant as I had not had sex for over five years. I also showed him the pigmentation and mentioned the exhaustion. I was given a tonic and told to rest in the afternoons.

I wondered if I was starting the menopause, but decided that I was too young. It was now over two years since the blue marks had appeared on my nails. The pigmentation had also spread to my chest; I was exhausted to the point of collapse, and too weary to care what might be wrong with me.

One day I bought fish for supper. Despite the shop being only about 10 minutes' walk away I gasped for breath. The fishmonger helped me into his van and took us home. The boys thought it smelly but fun. I put the cod in a handbasin of water in our bedroom then lay on the bed. We never ate the fish and I did not get up for weeks.

I ceased to feel guilty about my neglect of the children; in fact I had ceased to think about anything. I drifted vaguely in and out of consciousness, for how long I do not know. Fortunately, a friend visited us and was shocked by what she found. Two young boys fending for themselves, the mother immobile and barely conscious.

She at once took charge and sent for the doctor. Apparently she told him that he would have a dead woman on his hands if he did not do something at once. An ambulance took me to the Bristol Royal Infirmary and she took the boys to stay with her. I could barely repeat my own name. Soon I was in a warm bed and gradually the shivering stopped. I remember the sense of relief that at last, at long last, someone cared about my condition.

There was much activity about me. My blood pressure was taken every half hour; I had blood tests each day. I think it was two nights after admission that I had the relapse. Screens came round the bed, a second saline drip was added to the first. I was started on cortisone and dimly remember being told that I would have to take it for the rest of my life.

I was very fortunate to be in the care of the doctor who diagnosed Addison's disease when he came to visit me at home. My mother and my husband had access at all times. Because my mind was so confused, against all the rules my children were allowed to visit in the hope that I would be more settled about them, but not before I was able to speak coherently.

Almost a month after admission I left for convalescence in Bournemouth. I stayed for a month though the usual time was two weeks. Here I rested and walked, regained my strength, and tried to adjust to the medication of 10 g of sodium chloride and 35 mg of cortisone a day. As in hospital I found the sodium difficult to digest and was sick after each tablet. Some years later these doses were reduced and then slow sodium came on to the market, much to my relief.

The disease seemed to be well under control when I left Bournemouth, but overwork caused a relapse, though not as serious as before.

Many years later I had to be admitted to hospital with an Addison collapse. The cause was traced to persistent low sodium (hypothyroidism), but with 50 mg of thyroxine a day my sodium levels returned to normal. Sodium chloride was eliminated and replaced with 25 mg of cortisone acetate a day.

Four years ago I had a colostomy to remove a rectal carcinoma.

I have a dog, so walk at least 20 miles a week and swim regularly. I am very healthy, thanks to the excellent care I have received through the NHS.

Kathleen Hilditch Leamington Spa

If you would like to submit a personal view please send no more than 850 words to the Editor, BMJ, BMA House, Tavistock Square, London WC1H 9JR or email editor@bmj.com

COPYRIGHT 2000 British Medical Association
COPYRIGHT 2000 Gale Group

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