Addison’s Disease (Primary)

What Is Primary Addison’s Disease?

[dropcap]A[/dropcap]ddison’s disease is an autoimmune destruction of the adrenal glands by autoantibodies that target the adrenal cortex, or outer part of these glands, and is characterized by a slow progressive failure of the adrenal glands to adequately produce its steroid hormones.

Symptoms of adrenal fatigue or failure may not develop until the majority of adrenal tissue is destroyed. When untreated, progression leads to coma, called Addisonian crisis, which is a medical emergency.

There are two adrenal glands each located on top of a kidney and enclosed in a connective tissue capsule. Each is a small, triangular shape that is made of two parts: the outer region and the inner region.

The inner region, called the adrenal medulla, produces epinephrine and norepinephrine chemicals that are needed to deal with stress.

The outer region, called the adrenal cortex, produces adrenocortical (steroid) hormones and releases them into the bloodstream in response to pituitary stimulating hormone from the brain.

Q: What is the function of steroid hormones produced by the adrenal glands?

A: Functions of the three steroid hormones produced by the adrenal glands are:

1. Glucocorticoids restrain inflammation and metabolism of carbohydrates, fats and proteins to maintain a normal glucose blood level. The major glucocorticoid is hydrocortisone.
2. Mineralocorticoids regulate the retention and excretion of fluids and electrolytes by the kidneys. The most important mineralocorticoid is aldosterone.
3. Androgen (testosterone) is a male sex hormone.

Secondary adrenal insufficiency may develop from other causes that are not immune related such as chronic infections, tumor, and medications.

What Is Addison’s Disease In Celiac Disease and/or Gluten Sensitivity?

• Relationship between primary Addison’s disease and celiac disease. Primary Addison’s disease is an associated autoimmune disorder of celiac disease.
• Relationship between primary Addison’s disease and screening for celiac disease. The risk of developing celiac disease seems to be higher than can be explained by the common DR3-DQ2 gene association alone. It is often asymptomatic or associated with unspecific symptoms. Addison patients should be screened for the presence of celiac disease on a regular basis.¹
• Relationship between primary Addison’s disease and gluten. The association between celiac disease and other immune disorders may be due to the sharing of a common genetic background, such as HLA antigens. However, in a very large study, involving 909 patients with celiac disease, Ventura and his associates found that the development of immune disorders in celiac disease was clearly related to the duration of exposure to gluten.²
• Relationship between Primary Addison’s disease and vitamin D deficiency. The rate of Addison’s disease is significantly elevated in patients with vitamin D deficiency.³

How Prevalent Is Addison’s Disease In Celiac Disease and/or Gluten Sensitivity?

An Italian study found a prevalence of celiac disease in 5.4% of patients with Addison’s disease.⁴

A Norwegian study found a prevalence of celiac disease is 7.9% in patients with Addison’s disease.¹

What Are The Symptoms Of Primary Addison’s Disease?

Addison’s disease is marked in early stages by slowly developing weakness and fatigue progressing to these symptoms:

• Bluish-black discoloration of areolas and mucous membranes.
• Dark freckles.
• Decreased ability to handle stress when it occurs.
• Decreased tolerance to cold with low metabolism.
• Diarrhea that may become severe.
• Dizziness and fainting may occur.
• Hyperpigmentation (darkening) of skin, especially creases.
• Loss of appetite.
• Nausea.
• Vitiligo.
• Vomiting that may become severe.

Late stage symptoms include these:

• Elevated BUN (blood urea nitrogen). This is a common blood test.
• Fatigue that is exhaustive.
• Hyperkalemia (elevated blood potassium level). This is a common blood test.
• Hypoglycemia (low blood sugar) following fasting. This is a common blood test.
• Hyponatremia (low sodium blood level) due to loss of salt in urine (salt wasting). This is a common blood test.
• Orthostatic hypotension (blood pressure drops on standing up).Small heart size.Weight loss.

How Does Addison’s Disease Develop In Celiac Disease and/or Gluten Sensitivity?

• Primary Addison’s disease results from an associated autoimmune mechanism.

Does Addison’s Disease Respond To Gluten-Free Diet?

Yes. Celiac disease-related Addison’s disease responds to gluten free diet, which by removing gluten, removes inflammation and stress.

