2020

Written by Paul Margulies, MD, FACE, FACP, Medical Director, NADF. Retired Clinical Associate Professor of Medicine, Zucker School of Medicine at Hofstra/Northwell.

Q&A from NADF NEWS® March 2020

• I have had autoimmune Addison’s for more than 30 years. I have never had a crisis! I took 20 mg of hydrocortisone in the morning, and I seemed to function fine for the rest of the day. I went to a new endocrinologist and they lowered my dose to 15 mg every day. She told me to take my hydrocortisone twice or three times a day. I did that for about six years but I never felt as good as I did when I took all my hydrocortisone at the same time each day. So, I started taking it all at once again about 2 years ago. Since proper dosing to mimic circadian rhythm seems to be an issue for many, I wonder if it is okay that I continue with my once a day dosing preference?​

  Although most people with Addison’s disease do best with a split dose, your own experience feeling better with all the hydrocortisone in the morning is useful. As long as there is no let down in energy in the afternoon or early evening, it is perfectly appropriate to use your regimen of 20 mg in the morning. The fludrocortisone dose should depend on blood pressure, potassium level and renin level.

• I have Addison’s disease and recently discovered rooibos tea which I really enjoy. While doing some research on it, I discovered that it can reduce cortisol and aldosterone production. Should someone with Addison’s avoid this drink? Will our meds make up for any decrease the beverage might cause or would it possibly cause us to need more meds?

  Question (con’t): Here is one of the articles I found: http://www.ncbi.nlm.nih.gov/m/pubmed/22101210/

  Answer: There are a lot of plant-derived chemicals that have all sorts of effects on mammalian physiology. This is another reason to be careful about using herbal therapies. In this particular case, it seems that the active ingredient in rooibos can decrease the synthesis of steroid hormones, both glucocorticoids and mineralocorticoids in adrenal cells. This would not affect an Addisonian who is taking replacement steroids, but could have a serious effect on someone trying to taper off steroids, since it could reduce the adrenal reserve. On the other hand, it might be an interesting compound to help treat Cushing’s disease.

• My endocrinologist tested me for antibodies and it was negative, but I’ve had hypothyroidism for about 18 years. Since the test was negative, my doctor says it can’t be autoimmune and must be caused by something else. Before being diagnosed with hypothyroidism, I was hyperthyroid for 9 months but did not have radiation therapy. I was on medication, (I can’t recall what), and my thyroid went back to normal for several years. Is there another factor that could have caused my condition?

  he history of hyperthyroidism prior to the hypothyroidism is a fairly common story. It makes autoimmune thyroid disease a certainty. The hyperthyroidism (Graves’ disease) was treated with medication and went into remission, then as the underlying cause progressed manifested as hypothyroidism (Hashimoto’s thyroiditis). Graves’ and Hashimoto’s are two manifestations of one disease. Stimulating antibodies predominate in Graves’ and destructive antibodies predominate in Hashimoto’s. Transition from hyper to hypo is normal. Transition in the other direction can occur, but is less common. Although antibodies for Graves’ and Hashimoto’s are usually found when the disease begins, they are not always found, and are not necessary to make the diagnosis if the clinical presentation is consistent with either disease. Thyroid antibodies also tend to diminish or disappear over time, so with an 18-year history it’s likely the thyroid antibodies present earlier are long gone.

• I was diagnosed with Addison’s disease in 1988. I was wondering if anyone has tried CBD (cannabidiol) products to help with tiredness, joint pain, and muscle aches. If so, does it help, and are there any downsides to it?

  CBD products are now available without prescription because they contain no THC, the active cannabinoid in marijuana. Unfortunately, since the products are over the counter, manufacturers and distributors can make claims about benefits and purity that are unsubstantiated. We need controlled studies and better verification on the potency of these products. I am not an expert in the use of CBD oil or other products, but some of my patients without adrenal disease have reported short term help with anxiety and stress with the oil. I have no experience with CBD in Addison’s disease. I would express caution until there is more research and more consistency in the available products.

