{"id":469,"date":"2014-11-26T14:26:19","date_gmt":"2014-11-26T19:26:19","guid":{"rendered":"http:\/\/www.mynutriguide.com\/?p=469"},"modified":"2020-07-11T10:41:37","modified_gmt":"2020-07-11T14:41:37","slug":"autoimmune-polyglandular-syndromes-2","status":"publish","type":"post","link":"https:\/\/glutenfreeworks.com\/health\/autoimmune-polyglandular-syndromes-2\/","title":{"rendered":"Autoimmune Polyglandular Syndromes\u00a0"},"content":{"rendered":"<div id=\"attachment_6496\" style=\"width: 230px\" class=\"wp-caption alignleft\"><a href=\"https:\/\/glutenfreeworks.com\/health\/wp-content\/uploads\/sites\/10\/endocrine-glands.gif\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-6496\" class=\" wp-image-6496       \" src=\"https:\/\/glutenfreeworks.com\/health\/wp-content\/uploads\/sites\/10\/endocrine-glands-184x300.gif\" alt=\"Body image showing endocrine glands that may be affected by polyglandular autoimmune syndrome. Courtesy endocrine101.com \" width=\"220\" height=\"260\" \/><\/a><p id=\"caption-attachment-6496\" class=\"wp-caption-text\">Endocrine glands targeted in polyglandular autoimmune syndrome.<\/p><\/div>\n<h2><b>What Are Autoimmune Polyglandular Syndromes?<\/b><\/h2>\n<p style=\"text-align: justify\"><span class=\"dropcap\">A<\/span>utoimmune polyglandular syndromes (APS) are rare clusterings of two or more endocrine and non-endocrine autoimmune disorders in the same affected person.<\/p>\n<p style=\"text-align: justify\">Polyglandular is somewhat of a misnomer since many of the manifestations of the diseases do not concern endocrine glands.<a href=\"#footnote_1_469\" id=\"identifier_1_469\" class=\"footnote-link footnote-identifier-link\" title=\"W&eacute;meau JL, Proust-Lemoine E, Ryndak A, Vanhove L. Thyroid autoimmunity and polyglandular endocrine syndromes. Hormones (Athens). 2013 Jan-Mar;12(1):39-45.\">1<\/a><\/p>\n<p style=\"text-align: justify\">Endocrine autoimmune disorders involve the abnormal production of autoantibodies that\u00a0<span style=\"line-height: 1.5em\">target and\u00a0<\/span><span style=\"line-height: 1.5em\">destroy the body&#8217;s own endocrine tissues, causing loss of\u00a0<\/span><span style=\"line-height: 1.5em\">essential hormone\u00a0<\/span><span style=\"line-height: 1.5em\">production by the targeted glands.\u00a0Endocrine glands <\/span><span style=\"line-height: 1.5em\">include the pituitary, thyroid, adrenal, parathyroid, islets of Langerhans (pancreas), testes in males,\u00a0<\/span><span style=\"line-height: 1.5em\">and\u00a0<\/span><span style=\"line-height: 1.5em\">ovaries in females. <\/span><\/p>\n<p style=\"text-align: justify\"><span style=\"line-height: 1.5em\">First degree relatives (siblings of same parents, parents, children) have an increased incidence of latent, meaning not apparent, autoimmune pathology.<a href=\"#footnote_2_469\" id=\"identifier_2_469\" class=\"footnote-link footnote-identifier-link\" title=\"Femiano P, Castaldo V, Iossa C. Complex family association in autoimmune polyendocrine syndrome.&nbsp;Minerva Pediatrica. Apr 2003;55(2):163-70.\">2<\/a><\/span><\/p>\n<p><span style=\"color: #000000\"><strong>Q:<\/strong><\/span> How many autoimmune polyglandular syndromes are described?<\/p>\n<p style=\"text-align: justify\"><span style=\"color: #000000\"><strong>A:<\/strong> <\/span>Three syndromes have been identified and they are all inherited: APS type-1, APS type-2, and APS type-3.<\/p>\n<ul class=\"cp_check black\">\n<li style=\"text-align: justify\"><span style=\"color: #000000\"><strong><span style=\"text-decoration: underline\">APS type-1<\/span><\/strong><\/span> is a genetic mutation inherited in an autosomal recessive manner. A<span style=\"line-height: 1.5em\">\u00a0child<\/span><span style=\"line-height: 1.5em\">\u00a0with APS type-1 has inherited t<\/span><span style=\"line-height: 1.5em\">wo mutated copies of a gene called the AIRE (autoimmune regulator) gene, which is on the long arm of 21st chromosome present in each cell.<a href=\"#footnote_3_469\" id=\"identifier_3_469\" class=\"footnote-link footnote-identifier-link\" title=\"W&eacute;meau JL, Proust-Lemoine E, Ryndak A, Vanhove L. Thyroid autoimmunity and polyglandular endocrine syndromes. Hormones (Athens). 2013 Jan-Mar;12(1):39-45.\">3<\/a> The parents,<\/span><span style=\"line-height: 1.5em\">\u00a0called carriers,\u00a0<\/span><span style=\"line-height: 1.5em\">are\u00a0<\/span><span style=\"line-height: 1.5em\">unaffected <\/span><span style=\"line-height: 1.5em\">since they each have only a single copy of the AIRE mutated gene. Humans ha<\/span><span style=\"line-height: 1.5em\">ve<\/span><span style=\"line-height: 1.5em\">\u00a0a total of\u00a0<\/span><span style=\"line-height: 1.5em\">23 pairs of chromosomes that contain genes inherited from each parent. Mutations in the genes cause disease. <\/span><\/li>\n<\/ul>\n<p style=\"padding-left: 30px\"><span style=\"line-height: 1.5em\">D<\/span><span style=\"text-align: justify\">iagnosis criteria for autoimmune\u00a0<\/span><span style=\"line-height: 1.5em\">polyglandular<\/span><span style=\"line-height: 1.5em\">\u00a0<\/span><span style=\"line-height: 1.5em\">syndrome type-1 includes these three disorders:<\/span><\/p>\n<ol>\n<ol>\n<ol>\n<li style=\"text-align: justify\"><strong>Chronic candida infection<\/strong> (CMC), which\u00a0<span style=\"line-height: 1.5em\">usually develops first, typically attacks skin, but very commonly also nails, mouth, vagina, esophagus and intestine.