more on the Adrenals, everyone otta read over this one....Katy ck out appendix

[Guest guest]

Patty, and all ~

This is interesting, for about 2 years before everything went for me, I got very, very skinny.......and was so brown even thru the winter. Had the melasma on my face and neck. I also had what I thought was a horrible lupus flare that never stopped. A very rough couple years, then a couple months before my major organs shut down, I was totally bedridden about 5 out of 7 days. Then It was 24/7 and then I noticed I wasnt peeing so I collected it and found I wasnt ! and then I blew up in just a few days, I gained 36 lbs ! All of which I lost in the hospital due to the iv's of diuretics. Now here I am, sodium pump doesnt work, adrenal hormones very low, thyroid off, and look pregnant and gained 65 lbs ! I have these big smushy lumps between my collar bones and neck, they are huge, and very mushy. When I got my thyroid scanned, the guy ran it over the bulge and said he had never seen anything like it. but it was not on the report with my thyroid scan, guess cuz the doc didnt order that. Anyway.......I am thinking this all is telling a story for me. When I read here that steroids for asthma and such can cause your ACTH to not work and then there goes the domino effect. Well, I was on shitloads of steroids in all of the 90's inhalers, trigger point injections, kenalog shots, solumedrol for all those surgeries I had, medrol dose packs. I had like 9 or 10 surgeries during those years ! cervical cancer and all ! I bet ya I crashed ! !

This article is good........Everyone should read it, even Katy, as it refers to the appendics too ! ! ! ! ! ! ! ! ! ! !

Ya know, after implantation for many many people, it starts out slow, getting rashes here and there, you use the hydrocortisone cream on it so it wont itch or so it will go away, you get allergies, and maybe even have to have a kenalog shot, you may need to

use steroid inhalers, and of course, when you had the implants you were give steroids iv and maybe a medrol dose pack after the surgery. Geeze~~~~~~~here starts the downfall of the adrenals by the suppression of the ACTH ! ! ! It sounds like you can even have the suppression from just useing the cream sometimes for rashes and things, or the inhalers for asthma.......... Cortisone cream for bug bites, zits, etc...

never knowing it can suppress your acth, it can cause depression...........part of why I am sure kids with chronic acne are also depressed, and it is probably from steroid use for the face and suppression of the acth..........HUM........ I even read LEA in here, and I put her name in red by it.......Hope you enjoy this article !

Love Dede

Hypoadrenalism (underactivity of the adrenal glands)

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Hypoadrenalism (underactivity of the adrenal glands)

Written by Shern Chew, consultant endocrinologist

What is hypoadrenalism?The adrenal glands are two small but very important glands, situated one above each kidney, which produce a range of hormones, or 'chemical messengers'. Underactivity of the adrenal glands is called hypoadrenalism. Many of the symptoms of hypoadrenalism are due to a deficiency of the steroid hormone cortisol, which is a potentially fatal deficiency if left uncorrected. Each adrenal gland consists of two parts:

an outer ring - the cortex

an inner core - the medulla.The two parts have separate hormone functions and control mechanisms. The production of cortisol in the cortex is controlled by the hormone adrenocorticotropin (ACTH), which is produced by the pituitary gland at the base of the brain. The role of the pituitary gland in adrenal functionThe way in which the pituitary gland regulates the normal production of steroid hormones by the adrenal gland is through the secretion of ACTH.If the adrenal gland produces too little cortisol, then there will be a lower level of cortisol in the blood. This is sensed by the pituitary, which therefore will increase the release of ACTH, which in turn stimulates the adrenal cortex to produce more cortisol.Conversely, too much circulating steroid hormone will switch off the release of ACTH from the pituitary gland, which in turn reduces the adrenal gland production of steroids.What causes hypoadrenalism?

Primary hypoadrenalism or 's diseasePrimary hypoadrenalism, or 's disease, results from failure of the adrenal glands themselves. This is usually an 'autoimmune' disease, where the immune system produces antibodies that attack tissues of the body rather than a virus or bacteria. In 's disease, antibodies attack the adrenal cortex, causing damage and scarring. Antibodies to the adrenal cortex can be detected in the blood of some patients.

Secondary hypoadrenalism or ACTH deficiencySecondary hypoadrenalism, or ACTH deficiency hypoadrenalism, is caused by diseases of the pituitary gland, which lead to adrenal failure as a secondary effect.