Part of this positive dietary response is likely due to correction of a variety of nutrient deficiencies that have been causing stress and thus overloading the adrenal glands.

In order to normalize insulin and glucagon levels that have become unbalanced:

1. Strictly reduce sugar sources of glucose, such as table sugar, syrups, and honey. Limit carbohydrates, such as bread, baked goods, pretzels, and potatoes, in order to decrease circulating insulin. Remember, insulin removes excess glucose from the blood and glucose is the end product of starches. Too much glucose, too much insulin and this causes inflammation.
2. Include food sources of protein (egg, fish, meat, milk, poultry) at every meal and with snacks in order to increase glucagon output to combat excess insulin, which in turn reduces demand on adrenals.
3. Eat lots of green leafy vegetables  and broccoli to combat stress, which in turn reduces demand on adrenals.
4. Consume fish oil supplements to combat inflammation, which in turn reduces demand on adrenals.

6 Steps To Improve Addison’s Disease In Celiac Disease and/or Gluten Sensitivity:

• [dropcap]1[/dropcap]Remove the Trigger. Maintain a Strict, Nutritious Gluten Free Diet:

[box type=”shadow” ]Treatment. This condition responds to the complete elimination of gluten, which is the required treatment that improves both Addison’s disease and gut health.

• Gut health is the foundation to restore ALL health. Restored health will enable you to maintain a strict gluten free diet, just as other life tasks will be easier.
• A strict gluten free diet means removing 100% of wheat, barley, rye and oats from the diet.
• Cutting out bread and other obvious sources of gluten is not good enough for recovery. Even 1/8th teaspoon of flour or bread crumb is enough to sustain the inflammation that is damaging your small intestine, causing increased permeability (leaky gut) and allowing undigested gluten to enter your body where it can damage structures and function, and instigate immune inflammatory responses.

Correct Your Individual Nutritional Needs.

• Eat foods that can replenish missing nutrients. Find them under NUTRIENT DEFICIENCIES.
• Take nutritional supplements as needed. Find them under NUTRIENT DEFICIENCIES.

Recovery from celiac disease. You should begin to feel better within a week and notice more energy as inflammation subsides and the  absorbing cells that make up the surface lining of your small intestine are better able to function.

• Intestinal lining cells are replaced every 5 days. The healing process is like sunburn where the damaged surface layer of skin sloughs off and is replaced with new normal cells.
• Leaky gut normally resolves in two month after starting a gluten free diet and brings about a big improvement in health. Improvement in intestinal permeability precedes morphometric recovery (cell appearance and structure) of the small intestine in celiac disease.⁵
• The intestinal lining may take up to a year to heal.[/box]

• [dropcap]2[/dropcap] Reduce Inflammation. Foods to Eat and Foods Not to Eat:

Because gluten is inflammatory, eliminate OTHER inflammatory foods from your diet to reduce an additive effect to gluten. At the same time, try to eat foods that reduce inflammation (anti-inflammatory).

[box type=”shadow” ]Here Are Major Inflammatory Food Types That Reduce Healing:

• Damaging Foods. In susceptible persons, includes corn, dairy (cow), and soy. Lactose, the sugar in any animal milk disrupts intestinal permeability causing leaky gut.⁶
• Allergenic Foods. Includes foods that trigger the immune sytem to produce IgE antibodies. Allergy testing is the usual way to discover these offending foods.
• Shelf Stable Processed Foods. Includes any that contain additives and preservatives. Look for them on the nutrition label of the box or package. Additives and preservatives also disrupt intestinal permeability causing leaky gut.⁶
• Fats. Remove trans-fats entirely. Limit deep fried foods, saturated fats (animal fat/butter), and EXCESSIVE omega-6 fatty acid oils like corn oil. Do not eat rancid fats, sodium caprate (a medium chain fat), or sucrose monester fatty acid (a food grade surfactant) because they induce significant disruption of the intestinal barrier that causes leaky gut.⁶.
• Excessive Refined White Flours (bran layer removed). Includes products made from them such as cookies, bread, cakes, pies. Bran contains the vitamins and minerals that metabolize grains and slows the otherwise rapid entry of sugar from their digestion into the bloodstream. Also disrupt intestinal permeability causing leaky gut.⁶
• Refined Sugars.  Includes white sugar, corn fructose and high fructose corn syrup.
• Certain Spices. Includes paprika and cayenne pepper which disrupt intestinal permeability causing leaky gut.⁶
• Alcohol and Caffeine. Disrupt intestinal permeability causing leaky gut.⁶[/box]