\u00a0CMC in APS type-1 patients is usually mild, and in most cases, it is chronic. It is found in 73\u2013100 % of APS type-1 patients.\u00a0<\/span><\/li>\n<li style=\"text-align: justify\"><strong>Hypoparathyroidism<\/strong>, causing loss of parathyroid function (hypoparathyreosis) is found in 76\u201393 % of APS type-1 patients.<\/li>\n<li style=\"text-align: justify\"><strong>Autommune Addison\u2019s disease<\/strong>, also called autoimmune adrenalitis,\u00a0is found in 72-100 % of APS type-1 patients. Still many of them die for unrecognized or late diagnosed autoimmune Addison&#8217;s disease, so regular follow-up for children in suspicion of APS type-1 (with CMC or\/and hypoparathyroidism) is necessary.<a href=\"#footnote_4_469\" id=\"identifier_4_469\" class=\"footnote-link footnote-identifier-link\" title=\"http:\/\/autoimmune.pathology.jhmi.edu\/diseases.cfm?systemID=3&amp;DiseaseID=66\">4<\/a><\/li>\n<\/ol>\n<\/ol>\n<\/ol>\n<p style=\"padding-left: 30px\"><i>Other<\/i>\u00a0assocated disorders that may develop, but are not required for diagnosis, include: vitiligo,\u00a0premature menopause, pernicious anemia, parathyroid gland failure, alopecia, and celiac disease. Thyroid disease rarely occurs.<a href=\"#footnote_5_469\" id=\"identifier_5_469\" class=\"footnote-link footnote-identifier-link\" title=\"W&eacute;meau JL, Proust-Lemoine E, Ryndak A, Vanhove L. Thyroid autoimmunity and polyglandular endocrine syndromes. Hormones (Athens). 2013 Jan-Mar;12(1):39-45.\">5<\/a><\/p>\n<ul class=\"cp_check black\">\n<li style=\"text-align: justify\"><span style=\"color: #000000\"><strong><span style=\"text-decoration: underline\">APS type-2<\/span><\/strong><\/span> is linked to the inheritance of HLA antigens on chromosome 6 and\u00a0appears to be autosomal dominant with incomplete penetrance.\u00a0This suggests the contribution of environmental factors, such as bacterial and viral infections, medications, psychological factors, etc.<a href=\"#footnote_6_469\" id=\"identifier_6_469\" class=\"footnote-link footnote-identifier-link\" title=\"W&eacute;meau JL, Proust-Lemoine E, Ryndak A, Vanhove L. Thyroid autoimmunity and polyglandular endocrine syndromes.&nbsp;Hormones (Athens). 2013 Jan-Mar;12(1):39-45.\">6<\/a>\u00a0<span style=\"line-height: 1.5em\">It does\u00a0not have an identified mutation of the AIRE\u00a0<\/span><span style=\"line-height: 1.5em\">gene.<\/span><\/li>\n<\/ul>\n<p style=\"text-align: justify;padding-left: 30px\">Diagnosis criteria for \u00a0autoimmune\u00a0<span style=\"line-height: 1.5em\">polyglandular\u00a0<\/span><span style=\"line-height: 1.5em\">syndrome type-2 includes these two disorders:<\/span><\/p>\n<ol style=\"text-align: justify\">\n<ol>\n<ol>\n<li><strong>Autommune Addison\u2019s disease\u00a0<\/strong>combined with<\/li>\n<li><strong>Autoimmune thyroid disease<\/strong> (thyroid atrophy, hypertrophic goiter related to Hashimoto\u2019s thyroiditis, Graves\u2019 disease, asymptomatic autoimmune thyroiditis)<a href=\"#footnote_6_469\" id=\"identifier_7_469\" class=\"footnote-link footnote-identifier-link\" title=\"W&eacute;meau JL, Proust-Lemoine E, Ryndak A, Vanhove L. Thyroid autoimmunity and polyglandular endocrine syndromes.&nbsp;Hormones (Athens). 2013 Jan-Mar;12(1):39-45.\">6<\/a>\u00a0and\/or type I diabetes mellitus.\u00a0 The conditions may occur in any order.<\/li>\n<\/ol>\n<\/ol>\n<\/ol>\n<p style=\"text-align: justify;padding-left: 30px\">Polyglandular autoimmune syndrome type-2 \u00a0is also known as Schmidt\u2019s syndrome when adrenalitis (adrenal insufficiency) is associated with thyroiditis and Carpenter\u2019s syndrome for adrenal insufficiency with hypoparathyreosis (impaired function of parathyroid glands).<\/p>\n<p style=\"text-align: justify;padding-left: 30px\"><i>Other<\/i> disorders that may develop, but are not required for diagnosis, include: \u00a0type 1 diabetes (<span style=\"line-height: 1.5em\">50%),<\/span><span style=\"line-height: 1.5em\">\u00a0frequently gonadal failure or vitiligos, also celiac disease, autoimmune hepatitis, alopecia, pernicious anemia, and myasthenia gravis.<a href=\"#footnote_7_469\" id=\"identifier_8_469\" class=\"footnote-link footnote-identifier-link\" title=\"http:\/\/autoimmune.pathology.jhmi.edu\/diseases.cfm?systemID=3&amp;DiseaseID=67\">7<\/a>\u00a0Decades may arise between the onset of one disease and the onset of the second in the same patient.