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The Lesser Known Causes of Addison's Disease.

Please also see:- New cause of AD discovery?; Theory explained!.... CLICK HERE.

Prior to the discovery and use of sophisticated chemotherapeutic drugs and specific antibiotics, such as PAS and INAH, and Streptomycin, in the 1950's & 1960's the main cause of primary Addison's Disease was renal Tuberculosis spreading to the adrenal glands causing calcification (caseation) of these important glands of the endocrine system.

With the steady decline of TB at that time, autoimmune Addison's Disease came to the fore as the most common cause with up to 1:40000 of the UK population (less in the US) suffering from this non-infectious form of the disease. With the increase in cases of the former in the late twentieth century due to a reduction in the uptake by the public of immunisation against the causative agent, Mycobacterium tuberculosis, and increasing resistance by these pathogenic bacteria to the drugs used to treat it, renal TB has again had an impact, albeit relatively small, on the number of primary Addison's Disease patients.

It must not be forgotten however, that although these two causes account for the majority of cases, there remain a series of cases of this potentially fatal disease that cannot be attributed to TB or autoimmune disease of the adrenal glands.

On this page we are attempting to give an insite into these lesser known causes of Addison's Disease, starting with an article by Meg Blythe, a former nurse who suffers from Panhypopituitarism, a secondary form of Addison's.

Following publication of the article from Meg, we were pleased to receive a second article, this time from Angie Noah, who has a very interesting and unusual history
to tell. Angie's article is in two parts, the first being essentially her case history but the second is a report on her own investigation into the cause of her Addison's Disease. Because of the nature of it we decided in discussion with Angie that her article was better suited to our 'Lesser Known Causes of AD' page instead of the 'Case Histories' section. She is certain that her Addison's disease is the result of exposure to chemical toxicity. Angie has investigated the causes of her condition logically and explains in detail exactly why she comes to her conclusion. It is difficult to find fault with her arguments.

If you or a loved one suffer from one of the lesser known causes of AD and have some knowledge of the background to your specific condition, whether self taught or from your working background, we would be pleased to hear from you.

We are actively looking for articles to consider for publication on this page on this subject. If you are knowledgeable on your condition, but do not feel that you personally are able to write the article, we may be able to supply a 'ghost writer' for you who can take the information you supply relating to your specific cause of Addison's Disease, and turn it into an article for potential publication on your behalf.

Where technical or medical terminology has of necessity been used on this page, we have included explanatory notes within our 'A to Z guide' page.
If there remain any elements which you do not understand, please contact us and we will attempt to correct this.

Other causes of Addison's disease currently listed in order as follows.
Please click on any name to select.

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Return to list of alternative causes of Addison's disease/adrenal insuffiency

Panhypopituitarism

Meg Blythe
North East England, UK.

Panhypopituitarism is a clinical syndrome of deficiency in pituitary hormone production. This may result from disorders involving the pituitary gland, hypothalamus, or surrounding structures.

Panhypopituitarism refers to involvement of all pituitary hormones; however, only one or more pituitary hormones are often involved, resulting in partial Hypopituitarism. Pituitary hormones of clinical significance include adrenocorticotropic hormone (ACTH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), growth hormone (GH), prolactin, antidiuretic hormone (ADH) and thyroid-stimulating hormone (TSH, ie, thyrotropin). Referring to the GH (growth hormone) which is usually congenital, results in what is generally termed as Achondroplasia.

When pituitary hormone production is impaired, target gland hormone production is reduced because of a lack of trophic stimulus. Normally, subphysiologic target hormone levels stimulate the pituitary gland to increase trophic hormone production; however, in hypopituitarism, the pituitary gland response is absent, suboptimal, or inappropriate with biologically inert hormone production. This results in progressive secondary failure of the target glands.

Patients with hypopituitarism typically present with low target hormone levels accompanied by low levels of the corresponding trophic hormone. (Trophic hormones are any of those hormones which act as stimuli to the adrenal system. They are released and controlled by the pituitary gland. They act as a messenger service to various parts of the endocrine system.)

The trophic hormone level may sometimes be within the reference range, but when this is inappropriately low for the subphysiologic target hormone level, the trophic hormone level may be biologically inert.

As in most cases, Panhypopituitarism is exceedingly difficult to diagnose, but when a diagnosis is made, it is relatively easy to treat. Striking the correct balance of cortisol replacement however, can be a lengthy process. The patient must be aware of their own particular predisposition fully. It is usual for a day curve assessment to be carried out by the endocrinologist. Because cortisol levels reach a peak early morning and diminishing as the day progresses, a blood test is first carried out prior to the patient's first medication of the day. Blood tests are then carried out on an hourly basis to ascertain a true reading of the body's cortisol levels.

  1. Deficiency of ACTH with adrenal crisis or TSH with myxœdema may be life threatening. (Myxœdema, otherwise known as 'Moon face', a puffy appearance of facial & some other tissues.)