Other causesTuberculosis of the adrenal glands may also cause hypoadrenalism. This was a common cause of 's disease in Britain before the 20th century and remains a major cause in underdeveloped countries. Tuberculosis destroys the whole gland, both the cortex and the medulla. There are usually signs of tuberculosis in other organs, particularly the lungs. Destruction of the adrenal glands by tuberculosis is irreversible once hormonal deficiencies are clinically detectable.

Rare causesMany rare diseases may affect the adrenals. In general, at least 80 per cent of both adrenal glands have to be damaged in order for deficiencies to become clinically evident.

Rare conditions associated with primary hypoadrenalism

Adrenoleukodystrophy (a genetic disease in which the myelin sheath, or 'insulation', covering the nerve fibres within the brain is lost, along with degeneration of the adrenal gland).

Amyloidosis (a rare condition in which an abnormal substance called amyloid is laid down in various tissues, impairing their function).

Bilateral adrenalectomy (surgical removal of the adrenal glands).

Congenital adrenal hyperplasia (a common inherited condition in which an enzyme defect causes problems with the production of steroid hormones by the adrenal gland).

Drugs (eg ketoconazole (Nizoral), metyrapone (Metopirone), mitotane).

Familial glucocorticoid deficiency (ACTH receptor mutation).

Haemochromatosis.

Haemorrhage - usually in patients receiving anticoagulant drugs or in whom septicaemia ('blood poisoning') is present.

HIV-related adrenal inflammation.

Metastases (spread of cancer from another part of the body.

Sarcoidosis.