<a href=\"#footnote_8_469\" id=\"identifier_9_469\" class=\"footnote-link footnote-identifier-link\" title=\"http:\/\/www.dundee.ac.uk\/medther\/tayendoweb\/images\/polyglandular.htm\">8<\/a><\/span><\/p>\n<p style=\"text-align: justify;padding-left: 30px\">Therapy of APS type-2 consists of hormone replacement therapy for each separate condition, except that treatment for adrenal insufficiency must be given before thyroid therapy is started when the conditions occur together.<a href=\"#footnote_9_469\" id=\"identifier_10_469\" class=\"footnote-link footnote-identifier-link\" title=\"MAJERONI BA and PATEL P. Autoimmune Polyglandular Syndrome, Type II. Am Fam Physician. 2007 Mar 1;75(5):667-670.\">9<\/a> Thyroxin replacement may induce life-threatening adrenal failure in a patient with untreated Addison&#8217;s\u00a0disease. Thus, in case of doubt hydrocortisone should be given before the thyroxine administration is started.<a href=\"#footnote_10_469\" id=\"identifier_11_469\" class=\"footnote-link footnote-identifier-link\" title=\"Lipowsky C, Schorl-Schweikardt BA, Kehl O, Br&auml;ndle M. 19-year-old patient with adrenal cortex insufficiency&ndash;only the tip of the iceberg. Polyendocrine autoimmune syndrome type II (Schmidt syndrome). Praxis (Bern 1994). 2008 Jan 23;97(2):77-81.\">10<\/a><\/p>\n<ul class=\"cp_check black\">\n<li><span style=\"color: #000000\"><strong><span style=\"text-decoration: underline\"><span style=\"line-height: 1.5em\">APS t<\/span>ype-3<\/span><\/strong><\/span>\u00a0 has a strong genetic background.\u00a0Diagnosis criteria for autoimmune\u00a0<span style=\"line-height: 1.5em\">polyglandular\u00a0<\/span><span style=\"line-height: 1.5em\">syndrome type-3 involves these conditions:<\/span><\/li>\n<\/ul>\n<ol>\n<ol>\n<ol>\n<li style=\"text-align: justify\">\u00a0<strong>Autoimmune thyroiditis<\/strong> that occurs with another organ-specific autoimmune disease, but not with autoimmune Addison&#8217;s disease, and<\/li>\n<li style=\"text-align: justify\"><em>Other<\/em> autoimmune diseases can include diabetes mellitus, pernicious anemia, vitiligo, alopecia, myasthenia gravis, celiac disease, and Sj\u00f6gren\u2019s syndrome.\u00a0The most common APS type-3 combination is autoimmune disease of thyroid gland and pernicious anemia.<a href=\"#footnote_11_469\" id=\"identifier_12_469\" class=\"footnote-link footnote-identifier-link\" title=\"http:\/\/autoimmune.pathology.jhmi.edu\/diseases.cfm?systemID=3&amp;DiseaseID=68\">11<\/a><\/li>\n<\/ol>\n<\/ol>\n<\/ol>\n<p style=\"text-align: justify\"><span style=\"color: #000000\">Who is Affected in the General Population?<\/span><\/p>\n<ul>\n<li style=\"text-align: justify\">APS type-1 is usually apparent in childhood with the incidence of 1 in100,000 persons. It is more common among Finns (1 in 25,000), Sardinians (1 in 14,000), and Iranian Jews (1 in 6,500 to 1 in 9,000). The age of onset is usually early childhood, but new symptoms can develop throughout life. It affects both sexes equally.<\/li>\n<li style=\"text-align: justify\">APS type-2 has a peak onset in middle age, although the first signs usually develop between 20\u201330 years of age. Its prevalence is 1 in 20,000 persons. It is three times more frequent among women than men.<a href=\"#footnote_12_469\" id=\"identifier_13_469\" class=\"footnote-link footnote-identifier-link\" title=\"Van den Driessche A, Eenkhoorn V, Van Gaal L, De Block C. Type 1 diabetes and autoimmune polyglandular syndrome: a clinical review. Neth J Med. 2009 Dec;67(11):376-87.\">12<\/a><\/li>\n<li style=\"text-align: justify\">APS type-3 is most frequent among middle-aged women.<a href=\"#footnote_7_469\" id=\"identifier_14_469\" class=\"footnote-link footnote-identifier-link\" title=\"http:\/\/autoimmune.pathology.jhmi.edu\/diseases.cfm?systemID=3&amp;DiseaseID=67\">7<\/a>[\/box]<\/li>\n<\/ul>\n<h2 style=\"text-align: justify\">What Is Autoimmune Polyglandular Syndrome In Celiac Disease and\/or Gluten Sensitivity?<\/h2>\n<p><!--more--><\/p>\n<ul class=\"cp_check red\">\n<li style=\"text-align: justify\"><strong>Relationship between autoimmune polyglandular syndrome and celiac disease.<\/strong> Autoimmune polyglandular syndrome is an associated disorder in celiac disease.<\/li>\n<li style=\"text-align: justify\"><strong>Relationship between autoimmune polyglandular syndrome and gluten.\u00a0<\/strong>Autoimmune polyglandular syndromes seem to be related to gluten exposure. Gluten could represent a starting or a maintenance factor of autoimmune processes and the risk is proportional to the duration of exposure to gluten.\u00a0The 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.<a href=\"#footnote_13_469\" id=\"identifier_15_469\" class=\"footnote-link footnote-identifier-link\" title=\"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.