  2. GH deficiency causes morbidity in children rather than in adults.

  3. Sudden compromise of ACTH production may result in more profound morbidity than slowly progressive deficiency.

  4. Gonadotropin deficiency with hypogonadism may cause morbidity insidiously.

  5. Eostrogen and testosterone both stimulate endochondral growth and skeletal maturation. In both sexes below normal production of the gonadal hormones (reproductive organs e.g testes) will delay the appearance of secondary ossification centers and postpone the closure of epiphysial discs and sutures. Periosteal bone formation is also inhibited, resulting in gracile (meaning elongated/slim) skeletons with thin cortices, (cortexes) Since endochondral (bone development) growth is lengthened, normal skeletal proportions are altered. There is a disproportional length of the upper and lower extremities, elongation of the mandible, causing prognathism. (Prognathism is a term used for a mandible {jaw} which protrudes out far beyond the facial plain and it is usually caused by malformation of facial bones and misalignment of teeth.)

  6. Hypergonadism is the excessive production of gonadal hormones, by various abnormalities. The endochondral growth is stimulated, but the epiphysial plates result in a short and stocky skeleton. (Otherwise commonly known as Achondroplasia.)

    The author knows of a family personally and has made the following observations. The mother was prothnagismic. She gave birth to a son who suffered from Achondroplasia and another with Addisons disease. However, this happened before Thomas Addison wrote of his findings and therefore information was unavailable to this particular family. Unfortunately, the eldest son who suffered from what is now known as Addisons disease died. The other son with Achondroplasia lived until he was in his fifties. The mother died in her early fifties. Her other two children survived longer, but unfortunately the only daughter died from cancer. She did not have any endocrinological problems. The youngest son still survives relatively free of endocrinological disease. This is where I observed the genetic link.

  7. Morbidity is more profound in congenital hypopituitarism. (congenital = existing at birth)

  8. Post-partum hypopituitarism causes an overall increase in the prevalence of hypopituitarism in women (aka Sheehan Syndrome) & is caused by abnormal diminishment or cessation of pituitary gland functioning.

    The disorder affects females and is caused by necrosis (death of cells) of the anterior pituitary gland secondary to profound blood loss during and after childbirth, with vascular collapse and shock (post-partum collapse). In the case of the author however, she has never been pregnant or can associate this condition with childbirth. Due to gynaecological problems, profound blood loss can however be associated with post-partum hypopituitarism and this has been established with the author.

The causes of Panhypopituitarism can vary.

  1. Tumours - Craniopharyngiomas, pituitary adenomas.
  2. Infiltrative processes - Sarcoidosis, Histiocytosis Haemochromatosis.
  3. Infections - Tuberculosis, Meningitis ,Syphilis.
  4. Ischæmia and Apoplexy (Ischæmic attacks otherwise known as strokes) (This is also known as hemiplegia.)
  5. Empty Sella syndrome
  6. Iatrogenic (caused by treatment) - Radiation, surgery, withholding previous chronic glucocorticoid replacement.
  7. Trauma to the Hypophysis.
  8. Congenital - Kallmann syndrome.
  9. Autoimmune - Lymphocytic hypophysitis.
  10. Or, as with the author causes can be simply be idiopathic.

All ages are affected by panhypopituitarism. There are no racial predilections. The condition is more prevalent in women than in men.

Copyright © 2004 Meg Blythe & Mike Welch

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Chemical Toxicity

Angie Noah, Cottage Grove, Oregon, USA.

I had an 'on the job' chemical exposure (long term Carbon Monoxide poisoning) that went undiagnosed/ misdiagnosed for 8 years resulting in a diagnosis of Hypothyroidism, Addisons disease and no detectable estrogen. This is my story.

In 1992 I went to work as a Courier for Southland (7-11) convenience stores. My route consisted of 7 coastal stores totaling 158 mile round trip drive 3-5 days a week.

Because I worked for the company and not the franchise my van was my office. The company reimbursed me .28 a mile. At the end of every month I was responsible for taking down and hanging the new promotional banners ( 130 feet long 3 feet wide ) that advertised the Big Gulp and Hot dog specials.
The promotional banners would arrive via airplane 2 weeks prior to the hanging date. This meant that the banners would set in my van for 24 hours a day for at least 2 weeks a month for 1½ years. This would include my off time. Little did I know this job would not only diminish my quality of life it would also effect both my precious baby girls.

Shortly after I started my job I started experiencing a triad of health problems. My peaches and cream complexion was now one raw sore around my mouth and nose that would get a secondary infection causing me great pain. These sores would get worse with my cycles yet never totally healing. I saw a dermatologist for this. I was put on every antibiotic known to man with no luck. I was tired all the time. It was everything I could do to stay awake while I was doing my route. I actually would pull over and sleep for 2 to 3 hours before heading home.

My cycles were every 2 weeks for 2 weeks ( meaning I was bleeding all month ) & the flooding was borderline hemorrhaging. I would get diarrhoea accompanied by violent cramps and my blood pressure would drop so fast that I would pass out causing several black eyes. This went on for 8 years. Over the next 8 years, I had Bells Palsy twice (paralysis of the left side of my face.) I could not hear or see or chew on that side of my face. It would take me 5 years to become clinically stable (I still suffer from paralysis). I was one big bruise from the waist down. I had migraine headaches that made me want to throw up. I was experiencing severe fibromyolgia. I would wake up numb from the waist up. I was also experiencing shortness of breath and an intolerance to physical activities. I had become chemically challenged ( intolerance to the smell of newspaper and other common house-hold chemicals ). Occasionally I would experience a heart palpitation as well as high blood pressure ( I use to have LOW blood pressure).