Rare conditions associated with secondary hypoadrenalismThis means adrenal deficiency from causes acting on the pituitary gland rather than directly on the adrenal glands. The pituitary gland regulates adrenal cortisol production by responding to the amount of cortisol in the blood. However, the pituitary cannot distinguish between natural cortisol and synthetic steroid absorbed from medicines or steroid creams.If someone takes such treatment the pituitary production of ACTH will drop and as a result the adrenal cortex will become relatively inactive. If the steroid treatment is stopped abruptly then the patient may suddenly become deficient in cortisol as the adrenal gland takes some time - weeks or months - to regain its full manufacturing ability again. This is the reason that patients on medium or long-term steroid treatment are advised not to stop taking their medicine suddenly.Rarely, patients are affected by conditions that destroy the pituitary. Any cause of pituitary disease may cause ACTH deficiency.What is the course of hypoadrenalism?Autoimmune 's disease is chronic (ie long-standing), and antibodies to the adrenal cortex may be detected in a person's blood many years before damage to the adrenal cortex is apparent. There is no evidence that treatment can prevent this autoimmune attack, which may also affect other organs in the same person. Thus, people suffering from 's disease are at increased risk of other organ-specific autoimmune diseases including vitiligo, autoimmune thyroid disease, pernicious anaemia, and hypoparathyroidism.Patients with autoimmune diseases are also at increased risk of coeliac disease.Who is affected?Primary hypoadrenalism is relatively rare, for example it is found in about 6 in every 100,000 people in the North East Thames region. Much more common is ACTH deficiency caused by the intake of cortisol-like steroids for conditions such as asthma. Cortisol is required as part of the body's response to physical stress (eg emergency surgery). Failure to diagnose hypoadrenalism in an ill patient may lead to collapse and death.What are the symptoms of hypoadrenalism?The onset of symptoms in 's disease is usually subtle. Patients often feel faint and dizzy, and often experience weakness, fatigue and weight loss. At least 50 per cent of patients complain of vague stomachaches or other gut symptoms. Increased pigmentation of the skin (like a sun tan) is common in 's disease. Some patients will have a persistent tan long after a holiday. This is due to raised ACTH levels, which stimulate pigment cells (melanocytes) in the skin. Patients occasionally suffer mental problems, including depression. Some suffer joint and muscle pain. Very rarely, bleeding into the adrenal glands (see Figure 1 in appendix) causes acute severe back pain. This symptom should be particularly investigated in patients receiving anticoagulants, such as warfarin (eg Marevan), LEA which prevent blood clots. In some severe infections, particularly meningococcal septicaemia, bleeding may occur into the adrenal glands. The loss of cortisol results in hypotension (low blood pressure) that fails to respond to catecholamine hormones and medications (eg noradrenaline). How is 's disease diagnosed?The pigmentation of 's disease is characteristic, and is particularly evident on exposed or traumatised areas of the skin, such as the knuckles and elbows. Occasionally, the inner wall of the cheek, which is frequently bitten, also shows pigmentation. Any scars inflicted after the onset of the disease become pigmented. Patients may also have signs of organ-specific autoimmune disease. These include patches of abnormal pale skin called vitiligo and sometimes evidence of thyroid disease, such as a goitre (swelling of the neck). Blood pressure control is abnormal in severe cortisol deficiency. The patient may have an abnormal fall in blood pressure on standing (called postural hypotension). The highest blood pressure in 's disease is usually less than 110mmHg. Very low blood pressure is a sign that the patient is in imminent danger of collapse.A doctor suspecting 's disease will perform blood tests. Patients with a severe deficiency of cortisol and the related hormone aldosterone, often have a low sodium level and an increased potassium level. (However, potassium may be normal in 40 per cent of patients.) A high calcium level is also seen about 10 per cent of patients. Sometimes the blood sugar is low, although this is rare except in children, or in patients who have been undernourished for long periods, eg after major surgery. During acute illness, a cortisol level of less than 500nmol/l may be consistent with hypoadrenalism, while a level of less than 200nmol/l is highly abnormal and strongly supports the diagnosis. A level of 550nmol/l or above excludes the diagnosis.A blood count will show raised eosinophils (a type of white blood cell), and may reveal abnormally large red cells (macrocytes) because of co-existing pernicious anaemia. Blood tests should be carried out for thyroid function, vitamin B12, folate, iron and antibodies to other organs (thyroid, gastric parietal cells, endomysium) to check for associated autoimmune diseases.Specialist investigations, usually performed by an endocrine unit, may include a measurement of other adrenal hormones including ACTH, aldosterone, plasma renin activity, noradrenaline and adrenaline and Synacthen tests. In primary hypoadrenalism the ACTH level is usually greater than 80ng/l (high), because the pituitary gland tries to correct the cortisol deficiency by increasing the stimulus to the adrenal. If ACTH deficiency is due to pituitary disease or steroid suppression, the ACTH level is undetectable (generally less than 10ng/l). In Synacthen tests synthetic ACTH is injected into a vein and blood is then drawn to measure the cortisol response. The 'low dose' (250 micrograms) or 'short Synacthen test' will be abnormal in any cause of hypoadrenalism. High doses of Synacthen (1mg), especially given over several days, often produce a normal cortisol level in patients with ACTH deficiency, whereas those with primary hypoadrenalism experience no rise.Additional investigations should include a chest X-ray to check for tuberculosis. In some cases a CT scan of the adrenals may be performed to look for calcium deposits (a sign of tuberculosis). A skin test for tuberculosis may also be performed.What else could it be?Some patients with undiagnosed 's disease have been misdiagnosed as having an abdominal disease such as appendicitis. After operation a correct diagnosis may be reached because the scar turns brown and the appendix is normal.The main problem with diagnosis is that hypoadrenalism is simply not considered. Once hypoadrenalism is confirmed, there may be diagnostic problems related to the underlying cause of the adrenal failure. In this case further specialist tests may be needed to narrow down the cause.What can your family doctor do?Your GP can take blood for electrolytes (salt balance), kidney function, and cortisol level. Hydrocortisone replacement for cortisol may be started immediately after a blood sample is taken. A referral will be made to a specialist endocrine unit.What can you do yourself? Treatment is almost always life long. Failure to comply with treatment may be fatal, so patients with hypoadrenalism must take some simple precautions. The main problem is that the need for cortisol increases during physical stress, eg major surgery. All patients would be advised to carry a warning card stating their condition and explaining that they are dependent on adrenal replacement. This may save their life in the event of coma or collapse. Patients with 's disease should also keep extra supplies of tablets at home or when on holiday, as well as a vial of hydrocortisone that they can inject. Any medical professional can administer this if the patient is unconscious or unable to take oral medication.What can your specialist do?The best replacement therapy for cortisol is oral hydrocortisone (eg Hydrocortone tablets). This is very similar to normal cortisol, and the level is easily measurable in the blood. The correct level of cortisol can be checked by taking blood samples before the first hydrocortisone tablet of the day and then at regular timed intervals after the tablets, called a 'hydrocortisone day curve'. Samples should be taken into the early evening. The aim is to keep the cortisol level high in the morning (but not more than 1000nmol/l), and lower in the afternoon and evening (between 100 and 300nmol/l). This mimics the normal swing in cortisol level of the body during the day. The usual dose is 10mg taken on waking, 5mg before lunch and before the evening meal.Other corticosteroids may be used, including cortisone acetate, prednisolone (eg Deltacortril) and dexamethasone. However, it is difficult to judge the correct dose of prednisolone and dexamethasone. This may lead to the complications of long-term steroid treatment including avascular hip necrosis (destruction of the round head of the femur which forms the hip joint), osteoporosis, worsening of diabetes mellitus and hypertension. Cortisone acetate must be converted by the body into an active steroid, and the efficiency of conversion may vary between patients.Most patients with primary hypoadrenalism are deficient in another adrenal cortex hormone called aldosterone. This requires replacement with a synthetic form of aldosterone called fludrocortisone (Florinef). The usual dose is 100 micrograms as a single tablet taken on waking.The main hormone produced by the central part of the adrenal glands (the medulla) is adrenaline (a catecholamine) and this is not usually replaced as other catecholamine hormones are secreted from the rest of the sympathetic nervous system (of which the adrenal medulla is a component).Someone taking adrenal replacement therapy should double the dose of hydrocortisone for 48 or 72 hours if he or she develops an illness with fever or mild diarrhoea and vomiting. An injection of hydrocortisone into a muscle (intramuscular) or vein (intravenous) is required for the biological stress of a major illness or surgery.All patients should be followed up at least annually at a specialist endocrine clinic, and should have 24-hour access to specialist advice and treatment.What is the likely outcome?With appropriate treatment and monitoring, life expectancy and quality of life are normal.Figure 1: CT scan showing bleeding within the adrenal glands, causing hypoadrenalismThe patient depicted in Figure 1 suffered an adrenal haemorrhage eight days after major surgery. Anticoagulants ('blood thinning drugs') had been given to prevent clots in the veins following the operation (deep vein thrombosis). The main symptom was pain in the back and upper abdomen.The patient developed low blood glucose levels 14 days post operatively. The diagnosis was confirmed by an undetectable serum cortisol level and a CT scan of the abdomen showing enlarged adrenal glands (arrows) with abnormally high signal intensity consistent with the presence of blood. (L indicates the liver, and S the spleen).