&nbsp;World J Gastroenterol.&nbsp;2003;9(6):1377-1380.\">13<\/a>,<a href=\"#footnote_14_469\" id=\"identifier_16_469\" class=\"footnote-link footnote-identifier-link\" title=\"Iughetti L, Bulgarelli S, Forese S, Lorini R, Balli F, Bernasconi S. Endocrine aspects of coeliac disease.&nbsp;Journal of Pediatric Endocrinology &amp; Metabolism : JPEM. Jul-Aug 2003;16(6):805-18.\">14<\/a><\/li>\n<li style=\"text-align: justify\"><strong>Relationship between autoimmune polyglandular syndrome and diabetes mellitus.\u00a0<\/strong>Screening for a quick singling out of autoimmune pathologies is suggested for type 1 diabetes mellitus patients, their first relatives and for subjects affected by other autoimmune diseases or celiac disease.<a href=\"#footnote_15_469\" id=\"identifier_17_469\" class=\"footnote-link footnote-identifier-link\" title=\"Femiano P, Castaldo V, Iossa C. Complex family association in autoimmune polyendocrine syndrome.&nbsp;Minerva Pediatrica. Apr 2003;55(2):163-70.\">15<\/a><\/li>\n<li style=\"text-align: justify\"><strong>Relationship between autoimmune polyglandular syndrome and screening.\u00a0<\/strong>In patients and their relatives, who have\u00a0autoimmune\u00a0disorders, a search for autoimmune polyglandular syndrome\u00a0is crucial. Consequently, it would be appropriate that the patient and all family members are asked for clinical signs and symptoms of\u00a0autoimmune\u00a0disorders.<a href=\"#footnote_16_469\" id=\"identifier_18_469\" class=\"footnote-link footnote-identifier-link\" title=\"Lipowsky C, Schorl-Schweikardt BA, Kehl O, Br&auml;ndle M. 19-year-old patient with adrenal cortex insufficiency&ndash;only the tip of the iceberg. Polyendocrine autoimmune syndrome type II (Schmidt syndrome).&nbsp;Praxis&nbsp;(Bern 1994). 2008 Jan 23;97(2):77-81.\">16<\/a><\/li>\n<\/ul>\n<h2 style=\"text-align: justify\">How Prevalent Are Autoimmune Polyglandular Syndromes In Celiac Disease and\/or Gluten Sensitivity?<\/h2>\n<p style=\"text-align: justify\">Patients with celiac disease are at great risk for developing autoimmune polyglandular syndromes.<a href=\"#footnote_17_469\" id=\"identifier_19_469\" class=\"footnote-link footnote-identifier-link\" title=\"Iughetti L, Bulgarelli S, Forese S, Lorini R, Balli F, Bernasconi S. Endocrine aspects of coeliac disease.&nbsp;Journal of Pediatric Endocrinology &amp; Metabolism : JPEM.&nbsp;Jul-Aug 2003;16(6):805-18.\">17<\/a><\/p>\n<p style=\"text-align: justify\">In a study of 109 patients with autoimmune Addison&#8217;s disease,\u00a0celiac disease was present in 12.5% of the\u00a0autoimmune polyglandular syndrome\u00a0(APS) type-1 cases and in four out of 60 (6.7%) of the APS type-2 cases.<a href=\"#footnote_18_469\" id=\"identifier_20_469\" class=\"footnote-link footnote-identifier-link\" title=\"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&rsquo;s disease. Eur J Endocrinol. 2006 Feb;154(2):275-9.\">18<\/a><\/p>\n<h2 style=\"text-align: justify\">What Are The Symptoms Of Autoimmune Polyglandular Syndromes?<\/h2>\n<p style=\"text-align: justify\">Symptoms of autoimmune polyglandular syndromes depend on the individual disorders present in the individual.<\/p>\n<h2 style=\"text-align: justify\"><b>How Do Autoimmune Polyglandular Syndromes Develop In Celiac Disease and\/or Gluten Sensitivity?<\/b><\/h2>\n<ul class=\"cp_check red\">\n<li>Autoimmune polyglandular syndromes type-2 and type-3 result from these three features shared by\u00a0the associated diseases:<\/li>\n<\/ul>\n<ul class=\"cp_bullet red\">\n<li>\n<p style=\"text-align: justify\">Common autoimmune mechanisms,<\/p>\n<\/li>\n<li>\n<p style=\"text-align: justify\">Genetic susceptibility, and<\/p>\n<\/li>\n<li>\n<p style=\"text-align: justify\">Favorable environmental factors.<a href=\"#footnote_19_469\" id=\"identifier_21_469\" class=\"footnote-link footnote-identifier-link\" title=\"Fracchia M, Galatola G, Corradi F, et al. Coeliac disease associated with Sjogren&rsquo;s syndrome, renal tubular acidosis, primary biliary cirrhosis and autoimmune hyperthyroidism.&nbsp;Digestive and Liver Disease: Official Journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver.&nbsp;Jul 2004;36(7):489-91.\">19<\/a><\/p>\n<\/li>\n<\/ul>\n<h2 style=\"text-align: justify\">Do Celiac Disease-Related Autoimmune Polyglandular Syndromes Respond To Gluten-Free Diet?<\/h2>\n<p style=\"text-align: justify\">Studies are inadequate to determine how a gluten free diet could delay or mitigate the course of autoimmune polyglandular syndromes in genetically predisposed subjects.<a href=\"#footnote_20_469\" id=\"identifier_22_469\" class=\"footnote-link footnote-identifier-link\" title=\"Femiano P, Castaldo V, Iossa C. Complex family association in autoimmune polyendocrine syndrome.&nbsp;Minerva Pediatrica. Apr 2003;55(2):163-70.\">20<\/a><\/p>\n<p style=\"text-align: justify\">Treatment involves life-long follow up and screening for another glandular failure in patients already diagnosed with APS.