[box type=”shadow” ]Here Are Important Anti-Inflammatory Food Types to Promote Health:

• Fruits. Contain ample amounts of vitamins, minerals and phytochemicals which are naturally occuring components in plants that detoxify toxins, carcinogens (reducing the risk by 50%) and mutagens.
• Non-Starchy Vegetables. Support intestinal integrity and provide ample amounts of vitamins, minerals and phytochemicals. Includes green leafy vegetables such as lettuce and kale, also onion, broccoli, garlic, and others.
• High Quality Complex Carbohydrates. Provide vitamins, minerals, and fiber while boosting serotonin levels to help you relax and feel calm. Includes whole grains, legumes, and root vegetables such as carrots, parsnips, sweet potatoes, turnips, red beets, and others.
• Antioxidants. Protect the body from inflammatory oxidant molecules that continually occur and help us handle stress and reduce irritability. Includes vitamin C-containing foods such as lemon, grapefruit, apricot, Brussels sprouts and strawberries, and others. Also, includes vitamin E-containing foods such as nuts, seeds, avocado, olive oil, and others. Cocoa is good, too.
• Omega-3 Fatty Acids. Balance opposing omega-6 fatty acids and bad fats. Fish sources includes tuna, salmon, cod, and others. Plants sources include flax, chia seeds, canola oil, and others.
• Probiotics. Supply normal microbes needed for colon health and health of the body such as these fermented foods: yogurt, kefir, and unpasteurized apple cider vinegar.
• Prebiotics/ High Fiber Foods.  Food with fiber keeps our population of colonic microbes healthy.
• Protective Herbs and Spices.  See below #6 below for examples.[/box]

• [dropcap]3[/dropcap] Information Sheet You Can Take to Your Doctor or Other Health Professional:

Click here.

• [dropcap]4[/dropcap] Manage Your Medications Safely:

[box type=”shadow” ]

Certain medications can cause secondary adrenal insufficiency.  Ask your doctor or pharmacist about this possible adverse effect if you are taking any of the drugs listed below. Do not stop prescribed medications without supervision.

ANTI-INFLAMMATORIES disrupt intestinal permeability which complicates celiac disease.

• Corticosteroids (Prednisone, Medrol®, Aristocort®, Decadron) when their use is long-term or if they are stopped suddenly cause the adrenals to not produce cortisol.

Certain medications deplete vitamin D such as these common ones:

ANTACIDS / ULCER MEDICATIONS

• Pepcid®, Tagamet®, Zantac®  deplete Calcium, Iron, Vitamin D, Zinc, Magnesium, Copper.
• Magnesium and Aluminum Antacid preparations (Gaviscon®, Maalox®, Mylanta®) deplete Calcium, Iron, Vitamin D, Zinc, Magnesium, Copper.

ANTI-INFLAMMATORIES disrupt intestinal permeability which complicates celiac disease.

• Corticosteroids (Prednisone, Medrol®, Aristocort®, Decadron) deplete Calcium, Vitamin D, Magnesium, Zinc.

ANTICONVULSANTS

• Phenobarbital and Barbituates; and Dilantin®, Tegretol®, Mysoline®, Depakane/Depacon® deplete Calcium, Vitamin D, Copper, Zinc.

CHOLESTEROL DRUGS

• Colestid® and Questran® deplete Vitamin D, Iron.

WEIGHT LOSS DRUGS THAT BIND FAT also interfere with absorption of fat soluble vitamins.

• Zenicol (Orlistat®) depletes Vitamin D.

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• [dropcap]5[/dropcap]Nutritional Supplements To Help Correct Deficiencies:

[box type=”shadow” ]Always check with your doctor to avoid interactions with medications.

• Multivitamin/mineral combination once a day is useful to improve overall nutrient levels and combat stress.
• Fish oil as a reliable source of EPA and DHA omega-3 fatty acids to combat inflammation.
• Vitamin D3 as indicated by blood test to improve adrenal output.