Q&A from NADF NEWS® June 2020

• I’ve read that anti-inflammatory drugs can cause viral immunity suppression and should be avoided right now due to COVID-19. Are steroids to treat adrenal insufficiency also a problem?​​

  The fear about the COVID-19 virus is causing confusion, some of it coming from health authorities that make statements that are then used in different contexts. That is probably the reason for this confusion. First, it has nothing to do directly with NADF’s previous statements about individuals with adrenal insufficiency. Our recommendation for treating an individual with adrenal insufficiency who gets sick from any infection has not changed: take extra glucocorticoids according to the degree of symptoms and fever; treat the fever, hydrate and rest. Both acetaminophen and ibuprofen are effective in lowering fever. I generally favor acetaminophen primarily because it is less likely to cause heartburn or affect blood pressure, but I consider ibuprofen to be a safe choice. Some articles lump “anti-inflammatory drugs” with ibuprofen and glucocorticoids. This is inaccurate. Although we know that higher doses of glucocorticoids over time may have a mild effect on viral immunity, that does not mean we should stop treating acute infections with the appropriate stress doses to get through the acute illness.

• With the Covid-19 pandemic, what advice do you have for someone with primary hyperaldosteronism? I have to travel, and also have high blood pressure.

  Although everyone needs to be careful today, I would not consider hyperaldosteronism as a high-risk disorder because neither the disease nor the treatment affects the immune system. Age and the degree of hypertension are the major considerations for compromises to your health.

• I was put on a high dose of hydrocortisone due to a serious illness that led to hospitalization. Do you have any advice to taper down after two days of high doses (7 doses of 100 mg, every 6 hours)? My endocrinologist put me on a 10-day regimen to taper down. Is that needed?

  The rate of taper is based on the clinical status of the patient, not the diagnosis of adrenal insufficiency. A slow taper of 10 days would be appropriate if you are still ill and need continued stress dosing of the hydrocortisone. If you are completely back to normal and have good blood pressure, and are able to eat normally, then a more rapid taper would be appropriate.

• I will be 73 in one month and I have had Addison’s disease since 1989. I had my first trip to the ER for a crises 27 years after diagnosis. I have had 2 crises since then treated by injection at home. I realize I am very fortunate with my Addison history. Are adrenal crises more apt to increase with age?

  I have not seen any statistics on the incidence of adrenal crisis and age. Regardless of chronologic age, I think comorbidities (the presence of other medical conditions and need for medications) have an influence. On the opposite spectrum, I think children and adolescents are more vulnerable than adults because they have less experience and critical reasoning to take appropriate action early and prevent a full adrenal crisis.

• I wondered if you have any information about the bone building drug Prolia. Three of my doctors want me to try it, but when I Googled it, I came up with very bad reviews. I have Addison’s and a recent problem with hypothyroidism, so I certainly don’t need additional problems.

  Prolia is an injection given by a doctor every 6 months to treat osteoporosis. Most people with osteoporosis are initially treated with a bisphosphonate, such as Fosamax, Actonel or Boniva. These are given orally, and the major side effect is heartburn and sometimes achiness. They can be safely used for several years before using a holiday for 2 or 3 years. Prolia is usually prescribed when osteoporosis returns after bisphosphonates or if they have not been effective. It is safe and effective for most people. There are no GI side effects. It can also be used for several years. When researching these drugs, the internet is often misleading, suggesting a significant risk of two very rare side effects: osteonecrosis of the jaw and spontaneous fracture of the femur. It turns out that these are extremely unlikely with any of these drugs, but they are eliminated by taking a holiday for 1 to 2 years after continuous use for more than 7 years. All of these drugs are safe in people with adrenal insufficiency.

• Over the years, I have had several abdominal CT scans. All of them report my adrenal glands are “unremarkable.” I’ve had autoimmune Addison’s for 18 years. Others have said their scans show “small adrenal glands.” How does this compare to someone without Addison’s?

  PCT imaging of the abdomen is configured to have a specific resolution (similar to sharper focus on a camera). Older machines will have poorer resolution. Also, the setting of the resolution may be different depending on what the radiologist is looking for. Generally, radiologists are not looking for the size of the adrenals unless there is a specific reason, so the image of the adrenals in an abdominal CT is not a concern and is described in passing. The normal adrenals are quite small and flat. A typical CT may barely show one or both adrenals. If the adrenals are small, it may not necessarily show up as any smaller than normal. Usually, the radiologist will mention that the adrenals appear normal even when they are small. They will typically describe the adrenals only if they are larger than normal or have nodules or tumors. If there is a specific reason to assess the size of the adrenals, the ordering physician must ask for details about the adrenals, and then the radiologist will set the resolution to more sharply focus on the adrenals.