<\/p>\n<h2>6 Steps To Improve\u00a0Autoimmune Polyglandular Syndromes\u00a0In Celiac Disease and\/or Gluten Sensitivity:<\/h2>\n<ul class=\"cp_check green\">\n<li><em><span style=\"color: #800000\"><span class=\"dropcap\"><strong>1<\/strong><\/span><\/span><strong><span style=\"color: #800000\">Remove the Trigger. Maintain a Strict, Nutritious Gluten Free Diet:<\/span><\/strong><\/em><\/li>\n<\/ul>\n<p style=\"text-align: justify\"><div class=\"box shadow\"><div class=\"box-inner-block\"><i class=\"tieicon-boxicon\"><\/i>\n\t\t\t<b>Treatment<\/b>. This condition responds to the complete elimination of gluten, which is the required treatment that improves both \u00a0autoimmune disease and gut health.<\/p>\n<ul class=\"cp_bullet green\" style=\"text-align: justify\">\n<li>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.<\/li>\n<li>A strict gluten free diet means removing 100% of wheat, barley, rye and oats from the diet.<\/li>\n<li>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.<\/li>\n<\/ul>\n<p style=\"text-align: justify\"><strong>Correct Your Individual Nutritional Needs.<\/strong><\/p>\n<ul class=\"cp_bullet green\" style=\"text-align: justify\">\n<li>Eat foods that can replenish missing nutrients. Find them under\u00a0NUTRIENT DEFICIENCIES.<\/li>\n<li>Take nutritional supplements as needed.\u00a0Find them under\u00a0NUTRIENT DEFICIENCIES.<\/li>\n<\/ul>\n<p style=\"text-align: justify\"><strong>Recovery<\/strong>. You should begin to feel better within a week and notice more energy as inflammation subsides and the \u00a0absorbing cells that make up the surface lining of your small intestine are better able to function.<\/p>\n<ul class=\"cp_bullet green\" style=\"text-align: justify\">\n<li>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.<\/li>\n<li>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.<a href=\"#footnote_21_469\" id=\"identifier_23_469\" class=\"footnote-link footnote-identifier-link\" title=\"Cummins AG, Thompson FM, Butler RN, et al. Improvement in intestinal permeability precedes morphometric recovery of the small intestine in coeliac disease.&nbsp;Clinical Science. Apr 2001;100(4):379-86.\">21<\/a><\/li>\n<li>The intestinal lining may take up to a year to heal.\n\t\t\t<\/div><\/div><\/li>\n<\/ul>\n<ul class=\"cp_check green\" style=\"text-align: justify\">\n<li><em><span style=\"color: #800000\"><span class=\"dropcap\"><strong>2<\/strong><\/span><\/span><strong><span style=\"color: #800000\">\u00a0Reduce Inflammation. Foods to Eat and Foods Not to Eat:<\/span><\/strong><\/em><\/li>\n<\/ul>\n<p style=\"text-align: justify\">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).<\/p>\n<p style=\"text-align: justify\"><div class=\"box shadow\"><div class=\"box-inner-block\"><i class=\"tieicon-boxicon\"><\/i>\n\t\t\t<strong>Here Are Major Inflammatory Food Types That Reduce Healing<\/strong>:<\/p>\n<ul class=\"cp_bullet red\" style=\"text-align: justify\">\n<li><strong>Damaging Foods<\/strong>. In susceptible persons, includes corn, dairy (cow), and soy. Lactose, the sugar in any animal milk disrupts intestinal permeability causing leaky gut.<a href=\"#footnote_22_469\" id=\"identifier_24_469\" class=\"footnote-link footnote-identifier-link\" title=\"Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease.&nbsp;Journal of Gastroenterology and Hepatology. 2003;18:479-91.\">22<\/a><\/li>\n<li><strong>Allergenic Foods<\/strong>. Includes foods that trigger the immune sytem to produce IgE antibodies. Allergy testing is the usual way to discover these offending foods.<\/li>\n<li><strong>Shelf Stable Processed Foods.\u00a0<\/strong>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.<a href=\"#footnote_22_469\" id=\"identifier_25_469\" class=\"footnote-link footnote-identifier-link\" title=\"Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease.&nbsp;Journal of Gastroenterology and Hepatology. 2003;18:479-91.\">22<\/a><\/li>\n<li><strong>Fats.<\/strong>\u00a0Limit deep fried foods, trans-fats, saturated fats (animal fat\/butter), and EXCESSIVE omega-6 fatty acid oils like corn oil. Rancid fats, sodium caprate (a medium chain fat), and sucrose monester fatty acid (a food grade surfactant) induce significant disruption of the intestinal barrier that causes leaky gut.<a href=\"#footnote_22_469\" id=\"identifier_26_469\" class=\"footnote-link footnote-identifier-link\" title=\"Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease.&nbsp;Journal of Gastroenterology and Hepatology. 2003;18:479-91.\">22<\/a>.<\/li>\n<li><strong>Excessive Refined White Flours\u00a0<\/strong>(bran layer removed)<strong>.\u00a0<\/strong>Includes\u00a0products made from them such as cookies, bread, cakes, pies.\u00a0Bran contains the vitamins and minerals that metabolize grains and slows the otherwise rapid entry of sugar from their digestion into the bloodstream.