Storage Note: Store container tightly sealed, away from heat, moisture and direct light to avoid loss of potency. That is, in a safe kitchen cabinet – not in the bathroom or on the kitchen table.[/box]

• [dropcap]6[/dropcap]Manage Natural Remedies: 

[box type=”shadow” ]Hydration:

• Eight glasses of water are recommended per day unless there is a contraindication such as kidney or heart disease. The Institute of Medicine recommends approximately 2.7 liters (91 ounces) of total water, from all beverages and foods, each day for women and 3.7 liters (125 ounces) daily of total water for men.
• If you are thirsty, drink water. Add fresh, squeezed lemon to water. Lemon is anti-inflammatory, alkalizing and provides vitamin C.
• Hydration Test: Urine should be pale yellow. Fingertips should be plump, without pruning but this may not be reliable when fingers are swollen with edema. Lips should be plump, without puckering. The feeling of thirst can be unreliable.
• What is wrong with soda, coffee, tea, and alcohol? These drinks are dehydrating, increase acid, and deplete nutrients.[/box]

[box type=”shadow” ]Carminatives. The following  anti-inflammatory plant sources called carminitives help heal the digestive tract. They also tone the digestive muscles which improves peristalsis, thus aiding in the expulsion of gas from the stomach and intestine to relieve digestive colic and gastric discomfort.

Carminative Food Remedies:

• Raspberry.
• Carrot is also a cleansing digestive tonic.
• Grape is also bile stimulating and a cleansing remedy for sluggish digestion and laxative.
• Redbeets also stimulate and improve digestion and are easily digested.
• Cabbage also stimulates and improves digestion and is also a liver decongestant.
• Lettuce also stimulates and improves digestion and is also an alterative, meaning it improves the function of organs involved with the digestion and excretion of waste products to bring about a gradual change.
• Potatoes are antispasmodic (due to atropine like properties) and a liver remedy.

Carminative Herb Remedies:

• Sage is also a digestive, astringent, bile stimulant and energy tonic that heals the mucosa.  Drink as tea or use in cooking.
• Chamomile, lemon balm, and fennel, (as a tea) also help relieve nervous tension.
• Parsley also relieves indigestion.
• Rosemary as a tea and in cooking also is a nervous system tonic for stress and fatigue, bile stimulant, and can relieve headaches and indigestion.
• Thyme is also soothing remedy useful for stimulating digestion of rich, fatty foods.

Carminative Spice Remedies:

• Cloves are also antispasmodic.
• Nutmeg is also useful for indigestion.
• Ginger.[/box]

[box type=”shadow” ]Exercise Helps:

Exercise improves circulation and rids the body of toxins.

• Walking is aerobic exercise that reconditions the whole body to improve stamina. Read more about Exercise and Fitness.
• Weight training builds muscle. Read more about Exercise and Fitness.
• Stretching improves flexibilty. Read more about Exercise and Fitness.

Note: Exercise is important, but the amount and type of exercise undertaken depends on your health. Your first priority is to heal. [/box]

What Do Medical Research Studies Tell About Addison’s Disease In Celiac Disease and/or Gluten Sensitivity?

RESEARCH STUDY SUMMARIES

“Hospital admissions for vitamin D related conditions and subsequent immune-mediated disease: record-linkage studies.” This study investigating the reported association between vitamin D deficiency and the risk of developing immune-mediated diseases showed that  patients with vitamin D deficiency may have an increased risk of developing some immune-mediated diseases including Addison’s disease, although  reverse causality or confounding cannot  be ruled out.

Researchers analyzed a database of linked statistical records of hospital admissions and death registrations for the whole of England (from 1999 to 2011). Rate ratios for immune-mediated disease were determined, comparing vitamin D deficient cohorts (individuals admitted for vitamin D deficiency or markers of vitamin D deficiency) with comparison cohorts.

After hospital admission for either vitamin D deficiency, osteomalacia or rickets, there were significantly elevated rates of Addison’s disease, ankylosing spondylitis, autoimmune hemolytic anemia, chronic active hepatitis, celiac disease, Crohn’s disease, diabetes mellitus, pemphigoid, pernicious anemia, primary biliary cirrhosis, rheumatoid arthritis, Sjogren’s syndrome, systemic lupus erythematosus, thyrotoxicosis, and significantly reduced risks for asthma and myxoedema.³

“Celiac disease in North Italian patients with autoimmune Addison’s disease.” This study aiming to define the prevalence of celiac disease and of IgA deficiency in a group of Italian patients with autoimmune Addison’s disease found that in patients with Addison’s disease there is a high prevalence of both celiac disease and IgA deficiency.