• Can people feel “real scientifically-proven adrenal pain” with primary or secondary adrenal insufficiency?

  The adrenal glands do not have a lot of nerve endings. The only situation where adrenal pain may occur is when there is an acute hemorrhage into one or both adrenal glands due to a clotting disorder or from anticoagulants. This is a known but rare cause of primary adrenal insufficiency. With autoimmune primary adrenal insufficiency, the adrenal glands shrink slowly due to the chronic inflammation of the adrenal tissue, and that is painless. With secondary adrenal insufficiency, the lack of ACTH stimulation leads to a very slow shrinkage of the adrenal glands, which is also painless.

• I was on high-dose hydrocortisone, but stopped two months ago. I have heard it can weaken your immune system, so I’m wondering how long am I more susceptible to infections?

  The answer depends on the clinical situation. If you have adrenal insufficiency and read our warnings about the risk of getting viral infections due to the use of replacement glucocorticoids, then it is dangerous to stop the glucocorticoids because the adrenal insufficiency must be treated. Fear of viral infections is never a reason to stop steroid therapy altogether. It is always essential to take the best dose that prevents adrenal insufficiency symptoms. Avoiding viral infections requires the use of the usual measures, including masks, hand washing and social distancing. However, if you are without adrenal insufficiency but required a short-term use of hydrocortisone and are now off it for 2 months, then sensitivity to viral infections is probably back to normal. Two months should be adequate.

• I am an adult who struggles with extremely low aldosterone. I am currently on Florinef but my levels are still at the lowest point on the range when blood work is done. I struggle with extreme fatigue, have paralysis sometimes (full body except for the head) and tremors/shaking once the paralysis lifts. I’ve dealt with this for years.

  Aldosterone is the adrenal hormone that promotes salt retention and support of blood volume and blood pressure. When it is deficient, there is a tendency for low blood pressure, a further drop in blood pressure on standing (postural hypotension), and usually an elevated serum potassium. There are two major causes of low aldosterone: One is primary adrenal insufficiency (Addison’s disease), where the adrenals are destroyed and there is a loss of cortisol as well as aldosterone. The other is hyporeninemic hypoaldosteronism, caused by a kidney defect or disease where renin is deficient and cannot stimulate the adrenals to make aldosterone despite low blood volume. This defect is often seen in diabetes, but occurs in other kidney disorders as well. In this type, the adrenal glands are normal. The diagnosis is made by checking plasma renin and aldosterone at the same time. In Addison’s disease the renin is high, and the aldosterone is low. When both are low, it is hyporeninemic hypoaldosteronism. There are also some very rare cases of isolated aldosterone deficiency without cortisol deficiency. All types are treated with fludrocortisone because it is the only mineralocorticoid we have. The response is assessed by monitoring the blood pressure changes with posture, potassium and looking for excess replacement that can cause ankle swelling or an elevated blood pressure. Checking the level of aldosterone itself is useless because fludrocortisone is not measured in the assay. From your complaints about paralysis, I suspect that something else is going on besides hypoaldosteronism. A thorough neurologic evaluation is needed.

• I had my left adrenal gland removed in November of 2019. The doctor asked for a follow up with a CT scan on the right adrenal gland, and showed it enlarged. What treatment options would there be for this?​

  The proper response depends on the type of adrenal disease that warranted the original surgery. If you had a benign nonfunctioning adrenal adenoma removed, hyperplasia of the remaining gland would be normal. If you had Cushing’s syndrome with nodular hyperplasia, then the remaining gland could have the same pathology. You would need new baseline studies of adrenal function to assess the hormonal output of the remaining gland. If it is not producing excess cortisol and the size is less than 3 cm, it should be left alone.

• I have autoimmune Addison’s disease, and was diagnosed with hypothyroidism 18 years ago. I was tested for antibodies recently, and came up negative for the antibodies that would destroy my thyroid. Does that mean my hypothyroidism isn’t autoimmune related? Is there another link or cause connected to Addison’s?