\u00a0Also disrupt intestinal permeability causing leaky gut.<a href=\"#footnote_22_469\" id=\"identifier_27_469\" class=\"footnote-link footnote-identifier-link\" title=\"Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease.&nbsp;Journal of Gastroenterology and Hepatology. 2003;18:479-91.\">22<\/a><\/li>\n<li><strong>Refined Sugars.\u00a0<\/strong>\u00a0Includes white sugar, corn fructose and high fructose corn syrup.<\/li>\n<li><strong>Certain Spices<\/strong>. Includes paprika and cayenne pepper which disrupt intestinal permeability causing leaky gut.<a href=\"#footnote_22_469\" id=\"identifier_28_469\" class=\"footnote-link footnote-identifier-link\" title=\"Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease.&nbsp;Journal of Gastroenterology and Hepatology. 2003;18:479-91.\">22<\/a><\/li>\n<li><strong>Alcohol and Caffeine<\/strong>. Disrupt intestinal permeability causing leaky gut.<a href=\"#footnote_22_469\" id=\"identifier_29_469\" class=\"footnote-link footnote-identifier-link\" title=\"Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease.&nbsp;Journal of Gastroenterology and Hepatology. 2003;18:479-91.\">22<\/a><\/li>\n<li><strong>Cocoa and Black\u00a0Tea<\/strong>\u00a0increase blood sugar.<\/li>\n<li><strong>Rosemary.<\/strong>\u00a0Increases blood sugar levels and should not be used by persons with insulin resistance or diabetes. \n\t\t\t<\/div><\/div><\/li>\n<\/ul>\n<p style=\"text-align: justify\"><div class=\"box shadow\"><div class=\"box-inner-block\"><i class=\"tieicon-boxicon\"><\/i>\n\t\t\t<strong>Here Are Important Anti-Inflammatory Food Types to Promote Health<\/strong>:<\/p>\n<ul class=\"cp_bullet green\" style=\"text-align: justify\">\n<li><strong>Fruits<\/strong>.\u00a0Contain ample amounts of vitamins, minerals and phytochemicals which are\u00a0naturally occuring components in plants that detoxify toxins, carcinogens (reducing the risk by 50%) and mutagens.<\/li>\n<li><strong>Non-Starchy Vegetables.<\/strong>\u00a0Support 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.<\/li>\n<li><strong>High Quality Complex Carbohydrates<\/strong>. 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.<\/li>\n<li><strong>Antioxidants<\/strong>. Protect the body from inflammatory oxidant molecules that continually occur and\u00a0help 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\u00a0nuts, seeds, avocado, olive oil, and others. Cocoa is good, too.<\/li>\n<li><strong>Omega-3 Fatty Acids<\/strong>. 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.<\/li>\n<li><strong>Probiotics.\u00a0<\/strong>Supply normal microbes needed for colon health and health of the body such as these fermented foods: yogurt, kefir, and unpasteurized apple cider vinegar.<\/li>\n<li><strong>Prebiotics\/ High Fiber Foods<\/strong>. \u00a0Food with fiber keeps our population of colonic microbes healthy.<\/li>\n<li><strong>Protective Herbs and Spices<\/strong>. \u00a0See below #6 below for examples.\n\t\t\t<\/div><\/div><\/li>\n<\/ul>\n<ul class=\"cp_check green\" style=\"text-align: justify\">\n<li><em><span style=\"color: #800000\"><strong><span class=\"dropcap\">3<\/span>\u00a0Information Sheet You Can Take to Your Doctor or Other Health Professional:<\/strong><\/span><\/em><\/li>\n<\/ul>\n<p style=\"text-align: justify\">Click here.<\/p>\n<ul class=\"cp_check green\" style=\"text-align: justify\">\n<li><span style=\"color: #800000\"><strong><em><span class=\"dropcap\">4<\/span>\u00a0Manage Your Medications\u00a0Safely<\/em>:<\/strong><\/span><\/li>\n<\/ul>\n<p style=\"text-align: justify\"><div class=\"box shadow\"><div class=\"box-inner-block\"><i class=\"tieicon-boxicon\"><\/i>\n\t\t\t\n<p style=\"text-align: justify\">Certain medications promote inflammation and predispose to activation of autoimmune disease. Ask your doctor or pharmacist about this possible adverse effect if you are taking medications.<\/p>\n<p style=\"text-align: justify\">Also, some medication used to treat autoimmune diseases deplete nutrients. See below.<strong> Do not stop prescribed medications without supervision.<\/strong><\/p>\n<p style=\"text-align: justify\">This is not a complete listing.<\/p>\n<p><strong>ANTI-INFLAMMATORIES<\/strong>\u00a0disrupt intestinal permeability which complicates celiac disease.<\/p>\n<ul class=\"cp_bullet blue\">\n<li style=\"text-align: justify\">Corticosteroids (Prednisone, Medrol\u00ae, Aristocort\u00ae, Decadron) deplete Calcium, Vitamin D, Magnesium, Zinc, Vitamin C, Vitamin B6, Vitamin B12, Folic Acid, Selenium, Chromium, Phosphorus.<\/li>\n<li style=\"text-align: justify\">NSAIDS (Motrin\u00ae, Aleve\u00ae, Advil\u00ae, Anaprox\u00ae, Dolobid\u00ae, Feldene\u00ae, Naprosyn\u00ae and others) deplete\u00a0Folic acid.<\/li>\n<li style=\"text-align: justify\">Aspirin and Salicylates deplete\u00a0Calcium, Folic acid, Vitamin C, Iron, Pantothenate (vitamin B5).