One hundred and nine patients with Addison’s disease were enrolled and examined for tissue transglutaminase autoantibodies of the IgA class, circulating levels of IgA and adrenal cortex antibodies. The clinical, silent or latent form of celiac disease was present in six out of 109 (5.4%). This prevalence was significantly higher than that reported for the Northern Italian population which was equal to 0.063%. Specifically, celiac disease was present in 12.5% of the autoimmune polyglandular syndrome (APS) type 1 cases, in four out of 60 (6.7%) of the APS type 2 cases and in one out of 40 (2.5%) of the isolated Addison’s disease cases. IgA deficiency was present in two out of 109 patients (1.8%), all of whom had normal IgG anti-gliadin. Autoantibodies to the adrenal cortex were detected in 81 out of 109 patients (74.3%).Consequently, it is important to screen for celiac disease with tissue transglutaminase autoantibodies of the IgA class and for IgA levels.⁷

“High frequency of coeliac disease among patients with autoimmune adrenocortical failure.” This study investigating the prevalence of celiac disease among a large group of patients with autoimmune Addison’s disease demonstrated high prevalence of celiac disease (7.9%) in patients with Addison’s disease. Risk of celiac disease seems to be higher than can be explained by the common DR3-DQ2 association alone. Seventy-six patients (44 women) with Addison’s disease, 52% of whom had polyendocrine failure, were recruited from a registry of organ-specific autoimmune diseases in Norway. All sera were analysed for antibodies against gliadin (AGA), endomysium (EMA) and tissue transglutaminase (tTG). Patients with positive EMA and/or anti-tTG were offered endoscopy. The human leucocyte antigen (HLA) class II genotypes were determined. Five patients had antibodies against both endomysium and tissue transglutaminase. In these five patients, celiac disease was verified by biopsy. One patient had known celiac disease prior to the study. All six patients with celiac disease carried the celiac disease-associated HLA haplotype DR3-DQ2. Addison’s patients should be screened for celiac disease on a regular basis.¹

CASE REPORT SUMMARIES

“Multiple Disease Associations in Autoimmune Polyglandular Syndrome Type II. “ This case report describes the course of a patient with Autoimmune Polyglandular Syndrome Type II (APS II)  with a dramatic development of eight autoimmune diseases over the course of ten years. She developed Addison’s disease, hypothyroidism, type 1 diabetes, Hashimoto’s encephalopathy, vitiligo, celiac disease, sero-negative arthritis, and ulcerative colitis. This represents a particularly aggressive course of APS II and this combination of autoimmune diseases has not been previously reported. It highlights the potential complexity and severity of the clinical course of APS II.

A 25 year old female with a history of ulcerative colitis, celiac disease and type 1 diabetes presented with mental status changes. She was diagnosed with Hashimoto’s encephalopathy and treated with high dose steroids and intravenous immunoglobulin. She recovered well from her encephalopathy but her post-hospitalization course was complicated due to the development of Addison’s disease, vitiligo, sero-negative arthritis, and hypothyroidism.⁸

“Treatment-refractory hypothyroidism.” This case report describes diagnosing celiac disease and subsequent adrenal insufficiency showing autoimmune polyglandular syndrome type-2 in a 49-year-old man who was referred to an endocrine clinic because of rising thyroid-stimulating hormone (TSH) levels despite increasing doses of levothyroxine.

The patient had a history of Grave’s disease, which had been successfully treated with radioiodine ablation 15 years earlier. Over the past several years, his serum TSH levels had risen to 31.5 (normal 0.4–4.5) mU/L, and the dose of levothyroxine he was prescribed had been increased to 225 μg per day, or 2.7 (usual recommended dose 1.6) μg/kg daily. The patient’s adherence to the drugs he had been prescribed was confirmed, and to exclude impaired bioavailability of the medication,a medically supervised test for the absorption of levothyroxine was performed. The results of the test showed that only 30% of the medication administered was absorbed.

In the investigation of intestinal malabsorption, the screening serum test for gluten enteropathy was abnormal; the level of immunoglobulin A antibodies against transglutaminase was 75.4 (negative < 9.0, borderline 9–16, positive > 16.0) units/mL. A subsequent endoscopic biopsy of the patient’s bowel was consistent with a diagnosis of celiac disease. The patient was directed to follow a low-gluten diet. The patient’s histological abnormalities resolved, and his serum level of TSH normalized with his usual dose of thyroxine (225 μg daily).