  Most people with hypothyroidism have autoimmune (Hashimoto’s thyroiditis) hypothyroidism unless they have had surgery, congenital hypothyroidism or (rarely these days) a history of radiation to the neck for lymphoma. When the hypothyroidism exists along with autoimmune Addison’s disease, it is especially likely to be autoimmune. Thyroid antibodies tend to diminish or disappear over time, so with an 18-year history, this is likely autoimmune. It is also important to mention that many people with autoimmune hypothyroidism never have a positive blood test. The assumption here is that the lymphocytes within the thyroid make enough antibodies to injure the thyroid cells, but not enough to be see in the blood stream. We call this “seronegative Hashimoto’s thyroiditis.” It is quite common.Most people with hypothyroidism have autoimmune (Hashimoto’s thyroiditis) hypothyroidism unless they have had surgery, congenital hypothyroidism or (rarely these days) a history of radiation to the neck for lymphoma. When the hypothyroidism exists along with autoimmune Addison’s disease, it is especially likely to be autoimmune. Thyroid antibodies tend to diminish or disappear over time, so with an 18-year history, this is likely autoimmune. It is also important to mention that many people with autoimmune hypothyroidism never have a positive blood test. The assumption here is that the lymphocytes within the thyroid make enough antibodies to injure the thyroid cells, but not enough to be see in the blood stream. We call this “seronegative Hashimoto’s thyroiditis.” It is quite common.

• I have no pituitary and no adrenals. I also have diabetes and cirrhosis from fatty liver. My liver disease is progressing fast, and I cannot receive a transplant. I was wondering how to manage steroid doses. I am having to inject 100 mg for adrenal insufficiency symptoms. It perks me up but only for a day or 2 then I crash again. Could the liver disease have increased my steroid needs? I’m wondering how to dose. I read you can get AI from liver disease?

  It is difficult to provide specific guidance on the management of your specific adrenal insufficiency. Whatever the cause, the progressive liver disease is a serious complication. Liver disease does not cause adrenal insufficiency, but previous treatment may have included steroids, which may have caused secondary adrenal insufficiency. The use of sporadic injections of hydrocortisone is unusual. I suggest that an endocrinologist familiar with the complete history and current medical issues be directly involved in treatment.

Q&A from NADF NEWS® September 2020

• I was on high-dose hydrocortisone, but stopped two months ago. I have heard it can weaken your immune system, so I’m wondering how long am I more susceptible to infections?

  The answer depends on the clinical situation. If you have adrenal insufficiency and read our warnings about the risk of getting viral infections due to the use of replacement glucocorticoids, then it is dangerous to stop the glucocorticoids because the adrenal insufficiency must be treated. Fear of viral infections is never a reason to stop steroid therapy altogether. It is always essential to take the best dose that prevents adrenal insufficiency symptoms. Avoiding viral infections requires the use of the usual measures, including masks, hand washing and social distancing. However, if you are without adrenal insufficiency but required a short-term use of hydrocortisone and are now off it for 2 months, then sensitivity to viral infections is probably back to normal. 2 months should be adequate.

• I am an adult who struggles with extremely low aldosterone. I am currently on Florinef but my levels are still at the lowest point on the range when blood work is done. I struggle with extreme fatigue, have paralysis sometimes (full body except for the head) and tremors/shaking once the paralysis lifts. I’ve dealt with this for years.

  Aldosterone is the adrenal hormone that promotes salt retention and support of blood volume and blood pressure. When it is deficient, there is a tendency for low blood pressure, a further drop in blood pressure on standing (postural hypotension), and usually an elevated serum potassium. There are two major causes of low aldosterone: One is primary adrenal insufficiency (Addison’s disease), where the adrenals are destroyed and there is a loss of cortisol as well as aldosterone. The other is hyporeninemic hypoaldosteronism, caused by a kidney defect or disease where renin is deficient and cannot stimulate the adrenals to make aldosterone despite low blood volume. This defect is often seen in diabetes, but occurs in other kidney disorders as well. In this type, the adrenal glands are normal. The diagnosis is made by checking plasma renin and aldosterone at the same time. In Addison’s disease the renin is high, and the aldosterone is low. When both are low, it is hyporeninemic hypoaldosteronism. There are also some very rare cases of isolated aldosterone deficiency without cortisol deficiency. All types are treated with fludrocortisone because it is the only mineralocorticoid we have. The response is assessed by monitoring the blood pressure changes with posture, potassium and looking for excess replacement that can cause ankle swelling or an elevated blood pressure. Checking the level of aldosterone itself is useless because fludrocortisone is not measured in the assay. From your complaints about paralysis, I suspect that something else is going on besides hypoaldosteronism. A thorough neurologic evaluation is needed.