The ovarian cyctists had now taken over my life. Then at one point in 1998, out of the blue, my periods stopped for 4 months (not the norm for me). During this time I could have KILLED SOMEBODY, the rage was so bad. I also had one breast swell up to twice the size of the other. My Gynae Doctor was not concerned. I was put on medication to start my periods again, tested for Graves disease and sent on my merry way.

Prior to Jan 2000 I had been to 8 different Docs, all in different areas of expertise. I was diagnosed with everything from Acne to Bipolar disorder. I was put on anti-depressants and anti-anxiety medication as well as a slew of antibiotics. None of which did a thing for me other than make me feel like an UNPERSON or the LIVING DEAD.
Then in Jan of 2000 I added lactation, loss of eye site and hearing as well as loss of memory and MAJOR depression to my list of symptoms.

I also felt I needed to sleep 26 hours a day, had big dark circles under my eyes too, and felt I was dying!! Something was going to have to change and change soon. It was at this point that I decided to look into the chemical exposure theory. It was also at this time I contacted Oregon Health and Sciences University (OHSU) explaining my most recent symptoms. The person on the phone decided that a good place to start would be to see a breast specialist for the lactation and then go from there. So that's what I did.
The visit was a waist of time. I wanted an MRI done to rule out a Prolactinoma; I felt there were enough symptoms present to warrant one. The Dr. refused.
She did do a thyroid test though. My follow up visit was a joke. She told me my thyroid test came back normal. She told me that I needed to get my blood pressure under control and to stop smoking ( I don't smoke and never have!) She put me on birth control pills to regulate my periods and would see me in 3 months. The birth control pills made me sooooooooooo sick I stopped taking them after 5 days. (Later I would find in my chart that she suspected drug use was causing my problems. I was not too happy about that.) From there I made an appointment with one of OHSU’S Endocrinologists. They only had 2 and they only worked 4 days a month.

The appointment was for 7 months out. During this time the Endo’s office called to reschedule the appointment 2 more times. I was never going to get into see them. Then by chance I was taking my old phone book to be recycled when I dropped it. When I went to pick it up it was on the page for GLAND DR, otherwise known as Endocrinologists. I had been looking under Endocrinologists in the yellow pages; that explained why I couldn't t find any. They were listed under Gland Dr.'s. At any rate I called and was told they were not taking new patients but if I could get a referral she would make room for me.

At this point I now longer had private insurance and was on the Oregon Health Plan (OHP). I got lucky and the Dr. was taking OHP patients.
I phoned my Allergy Dr. (my family Dr. was out of town ) and asked him for the referral. Within 20 minutes Dr. Smulovitch's office called me back to give me an October appointment. Once I got this news I sat down at the computer and put together a document that listed the Dr.'s I had seen since I started working for Southland ( 7-11), what I had seen them for, what the diagnosis was, what treatment was recommended, and how I responded to the treatment. (I always did as they said even if I disagreed with them.) I felt that since my memory was going and that I had experienced so much for so long it tended to sound like rambling when talking to a new Dr. so this documentation was the best way to avoid that situation.

Upon my first appointment I handed him two documents. One said “ Dr.'s seen” and the other said “ Chemical Exposure”.
He sat quietly and read all of them, then ordered an MRI as well as an ACTH test and other blood tests. I went back on Halloween and was told that I was hypothyroid, (why didn't the breast specialist 3 months prior catch this ???) had low cortisol, and no detectable estrogen. I was put on levxoyl and HRT.
Five months later( March 2001) I woke up with every joint in my body swollen up. I could not move, it hurt so bad. It took me 3 hours to get out of bed and down the hall way to use the bathroom. This went on for 2 weeks (that's how long it took for me to get an appointment). I was tested for Rheumatoid Arthritis with the results finding I had a raised RA factor . I was put on 25 mg of Vioxx and sent to a Rheumatologist. (He said I did not have RA, rather severe fibromyolgia.) The Vioxx does wonders for me.
The depression that goes with having RA is something that I fear. I NEVER want to go back to that. I was also seeing a gynaecologist for the ovarian problems I was having even though I was on HRT. This specialist put me on Menets and Prometrium. They seemed to do the trick. My cycles were under control as were the cysts. I was still having problems with sleeping 14-16 hours a day and the fatigue was extreme. I was not dealing with the heat very well. I felt like I was loosing my mind. I continued seeing my Endo every 3 months as ordered. Then in Dec 2002 I told him I thought I was loosing my mind. It was at this time he diagnosed me with Addisons (this had been ruled out on 2 other occasions.) and put me on 40 mg of Hydrocortisone daily. (Once put on the HC my facial sores healed up for the first time in 10 years and have never come back). That same month I experienced SEVERE tendonitis (or so they say), both my hands and fore arms were red hot and swollen. It hurt to look at them. My hands were cracked and bleeding all the time. I was given flexaril three times a day.

By March 2003 I had gained 30 lbs in 2 weeks ( I went from a size 5 to a 13 overnight ). As it turned out I was being over dosed on estrogen. My OBGYN never told me to stop taking the HTR prescribed by my Endo. By April I started having seizure-like fits in my sleep. I went back in and was given water pills. By August I was experiencing chest pains and high blood pressure. I was also suicidal. Did I mention that I was peeing up to 30 times a day, most of it after midnight. (A real pain in the ass. Sleep deprivation was setting in from getting up so much) I was put on Zypraxa (it is for psychotic episodes. I love it and fear the day the state of Oregon no longer covers the $200.00 price tag. I never want to go back to the mental hell this illness put me through.)