<\/li>\n<\/ul>\n<p style=\"text-align: justify\">\n\t\t\t<\/div><\/div>\n<ul class=\"cp_check green\" style=\"text-align: justify\">\n<li><em><span style=\"color: #800000\"><strong><span class=\"dropcap\">5<\/span>Nutritional Supplements To Help Correct Deficiencies:<\/strong><\/span><\/em><\/li>\n<\/ul>\n<p style=\"text-align: justify\"><div class=\"box shadow\"><div class=\"box-inner-block\"><i class=\"tieicon-boxicon\"><\/i>\n\t\t\t\n<p style=\"text-align: justify\">The type and quantity of nutritional supplements that may be needed depend on which nutrients are deficient.<\/p>\n<ul class=\"cp_bullet orange\" style=\"text-align: justify\">\n<li>Multivitamin\/mineral combination that provides 100% once a day is useful to improve overall nutrient levels. This is a safe dose, but always check with your doctor to avoid interactions with medications.<\/li>\n<\/ul>\n<p style=\"text-align: justify\"><strong>Storage Note<\/strong>:\u00a0<em>Store container tightly sealed, away from heat, moisture and direct light to avoid loss of potency. That is, in a safe kitchen cabinet &#8211; not in the bathroom or on the kitchen table<\/em>.\n\t\t\t<\/div><\/div>\n<ul class=\"cp_check green\" style=\"text-align: justify\">\n<li><span style=\"color: #800000\"><em><strong><span class=\"dropcap\">6<\/span>Manage Natural Remedies:\u00a0<\/strong><\/em><\/span><\/li>\n<\/ul>\n<p style=\"text-align: justify\"><div class=\"box shadow\"><div class=\"box-inner-block\"><i class=\"tieicon-boxicon\"><\/i>\n\t\t\t<strong>Hydration<\/strong>:<\/p>\n<ul class=\"cp_bullet green\" style=\"text-align: justify\">\n<li>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.<\/li>\n<li>If you are thirsty, drink water. Add fresh, squeezed lemon to water. Lemon is anti-inflammatory, alkalizing and provides vitamin C.<\/li>\n<li>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.<\/li>\n<li>What is wrong with soda, coffee, tea, and alcohol? These drinks are dehydrating, increase acid, and deplete nutrients.\n\t\t\t<\/div><\/div><\/li>\n<\/ul>\n<p style=\"text-align: justify\"><div class=\"box shadow\"><div class=\"box-inner-block\"><i class=\"tieicon-boxicon\"><\/i>\n\t\t\t<strong>Carminatives.\u00a0<\/strong>The following \u00a0anti-inflammatory\u00a0plant 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.<\/p>\n<p style=\"text-align: justify\"><strong>Carminative Food Remedies<\/strong>:<\/p>\n<ul class=\"cp_bullet green\" style=\"text-align: justify\">\n<li>Raspberry.<\/li>\n<li>Carrot is also a cleansing digestive tonic.<\/li>\n<li>Grape is also bile stimulating and a cleansing remedy for sluggish digestion and laxative.<\/li>\n<li>Redbeets also stimulate and improve digestion and are easily digested.<\/li>\n<li>Cabbage also stimulates and improves digestion and is also a liver decongestant.<\/li>\n<li>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.<\/li>\n<li>Potatoes are antispasmodic (due to atropine like properties) and a liver remedy.<\/li>\n<\/ul>\n<p style=\"text-align: justify\"><strong>Carminative Herb Remedies:<\/strong><\/p>\n<ul class=\"cp_bullet green\" style=\"text-align: justify\">\n<li>Sage is also a digestive, astringent, bile stimulant and energy tonic that heals the mucosa. \u00a0Drink as tea or use in cooking.<\/li>\n<li>Chamomile, lemon balm, and fennel, (as a tea) also help relieve nervous tension.<\/li>\n<li>Parsley also relieves indigestion.<\/li>\n<li>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. However, because it increases blood sugar levels, it should not be used by persons with insulin resistance or diabete.<\/li>\n<li>Thyme is also soothing remedy useful for stimulating digestion of rich, fatty foods.<\/li>\n<\/ul>\n<p style=\"text-align: justify\"><strong>Carminative Spice Remedies:<\/strong><\/p>\n<ul class=\"cp_bullet green\" style=\"text-align: justify\">\n<li>Cloves are also antispasmodic.<\/li>\n<li>Nutmeg is also useful for indigestion.<\/li>\n<li>Ginger.\n\t\t\t<\/div><\/div><\/li>\n<\/ul>\n<p style=\"text-align: justify\"><div class=\"box shadow\"><div class=\"box-inner-block\"><i class=\"tieicon-boxicon\"><\/i>\n\t\t\t<strong>Exercise Helps<\/strong>:<\/p>\n<p style=\"text-align: justify\">Exercise improves circulation and rids the body of toxins.<\/p>\n<ul class=\"cp_bullet green\" style=\"text-align: justify\">\n<li>Walking is aerobic exercise that reconditions the whole body to improve stamina.\u00a0Read more about<a href=\"https:\/\/glutenfreeworks.com\/health\/2014\/07\/08\/fitness-guide\/\">\u00a0Exercise and Fitness<\/a>.<\/li>\n<li>Weight training builds muscle.\u00a0Read more about\u00a0<a href=\"https:\/\/glutenfreeworks.com\/health\/2014\/07\/08\/fitness-guide\/\">Exercise and Fitness<\/a>.<\/li>\n<li>Stretching improves flexibilty.\u00a0Read more about\u00a0<a href=\"https:\/\/glutenfreeworks.com\/health\/2014\/07\/08\/fitness-guide\/\">Exercise and Fitness<\/a>.