Figure 2: Contents of the bathroom cabinet of a patient with hypoadrenalism due to ACTH deficiencyA patient was referred with tiredness and an undetectable cortisol level.Our investigations revealed an undetectable ACTH level. There was no clinical evidence of pituitary disease, the rest of the pituitary hormones were normal and a MRI scan of the pituitary gland was normal. The patient denied steroid use, but did use various skin creams. When asked to bring all the creams into the hospital, a steroid-containing skin cream was found (arrow). The patient had used this cream as an acne cure and the steroids in the cream were suppressing ACTH.Three months after ceasing use of the steroid cream the patient had a normal serum cortisol level and a normal response to a Short Synacthen test.

Figure 3: 's disease caused by tuberculosisThe patient had vomiting and abdominal pain for several weeks. The serum cortisol was undetectable and the plasma ACTH was high.Photograph 3A shows pigmentation of skin creases (arrow). Photograph 3B shows patchy pigmentation on an elbow (arrows). The tubing for the patient's blood tests is also seen. A CT scan of the abdomen showed both adrenals were enlarged and contained specks of calcium (3C, arrows). This is highly suggestive of tuberculosis affecting the adrenal glands. The tuberculin skin test for tuberculosis was strongly positive. A full course of anti-tuberculosis drugs was started. Anti-tuberculosis drugs increase the breakdown of hydrocortisone, making careful assessment of the hydrocortisone levels in the blood essential to proper replacement. (Pictures shown with the full consent of the patient).

Figure 3A

Figure 3B

Figure 3C

References Bhatia E, Jain SK, Gupta RK, Pandey R. Tuberculous 's disease: lack of normalization of adrenocortical function after anti-tuberculous chemotherapy. Clin Endocrinol 1998; 48: 355-9.Chew SL. 's disease. In: Handbook of Current Diagnosis and treatment. Eds, Pounder R and Hamilton M. Churchill Livingstone, London; 1995: p. 10-11.Kaukinen K, Collin P, Mykkanen AH, Partanen J, Maki M, Salmi J. Celiac disease and autoimmune endocrinologic disorders. Dig Dis Sci 1999; 44: 1428-33.Laureti S, De Bellis A, Muccitelli VI, Calcinaro F, Bizzarro A, Rossi R, Bellastella A, Santeusanio F, Falorni A. Levels of adrenocortical autoantibodies correlate with the degree of adrenal dysfunction in subjects with preclinical 's disease. J Clin Endocrinol Metab 1998; 83: 3507-11.Leong KS, Wallymahmed M, Wilding J, MacFarlane I. Clinical presentation of thyroid dysfunction and 's disease in young adults with type 1 diabetes. Postgrad Med J 1999; 75: 467-70.

Last updated 01.08.2005

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