It was at this time my husband told me he wanted out. He wanted me to leave. I had not worked for 3 years due to being ill. I had no place to go. I had to walk away from my kids as well as my family. Family was every thing to me. So for the next year and a half I lived out of a suitcase going between my moms home in Rainier Oregon and her Boat House in Portland Oregon (2-4 hours from Cottage Grove Or where I had lived.) I had no money and was still to sick to work.

It was during this time I finally told my spirit guide ( I believe in life after death and that everything happens for a reason, although I haven't quite figured out what my reason is yet) I could no longer do this on my own. I was going to just go with the flow ( the zyprexa helped my mental state a lot. I no longer obsessed over not having a job and loosing my marriage and my children. What did my future hold? How was I going to survive? I couldn't live with my Mom and her husband forever.)In fact I did nothing but eat sleep and go to my Dr.'s appointments for that 1½ years. I got my disorder, Schmidt’s syndrome ( Addison's co-existing with hypothyroidism) under control to the best of my abilities during that time. I was 100% better than I was in Oct 2000 but not 100% the person that I use to be.

In June of 2003 by the grace of God I was able to move back to Cottage Grove where my daughters are. My SSD case has been on going for 4 years now. I am getting assistance from the State. That could change at any given time, leaving me homeless, but I don't let it get to me. I am still having trouble with brain fog, sleeping 16 hours a day as well as poor concentration, no motivation or focus or drive. I experience panic attacks when I drive among other things. It ultimately took 10 years to diagnose my Addisons (2 yrs of seeing an Endo before he found it)I am on $400.00 worth of meds a month. I am on Levoxyl, Vioxx, Atenonol, Hydrocortisone, Lipitor, & Zyprexa and feel this is probably the best it’s going to get for me. The journey to diagnosis was a very long and hard path. I wish this on no one.

CHEMICAL EXPOSURE

In May of 2000 I added lactation to the triad of symptoms I had. It was at this time I decided to look into the possibility of an on-the-job chemical exposure being responsible for my misdiagnosed / undiagnosed illnesses.

I had seen 8 different Dr.'s in different areas of expertise over the past 8 years, all of whom had a little piece of the puzzle none seeing the WHOLE picture. Not one Dr. had all the symptoms I suffered making it hard to see the 'Big Picture'.

This is my story regarding how my Addison's came to be..........

After I made the appointment with the breast specialist in May of 2000 I called the company (Southland 7-11) that I use to work for and requested the name of the company that printed the banners that I use to transport. I explained my situation and assured them that I was not out to sue or anything (statute of limitations was possibly expired). I was on a damage control mission. I was told not only NO but HELL NO! So with that I decided to go to OSHA and see if they could help me obtain a Material Safety Data Sheet (MSDS) on the ink in question. One may or may not exist. If one did not then I could rule out the chemical exposure theory. If one did exist (which I was pretty sure it did ) then my chemical exposure theory may be valid. Remember 8 years ago there was not that much info on the chemical effects on humans so any thought I may have had 8 years ago were put aside due to lack of documentation, that’s not to say I didn't tell my Dr.'s my thoughts on the chemical exposure theory, because I did.

OSHA obtained the MSDS on the ink used to print the banners that I carried in my van for 24 hours a day for 2 weeks at a time for 1½ yrs. When I got the MSDS I was not surprised to find 6 hazardous ingredients, all of which were listed with the 'TOXIC SUBSTANCE CONTROL ACT', plus the 'FEDERAL HAZARDOUS SUBSTANCE ACT' and the 'POLLUTION PREVENTION PROTECTION ACT', (as well as the TOXIC SUBSTANCE CONTROL ACT).....

The chemicals in question are:

Upon researching each chemical individually found that they all were capable of being reproductive effectors, endocrine disrupters and could cause changes in blood (RBS count and other cell counts), behavioural problems, changes in kidney tubules including acute renal failure. Enzyme inhibition could occur upon inhalation of fumes.

The reproductive effectors could explain my lack of estrogen and all the ovarian cysts problems I had experienced over the years. It would explain the sores in my mouth that I experienced when my cycles got real bad. It would also explain my endocrine problems. For me I had found the culprit.
I gathered and documented all my findings and contacted OHSU’S poison control center. There was no longer a poison control center but there was a toxicology department. I was hoping they could give me some different documentation that would help me prove my case.

I spoke with a Mr. Berman, the Director of the Toxicology Dept. He told me to send him what I had and he would look it over and let me know if he could help me or not. So I sent him:-

  • Chemical Exposure Document
  • Doctors seen document (9 pages)
  • MSDS from Garner Printing
  • "Your OBGYN friend or Foe"
  • OPPT chemical fact sheet for Trimethybenzene
  • EDSTAC recommendations on Endocrine disrupting chemicals (Ethyl Glycol)
  • Environmental Health Prospective (Phthalates)
  • Pilot testing of case studies in Environmental Medicine

I also had explained the whole situation on how I carried these banners in my van for long periods of time and that I was convinced that there was an off-gassing that occurred causing my problems.( Remember I had not yet been to the Endocrinologist to be diagnosed yet) After he reviewed all the info, he replies with an opinion that there was no way that the chemicals in question could cause my health problems. That he was convinced that my problem was organic and he wished me well. He mentioned that he thought that maybe carbon monoxide from my van was responsible for my daughters illness when ever she rode in my van.
CARBON MONOXIDE ???? I knew that my van did not have a carbon monoxide leak. Although I was sick I was not experiencing any of the symptoms I had experienced in the van 7 years prior.