• I had my left adrenal gland removed in November of 2019. The doctor asked for a follow up with a CT scan on the right adrenal gland, and showed it enlarged. What treatment options would there be for this?

  The proper response depends on the type of adrenal disease that warranted the original surgery. If you had a benign nonfunctioning adrenal adenoma removed, hyperplasia of the remaining gland would be normal. If you had Cushing’s syndrome with nodular hyperplasia, then the remaining gland could have the same pathology. You would need new baseline studies of adrenal function to assess the hormonal output of the remaining gland. If it is not producing excess cortisol and the size is less than 3 cm, it should be left alone.

• I have autoimmune Addison’s disease, and was diagnosed with hypothyroidism 18 years ago. I was tested for antibodies recently, and came up negative for the antibodies that would destroy my thyroid. Does that mean my hypothyroidism isn’t autoimmune related? Is there another link or cause connected to Addison’s?

  Most people with hypothyroidism have autoimmune (Hashimoto’s thyroiditis) hypothyroidism unless they have had surgery, congenital hypothyroidism or (rarely these days) a history of radiation to the neck for lymphoma. When the hypothyroidism exists along with autoimmune Addison’s disease, it is especially likely to be autoimmune. Thyroid antibodies tend to diminish or disappear over time, so with an 18-year history, this is likely autoimmune. It is also important to mention that many people with autoimmune hypothyroidism never have a positive blood test. The assumption here is that the lymphocytes within the thyroid make enough antibodies to injure the thyroid cells, but not enough to be see in the blood stream. We call this “seronegative Hashimoto’s thyroiditis.” It is quite common.

• I have no pituitary and no adrenals. I also have diabetes and cirrhosis from fatty liver. My liver disease is progressing fast, and I cannot receive a transplant. I was wondering how to manage steroid doses. I am having to inject 100 mg for adrenal insufficiency symptoms. It perks me up but only for a day or 2 then I crash again. Could the liver disease have increased my steroid needs? I’m wondering how to dose. I read you can get AI from liver disease.

  It is difficult to provide specific guidance on the management of your specific adrenal insufficiency. Whatever the cause, the progressive liver disease is a serious complication. Liver disease does not cause adrenal insufficiency, but previous treatment may have included steroids, which may have caused secondary adrenal insufficiency. The use of sporadic injections of hydrocortisone is unusual. I suggest that an endocrinologist familiar with the complete history and current medical issues be directly involved in treatment.

Q&A from NADF NEWS® December 2020

• I have a 1.3 cm adrenal adenoma that was found during a CT scan. Later, I had another CT scan done for a different reason, and the results said “adrenals unremarkable.” Do these adenomas go away or are there different levels of CT scans? I was told they can cause problems sometimes, but most are benign.

  Adrenal nodules as an incidental finding on CT and MRI of the chest and abdomen are very common. Most are nonfunctioning adenomas that do not grow and cause no harm. I think it is appropriate for an internist or endocrinologist to clinically evaluate anyone with this finding. Most of the functioning adenomas will cause signs and symptoms. The major syndromes are pheochromocytoma, Cushing’s syndrome and Conn’s syndrome. Each of these can be ruled out by basic history, physical exam and some basic laboratory tests. Even in the absence of any findings, it is useful to do an overnight dexamethasone test to rule out subclinical Cushing’s. At least one follow-up imaging 6 to 12 months later is useful to rule out significant growth of the nodule. In the case of a large nodule (over 3.5 cm) or a rapidly growing nodule, surgical removal is necessary because of the risk of cancer. Generally, adrenal adenomas do not go away. However, different techniques used in imaging the area might miss a tiny adenoma or misjudge the size.

• I have secondary adrenal insufficiency, and I suspect my daughter does as well now. What are the chances of that? Is somehow secondary AI able to run in families?

  It all depends on the cause of the adrenal insufficiency. The most common cause is prolonged steroid use, so this would not be a familial situation. If the cause is pituitary, there are families with pituitary tumors from MEN1 which also includes hyperparathyroidism and neuroendocrine pancreatic tumors.

• I have Addison’s disease, and now evidently have an issue with my blood sugar staying in the 200-250 range, and my blood being way too thin. Nobody seems to have a clue what to do. I’m 5’10” and weigh 153 lbs. I eat a healthy diet and exercise regularly, so I don’t know why I’m having these issues.