Because of the patient’s previous Grave’s disease, an autoimmune polyglandular syndrome was investigated. Subsequent tests showed elevated antiadrenal and 21-hydroxylase antibodies, suggesting autoimmune adrenalitis. A short intravenous adrenocorticotropic hormone (ACTH) stimulation test was consistent with diminished adrenal cortisol reserve.⁹

“Moderate Dose Inhaled Budesonide Disguising Symptoms of Addison’s Disease in An Asthmatic Boy with Silent Celiac Disease.” This case report describes finding celiac disease in an 11 year-old boy who had asthmatic symptoms since age four and developed Addison’s disease, which was not diagnosed promptly because of the steroid effect of his inhalers.  Inhaled corticosteroids are first-line treatment for asthma. Moderate doses of budesonide have been supposed not to affect hypothalamic-pituitary-adrenal axis function. We report the case of a boy with asthmatic symptoms and a late diagnosis of celiac disease, in whom inhaled budesonide in a dose used in conventional asthma therapy seems to have been systemically absorbed in amounts large enough to temporarily disguise the symptoms of a developing adrenal insufficiency. Inhaled corticosteroids in a dose used in standard asthma therapy seem to have the potential of disguising a developing Addison’s disease. Furthermore, celiac disease, especially if diagnosed in late childhood, may be associated with Addison’s disease causing a complex symptom pattern.¹⁰

Sources:

1. Myhre AG, Aarsetøy H, Undlien DE, Hovdenak N, Aksnes L, Husebye ES. High frequency of coeliac disease among patients with autoimmune adrenocortical failure. Scand J Gastroenterol. 2003 May;38(5):511-5. [↩] [↩] [↩]
2. La Villa G, Pantaleo P, Tarquini R, Cirami L, Perfetto F, Mancuso F, Laffi G. Multiple immune disorders in unrecognized celiac disease: a case report. World J Gastroenterol. 2003;9(6):1377-1380, Available at: http://www.wjgnet.com/1007-9327/9/1377.asp. [↩]
3. Ramagopalan SV, Goldacre R, Disanto G, Giovannoni G, Goldacre MJ. Hospital admissions for vitamin D related conditions and subsequent immune-mediated disease: record-linkage studies. BMC Med. 2013 Jul 25;11:171. doi: 10.1186/1741-7015-11-171. [↩] [↩]
4. Betterle C, Lazzarotto F, Spadaccino AC, Basso D, Plebani M, Pedini B, Chiarelli S, Albergoni M. Celiac disease in North Italian patients with autoimmune Addison’s disease. Eur J Endocrinol. 2006 Feb;154(2):275-9. [↩]
5. Cummins AG, Thompson FM, Butler RN, et al. Improvement in intestinal permeability precedes morphometric recovery of the small intestine in coeliac disease. Clinical Science. Apr 2001;100(4):379-86. [↩]
6. Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease. Journal of Gastroenterology and Hepatology. 2003;18:479-91. [↩] [↩] [↩] [↩] [↩] [↩]
7. Betterle C, Lazzarotto F, Spadaccino AC, Basso D, Plebani M, Pedini B, Chiarelli S, Albergoni M. Celiac disease in North Italian patients with autoimmune Addison’s disease. Eur J Endocrinol. 2006 Feb;154(2):275-9. [↩]
8. Maturu A, Michels A, Draznin B. Multiple Disease Associations in Autoimmune Polyglandular Syndrome Type II. Endocr Pract. 2014 Aug 22:1-13. [↩]
9. Ramadhan A, Tamilia M. Treatment-refractory hypothyroidism. CMAJ. 2012 Feb 7;184(2):205-9. doi: 10.1503/cmaj.110994. [↩]
10. Stenhammar LC, Högberg LM, Nordwall M, Strömberg LG. Moderate Dose Inhaled Budesonide Disguising Symptoms of Addison’s Disease in An Asthmatic Boy with Silent Celiac Disease. J Pediatr Pharmacol Ther. 2005 Apr;10(2):100-3. doi: 10.5863/1551-6776-10.2.100. [↩]