Carbon Monoxide?....... I remember reading something about CO in the MSDS. So I went back to the MSDS and found it.........

On page 3 of the MSDS, SECTION IV, REACTIVE DATA, it states:-

  • Incompatibility : Oxidizing agents, strong acids and bases
  • Conditions to avoid: HEAT ,SPARKS OR FLAMES
  • Hazardous decomposition products: Thermal decomposition may yield CO, CO2, and other toxic fumes.
...and in SECTION VIII, SPECIAL PROTECTION INFORMATION,
  • Adequate ventilation is a must.

With that information I looked up Carbon monoxide on the Internet and was taken to a web site CARBONMONOXIDEKILLS.COM
Dr. David Penny of Wayne State University is considered the world's top CO expert. Once I went to his site and I went NUMB. That was me....!

"The Central Major sites of Nervous system damage include the Hippocampus (effects on short to long term memory, limbic system), Cerebellum (produces ataxia, slurring of speech, Purkinje cells & Dentate nuclei), Cerebral Cortex (effects on learning,memory, executive functioning, multitasking, emotion, etc.), and the Hypothalamus( alters multi-glandular control, possibly body temperature, deregulation, hypothyroidism). Peripheral damage include various nerves (peripheral neuropathy: loss of sensation.) CO poisoning affects underlying executive functions well as short term memory, sensory motor Function, visual perception / visual analytic and information processing. Other residual dysfunction effects that may be present include : headaches, fatigue, muscle/ joint pain, nausea / vomiting, dizziness, shortness of breath, phonophobia ( noise sensitivity), tinnitus, photophobia (and many other visual effects ) MCS, alteration of smell and/or taste, temperature deregulation, and many others."
The list is too long for me to mention.

So I am convinced that thermal decomposition ( heat sparks or flames )of the ink used on the banners off-gassed CO and other toxic fumes in my poorly ventilated van resulting in my hypothyroidism, Addison's, and no detectable estrogen. The thermal decomposition (heat) did not have to be very hot. You know how hot it can get in a car sitting in the sun. During the winter the longest part of my trip (60 some miles) I had my windows closed and the heater cranked. This is when I started to experience the effects of the CO (all listed at the CO web site ). During the summer the temperatures reached up into the 90’s at times. I would be in and out of my van with the internal temp of my van reaching 100+ degrees from just sitting in the sun.

While waiting for my appointment with the Endocrine Doctor, I had contacted Dr. Penny who, as I mentioned, is the worlds foremost expert on CO and also is the Director of Surgical Research & Professor of Physiology at Wayne State University. Over the next couple of years I contacted Dr. Penny explaining my situation asking about testing of the banners in question and if he could do it. I had a SSD claim going and needed an expert to confirm CO exposure. Dr. Penny told me that he thought he could help my SSD claim.

I needed to send him all the info I had and fill out 3 CO questionnaires. This would cost $500.00 for his review of the questionnaires results as well as the info I sent him ( I begged borrowed and stole to get the $500). This info was sent in Jan of 2002. In March 2002 a few months shy of being diagnosed with Addisons I got a letter from him stating that he was convinced that I was exposed to large amounts of CO and that testing of the banners in question was warranted. I have never been able to come up with another $500.00 so he can review all my medical records and other info.

So, I was able to connect my hypothyroidism to the CO exposure. At one point in my research I went to a site that Albert Donnay had. He had a questionnaire on his site but I had just missed the deadline. At any rate I think that in his research on CO he mentioned Addisons being the result of CO poisoning. I have just e mailed him asking him if in fact it was his site I saw this information.

It’s been 12 years since exposure; I have been treated for hypothyroidism for 4 years, no estrogen for 4 years and 3 years for the Addison' Diseases.

I am on Levoxyl, Vioxx, Atenonol, Hydrocortisone, & Lipitor totaling over $400.00 a month. I guess that I would be considered clinically stable at this point.
I am still having problems with brain fog, poor concentration, word finding problems, poor multi tasking problems, slow processing, MCS, lack of motivation, poor memory and sleeping 16 hours a day. My Endo Dr. retired in May 2003 so I am seeing an Internist. His answer to my remaining symptoms is Strattera. This is an ADD medication. I on the other hand believe that it is a syndrome induced by chronic CO poisoning. This syndrome effects the somatic/physical symptoms, cognitive/memory impairments, affective disorders (emotional/personality effects), sensory & motor disorders (visual, auditory, etc.) and gross neurological disorders.
This would explain why medication can't fix it, i.e. because it is residual from the CO poisoning. I have since given my Endo and now my internist all the info concerning the CO exposure. They assure me that this is not the case; that CO could not cause my illnesses. They disagree with the expert. This past year I told my Dr. (Internist) it doesn't matter how I got to this point only that I am here and need him to work with me in getting a handle on my health. I have decided that on my next appointment I am going to challenge his knowledge on CO and it’s long term effects . I am assuming that he did not read the letter that is in my chart from Dr. Penny. Eugene, Oregon, does not have another specialist. The only other option I have is to go to Portland to OHSU where the Dr.'s have compromised their ethics for $$$$$$$$$$$$!
I have been told that I would never get a workman's compensation claim for chemical exposure nor would I get a Dr. in Oregon to state my disorders are CO related. So I am kinda in a catch 22. Oh! and did I mention that 3 months after I was diagnosed as being hypothyroid so were both my girls. They were 8 & 10 at the time ,they are now 13 & 15. I know that due to diabetes and Graves disease in the family that I am predisposed to autoimmuine disorders as are my daughters. I am sure Carbon Monoxide is responsible for our hypothyroidism and my Addisons. Nothing will ever change my mind. I was not only sick for 8 years so were both my children. I lost everything due to the CO exposure. I lost my marriage, my kids, my self respect,my life and my mind. I tried suicide and the Angels saved me for some reason. So all I have left at this point in time is Faith.