  The elevated blood sugars indicate diabetes mellitus. It is most likely type-2, but your endocrinologist can quickly prove this and rule out type-1, which would require insulin treatment. If it is type-2, management with oral medication such as Metformin and other drugs should be adequate. Keep in mind that replacement doses of hydrocortisone should not cause the elevated blood sugar, but if high doses are taken, the blood sugar will rise. If “thin blood” means there is inadequate clotting, it could be from a platelet disorder or an abnormality in the circulating clotting factors. A hematology consult would be useful.

• I’m having serious issues with fluid retention. I need hydrocortisone due to a pituitary malfunction: good stim, low baselines. Sometimes random testing is normal on ACTH and cortisol, though. But I was told to take no less than 15 mgs hydrocortisone per day. I have Hashimoto’s as well with many symptoms: swollen, 15 lbs. overweight when I am unable to eat because of slowed digestion. I’m on thyroid meds, but those aren’t helping. When I take hydrocortisone, I retain even more fluid, without any benefit. Why would someone who needs the cortisol, get worse edema, on a dose that is physiological 15-20 mgs?

  The question you ask is whether replacement doses of hydrocortisone can cause fluid retention. The answer is yes, if the dose is more than replacement for your specific needs. Many other factors can contribute to fluid retention, including the thyroid disease that you have, but also heart disease, kidney disease and vascular abnormalities. From your notes, it is not certain that you actually need hydrocortisone replacement. If you do, the baseline dose of 15 mg may be too much. Since pituitary disease is the primary problem, even if adrenal insufficiency is present, most likely aldosterone production is still adequate. Therefore, the mineralocorticoid content of hydrocortisone may be unnecessary and would contribute to the fluid retention. A switch from hydrocortisone to prednisone may solve that issue. The dose of prednisone should then be adjusted to keep you comfortable and to avoid gaining any fat. Please discuss this with your endocrinologist.

• I read a study about increased renin levels in Addison’s disease causing a higher mortality rate due to cardiovascular disease. I take 0.5 mg fludrocortisone daily, and my renin levels are over 1000. My sodium and potassium levels are always normal. Can you please tell me if you are familiar with this study, what it means, and if you feel I am taking the appropriate dose of fludrocortisone given my high renin levels, but normal sodium and potassium?

  Elevated renin in Addison’s disease reflects diminished blood volume from a deficiency of mineralocorticoids. Usually potassium will also be elevated in this situation, but not always. The most important symptom related to low blood volume is postural hypotension with resulting dizziness and salt craving. The elevated renin itself should not cause an increase in cardiovascular disease, but hypotension is a risk. A dose of 0.5 mg of fludrocortisone is a higher than average dose, suggesting some degree of mineralocorticoid resistance. It is rare, but I have been treating a patient who needs 4 times that dose. I would focus on sense of wellbeing and a lack of adrenal insufficiency symptoms with appropriate hydrocortisone replacement in addition to a dose of fludrocortisone that optimizes blood pressure.

• We recently corresponded in relation to my mom who suffers from Addison’s disease. Just to review, my mom was diagnosed almost 30 years ago and has taken a combination of steroids over time to treat the disease. My mom just turned 73 and she is starting to suffer more complications related to AD. One symptom is that she is having some cognitive trouble. Certainly, we understand that is common symptom for AD. However, the cognitive trouble seems to be on the increase. Her endocrinologist recently saw her and noticed her glucose levels were up indicating a possible change into Diabetes 2 along with her AD. Furthermore, she did an MRI of brain and noticed that there was some ‘shrinkage’ of the brain, possibly due to vascular restrictions caused by AD or Diabetes 2. These findings were not deemed significant but she is now being referred to a neurologist for more testing.

  Most people with Addison’s disease do not die of the disease or from an adrenal crisis. Therefore, people can live with disease and may develop problems related to aging that are not necessarily caused by the adrenal insufficiency or treatment with replacement steroids. Two of the common disorders of aging are type 2 diabetes and cognitive issues. Each one deserves attention. Type 2 diabetes in the setting of Addison’s disease can be managed with the same techniques as in people without adrenal insufficiency: diet that reduces sugar and simple carbohydrate, exercise, weight management and medications. Cognitive changes should be evaluated by a neurologist. The presence of vascular shrinkage may be simply an age factor. it is not due to the Addison’s disease. Most neurologists can do a baseline cognitive assessment and will look for treatable causes. Medications can sometimes help and are not contraindicated by the Addison’s disease.