The Final Outcome.

September 27th 2002 I received an "UNFAVORABLE" decision from the Social Security Administration.
I cried and cried and cried. What was I going to do ? Where was I going to live being so sick and unable to work? I was never going to see my kids again. My whole world finally hit rock bottom or so I thought. My attorney filed an appeal on the grounds that the Administrative law judge did not review all the facts, nor did he allow key evidence to the exhibitions. He was predjudiced.
December 18th 2003, a remand order was issued by the Appeals Councl. It wasn't over yet. There would be a 2 year back log before I would get a hearing.

During that time I pulled myself together the best that I could.
It was during this time I secured low-income housing so I could get my kids back. Then I applied for welfare (this was the most degrading thing I have ever had to do). Since I was awaiting a SSD decision I was exempt from working. I was living off $427.00, $250 of which was from child support. February 2005 rolls around and I'm stressing because any day now I would be receiving a hearing date. It finally came in March. May 9th was my hearing. I was a total wreck by this time.

May 3rd I receive something from SS. Thinking it was more papers to fill out, I tossed it on the table and went about my business. Two hours later I opened it.
My eyes focussing on the sentence:- "I conclude that a fully favorable decision can be issued without the necessity of a hearing." I wasn't sure if I was understanding it right, so I called my Attorney. His assistant congratulated me on my victory.
'OH! MY GOD....There was a SSD GOD.'
I started to cry hysterically and couldn't stop shaking. After 5 long years it was over. Although it was a happy stress it still took its toll on me and I almost started to crash.

I was going to get 4½ years RETRO payments ($35,000 - 25 % Attornies fees ), SSD for the girls (amount undetermined at this time) and Medicaide. I will still be living on a strict budget, but now I can afford to buy the medications that were too expensive before. Although I did not get it due to having Addisons, the ALJ concluded that I had the following impairments which is considered to be "severe" under the Social Security Act: 'Somatoform disorder, undifferentiated.
Her decision weighed heavily on the documentation I supplied on my chemical exposure as well as the letter from Dr Penny, the worlds top carbon monoxide expert, as well as the State Doctors.

So the moral to the story is : $ may be the root of all evil, but it's going to buy me and my girls a 5 day cruise to Jamaica.
I put a lot of responsibility on my girls (especially my oldest) while I was sick. Joking aside, DOCUMENTATION is so very important (I had 76 pages I submitted and that didn't include any of my medical records.)

Things do get better. You just have to have FAITH (and a good Lawyer Ha Ha ).
Angie.

Copyright © 2004-2005 Angie Noah & Mike Welch

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Adrenal haemorrhage

By Joy Evers
Southern Florida, USA.

In Spring 2006, we were approached by Joy. Her daughter Faith, 5 years old at the time, had suffered trauma during birth (not from any fault of Joy herself).
It is unusual to discover a patient who has suffered permanent adrenal damage from birth trauma.

Joy had seen the invitation on this ADNetwork web site inviting the submission of articles on 'Other causes of Addison's disease' and outlined to us, her daughter's story. Subsequently we invited Joy to write an article for publishing on this page and we are pleased to now present this:

A LESSON IN 'FAITH'

When I learned that I was going to have my first baby, I was both elated and terrified. Thankfully the pregnancy was uneventful and the only problem that came up during pregnancy was gestational diabetes, a pretty common ailment. Since both my parents had died of diabetes I was pretty upset that I now seemed to be afflicted with it, but I was going to have a baby so I needed to focus on that. Two weeks before my delivery date, they did an ultra sound on the baby and discovered that she was growing at an alarming rate, and that they needed to induce labor because she would be about thirteen pounds if I waited till my due date to deliver.

On the date of inducement, I was terrified of the whole process and asked for an epidural. The anesthesiologist asked me how tall I am and when I replied 6ft 1 in, he gave a long whistle and rolled his eyes. I asked why he responded that way. He explained that the dosage of medicine given with epidurals was based on the length of the spine and how far the medicine has to travel, and he had never done an epidural for a woman who was so tall. I thought nothing of it and trusted that he would know just how much was appropriate to give to me.

Hours into the delivery they told me that it was time to push. Due to the excessive amount of epidural I was unable to do a thing. I overheard the gynecologist and anesthesiologist talking.....
I had apparently been given about 50% more epidural drug than the average woman. The gynecologist’s eyes got large and she told him to back off the meds immediately, but by that time it was too late, I would be essentially paralyzed from the hips down for a long time to come. They did everything possible to help deliver the baby once she began to crown; forceps, vacuum suctioning, nurses with their elbows shoved into my midsection to try to force her out, and at one point the doctor even had one foot on the end of the bed using it as leverage while she tried to pull the baby out.

This went on for hours until finally she was delivered.
During that time they did have a monitor attached to her head to make sure that all her vital signs were normal, and they seemed to be, except for her heart rate, which seemed to be too fast at times.

As soon as the cord was cut a team of 6 or so people from Neonatal ICU came to work on her. She was badly bruised and the cord was twisted around her neck, and she was turning blue. They took her away after I got one quick look at her and hours later I was told that they were going to keep her overnight to check out her sugar levels, due to the diabetes.

The next day they informed us that her blood levels were coming back abnormal, and they would have to keep her for a few days to figure out why. It seems that because of the diabetes, they kept her to check her for sugar levels. If it had not been for that, they probably would have sent her home within a couple days without discovering the adrenal issues. If that had happened, she more than likely would have gone into crisis shortly after coming home and no one would have had any answers – thanks to the diabetes my little baby was saved!

Two weeks later they still had no idea what was going on. The baby was so jaundiced that they had her under the special bilirubin lights [phototherapy] and I was unable to hold her because they wanted as much exposure to the lights as possible. They mentioned that if her jaundice got too high it could “possibly” cause mental retardation.
[This is a rare condition called 'kernicterus' in which a build up of bilirubin can stain a small almond shaped piece of tissue in the centre of the brain, & which, had it done so, might in the first few days after birth have caused the potential problems that Joy has mentioned: MLW]

Finally a pediatric endocrinologist was called in and he ordered an ultrasound of her adrenal glands. The medical staff thought he was “barking up the wrong tree,” but they did it anyway. This ultrasound showed a hemorrhaged adrenal gland and they finally had their answer. They started her on Florinef and liquid cortisol and let her go home a few days later.

I was told the dosage to give her, told what sort of things to look out for that could be of harm to her, fever, dehydration, any sort of physical trauma, etc. The endo told us that he had only had one other case like hers in his thirty-year practice, but that the child had been able to recover; his adrenal glands healed and began working around age three. This endocrinologist thought that this might happen with Faith also. (She got that name because this whole experience was a lesson in having Faith for us.)

So we carried on, thinking, hoping, that one day our daughter would be off the meds and it would only be a matter of time, although her doctor certainly had made no promises to that effect.

At around age 4, her endocrinologist informed us that it looked like a permanent thing, and that he did not think her adrenal glands would ever work. This was quite a blow to me, as I had always seen this as a temporary illness. Now it seemed that there was a whole life with all the long-term issues that we now had to consider.

Since then her only real scare has been when she got rotavirus at about 5 months of age. It took three visits to the ER and one loud altercation with the ER staff to convince them that this severely dehydrated baby needed more care than just Tylenol for fever. Finally, on the third visit they admitted her and consulted her endocrinologist.
It seems that the ER staff is poorly educated on adrenal issues and was unwilling to listen to me, a layperson.

We have been very fortunate in that Faith has not suffered any Addison’s crisis. Sending her to pre-school and elementary school has been trying, as I am afraid to send her anywhere that they may not be fully educated on her condition. Her doctor tells me that her case is not actually Addison’s, but it is simply adrenal insufficiency. My understanding is that the only difference is the way the condition is contracted, hers being trauma at birth, and not genetic or from antibodies reacting in her system.

At this point she is just over 4 ft tall, growing well, and about 75 pounds, a little on the heavy side, I assume partly from the steroids. We recently had to up her dosage of hydrocortisone to 20 mg/day from 15 mg/day. This seems like a lot to me, and her doctor agrees that it is more than he thinks her body should need, but it is what her blood work is indicating is necessary to keep her stable. This latest round of blood work also suggests that something is now happening with her adrenal cortex, and she may have to go back on Florinef, which she had been taken off of at about age 1½ years.

The doctor thinks maybe antibodies are attacking, but has no real answer yet. He continues to seek advice and information from others in the field and has suggested us going to the NIH (National Institute of Health) in the near future to see if they can advise us.

All things considered, we have been blessed and her condition seems to be well under control. My real concern is the drugs and the effects they will have on her later in life, but it seems that at this point I have no other options and must continue to rely on faith to help find the answers and find peace within to deal with this confusing condition.

I know that there is a reason for all things that happen, and that I may not ever know the reason behind her condition, but I can only hope that she uses her experiences with this condition to help others, as it seems that so many people on this site are doing.

Joy Evers, on behalf of her daughter, Faith.

Copyright © 2006 Joy Evers & Mike Welch

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.

New Discovery?: High Cortisol Binding Globulin as cause of Addison's?

Mike Welch, Devon,UK.

First published: 14 February 2006

Since late 2004 it has become increasingly obvious that a proportion of patients who present to their General Practitioner (GP), Primary Care Physician (PCP), or Endocrinologist, with a multitude of signs and symptoms which closely resemble or are identical to those often seen with adrenal insufficiency, or Addison's Disease per se, when tested do NOT exhibit the classical results which may have been expected with the condition.

It is well known that the body may be expected to respond to stress with an increase in the level of cortisol. When a random sample of blood plasma is analysed for cortisol, patients with adrenal insufficiency may be seen to exhibit a low, low normal, or normal level of this hormone. However, for years it has been the norm to confirm the diagnosis of Addison's Disease by means of the SynActhen (Synthetic ACTH enhancement) test, known in the USA and some other countries as the Stim (ACTH stimulation) test.
This test is traditionally performed on patients who are not on any supplementary corticosteroid therapy (i.e. hydrocortisone or prednisolone). However in an emergency patients who have been prescribed the alternative corticosteroid, dexamethasone, may have the SynActhen test performed without results being adversely affected or skewed. A baseline cortisol assay sample of blood is taken. The patient is then given the appropriate dose of ACTH, following which repeat samples of blood are taken after 30 minutes & often another at 60 minutes for further cortisol assays to determine what response has been generated by the adrenal glands.

It has been noted that a few patients who, clinically, have been judged by their physician to exhibit classic signs of Addison's disease, have reported to me personally or via the 'Yahoo' Addison's disease discussion group that they have been told by their physician that their SynActhen test results have not supported a diagnosis of Addison's disease. Where these particular patients have had access to copies of the results of these tests or the results have been explained to the patient by the physician, it has often been related that the cortisol response has either been sub-optimal from a normal or low normal baseline level, or that the result appears to be 'normal'. Several of this group of patients have subsequently had repeat SynActhen tests performed and found that the results have varied from the previous tests. Not all the patients who have initially had sub-optimal or normal results have had repeat tests carried out.
In the United States, an alternative diagnosis if 'adrenal fatigue' is often offered for example, where the ACTH stimulation test fails to provide the expected results in the face of clinical signs & symptoms highly suggestive of Addison's disease.

I am a retired Chief Biomedical Scientist with over 36 years experience in pathology and I believe these results from patients who were clinically suffering from symptoms of adrenal insufficiency suggest that something else was interfering, in those patients' blood stream, with their cortisol levels. I had already noticed that most of this group of patients were female and that many had reported they also suffered from an established diagnosis of hypothyroidism or Hashimoto's disease. One female patient in the group who also had Hashimoto's disease reported that her replacement dose of thyroxine had at one time required increasing over a period of several months from 200µg/day (often recognised as full replacement dose) to 400µg/day at the time of an apparently unrelated medical condition. This required increase had been investigated by her endocrinologist and discovered to be the result of an elevated level of thyroid binding globulin (TBG).

From research on the Internet, I discovered a paper by Wyeth Lederle, a well known drug company, in which they related the fact that patients with increased TBG levels also were often found to also have elevated levels of both sex hormone binding globulins (SHBG) and cortisol binding globulins (CBG). I also uncovered another report by the Department of Chemical Pathology at Hong Kong University Hospital in which they mentioned in a ward manual that high CBG could affect cortisol response to ACTH, 'often from a normal baseline'.

Following discussion with an endocrinologist in the United States, with patients who have encountered similar problems in establishing an adequate diagnosis by their physicians, and after further extensive research on the Internet, I submit the following theory which I confidently believe explains the previously unknown or 'atypical' form of Addison's disease, its cause, and the tests required to assist the clinician to establish the diagnosis:-

The Theory of High CBG Addison's Disease.

The cause of primary Addison's disease in the 21st century is autoimmune in approximately 70% of cases, with antibodies (where found) directed against adrenal tissue.
The SynActhen test as described currently remains the method of choice to establish if adrenal insufficency exists.

In a small proportion of patients (see below) who clinically manifest the signs and symptoms of adrenal insufficiency, the SynActhen test as currently performed fails to support the diagnosis of Addison's disease. Instead it may show either an unexpected normal result, or a sub-optimal response to ACTH from, often, a normal baseline. Furthermore, results may vary on subsequent repeated SynActhen tests from previous investigations.

It is suggested that an elevated level of Cortisol Binding Globulin, which are known to have been reported in patients with pre-existing raised Thyroid Binding Globulin levels, binds to the free cortisol in the blood plasma, thus giving false negative or variable non-responsive results when a SynActhen test is performed under current conditions.

Tests Required to Confirm or Exclude High CBG Addison's Disease.

Current methodology for SynActhen tests measures total plasma cortisol levels, i.e. free plus protein bound plasma cortisol.
Bound cortisol cannot be easily metabolised by the human body, thus the measured levels of cortisol in the SynActhen test may not truly reflect the amount of free cortisol available for use within the body.

A modification to the SynActhen test whereby free cortisol in plasma is the required measurement, together with an assay of CBG, may be required to enable the clinician
to establish a diagnosis of atypical, or high CBG, Addison's disease.

Current methodology for plasma free cortisol assay is not yet established as an accredited technique. This requires urgent attention. In discussion with my own endocrinologist (who accepted that the CBG AD theory is correct) I understand that work is in progress to establish an accredited method for this test within the UK.

Criteria for Patients With Suspected High CBG Addison's Disease.

The patients who should be considered as suffering from High CBG Addison's disease and who should be tested as above fit into a fairly tight group of criteria.

They appear to satisfy most or all of the following criteria:

Expected Results:

Patients suffering from 'High CBG Addison's Disease' may expect to show the following ranges of test results:-