<\/li>\n<\/ul>\n<p style=\"text-align: justify\"><strong>Note<\/strong>: Exercise is important, but the amount and type of exercise undertaken depends on your health. Your first priority is to heal. \n\t\t\t<\/div><\/div>\n<h2 style=\"text-align: justify\">What Do Medical Research Studies Tell About Autoimmune Polyglandular Syndromes with Celiac Disease?<\/h2>\n<h4><strong>RESEARCH STUDY SUMMARIES<\/strong><\/h4>\n<p style=\"text-align: justify\"><b>\u201cScreening for autoimmune polyglandular syndrome in a cohort of patients with type 1 diabetes mellitus.\u201d<\/b> This study aimed to characterize a cohort of 151 patients with\u00a0type 1 diabetes mellitus\u00a0(T1DM) on the presence of other autoimmune disorders that could establish the diagnosis of autoimmune polyglandular syndrome (APS). The following clinical parameters were analyzed: gender, current age,\u00a0disease duration, previous history of autoimmune disorders, and familial history for diabetes mellitus. Each patient was analyzed to detect autoimmune markers of thyroiditis, adrenocortical insufficiency, gastritis, and\u00a0celiac disease, as well as possible associated dysfunctions.<\/p>\n<p style=\"text-align: justify\">A cohort with 51.7% males, average current age of 33.4 \u00b1 13 years and\u00a0disease\u00a0duration of 14.4 \u00b1 9.6 years was analyzed. Previous history of autoimmunity was found in 2%, and familial history for diabetes mellitus in 31.1% of the cohort. Frequency of autoimmune markers was 24% for thyroiditis, 9.4% for adrenocortical insufficiency, 17.2% for gastritis, and 2% for\u00a0celiac disease. APS was diagnosed on 25.2% of the patients. APS and autoimmune thyroiditis risk was higher in females.\u00a0Disease\u00a0duration correlated directly with gastric autoantibodies, and inversely with positive islet cell, glutamic acid decarboxylase, and tyrosine phosphatase antibodies. There was a correlation between autoimmune markers for thyroiditis and gastritis, as well as between\u00a0celiac disease\u00a0and adrenocortical insufficiency. Considering APS prevalence and prognosis, the need for APS screening in patients with T1DM is emphasized.<a href=\"#footnote_23_469\" id=\"identifier_30_469\" class=\"footnote-link footnote-identifier-link\" title=\"Gouveia S, Gomes L, Ribeiro C, Carrilho F. Screening for autoimmune polyglandular syndrome in a cohort of patients with type 1 diabetes mellitus. Arq Bras Endocrinol Metabol. 2013 Dec;57(9):733-8.\">23<\/a><\/p>\n<p style=\"text-align: justify\"><b>\u201cClinical profile of coexisting conditions in type 1 diabetes mellitus patients.\u201d<\/b> This study investigating Type 1 diabetes mellitus\u00a0(T1DM) for various genetic and autoimmune diseases implicated in its etiopathogenesis found that various conditions including genetic (Down, Turner, Noonan, and Klinefelter&#8217;s), autoimmune (thyroid and adrenal disorders, myasthenia gravis, SLE, rheumatoid arthritis) and central nervous system diseases were the associated diseases encountered in our patients.<\/p>\n<p style=\"text-align: justify\">Consecutive patients of T1DM presenting to department of Endocrinology from May 1997 to December 2011 were retrospectively analyzed in context of associated clinical profile. Among 260 patients diagnosed as T1DM, 21 (8%) had hypothyroidism, 4 (1.5%) had hyperthyroidism and 2 (0.7%) had primary adrenal insufficiency. Eighteen patients (7%) had\u00a0celiac disease, 9 (3.5%) had Turner&#8217;s syndrome, 5 patients (1.9%) had Klinefelter&#8217;s syndrome, whereas Down&#8217;s syndrome and Noonan&#8217;s syndrome was present in 2 and 1 patients (0.7%) respectively. One patient had Wolframs&#8217; syndrome and 1 patient had myasthenia gravis. Systemic lupus erythematosus and rheumatoid arthritis were present in 3 and 1 patients respectively. Total of 5 patients with cerebral palsy, 4 cases with deaf mutism, 4 cases with acute psychosis and 16 patients with depression were noted. Mean age of study patients was 20.8\u00b19.8 years (range, 3-23 years). Routine screening is required for early diagnosis and treatment of associated co morbidities.<a href=\"#footnote_24_469\" id=\"identifier_31_469\" class=\"footnote-link footnote-identifier-link\" title=\"Kota SK, Meher LK, Jammula S, Kota SK, Modi KD. Clinical profile of coexisting conditions in type 1 diabetes mellitus patients. Diabetes Metab Syndr. 2012 Apr-Jun;6(2):70-6. doi: 10.1016\/j.dsx.2012.08.006.\">24<\/a><\/p>\n<p style=\"text-align: justify\"><strong>&#8220;Celiac disease in North Italian patients with autoimmune Addison&#8217;s disease.&#8221;<\/strong>\u00a0This study aiming to define the prevalence of celiac disease and of IgA deficiency in a group of Italian patients with autoimmune Addison\u2019s disease (AAD) found that in patients with AAD there is a high prevalence of both celiac disease and IgA deficiency.<\/p>\n<p style=\"text-align: justify\">One hundred and nine patients with AAD were enrolled and examined for tissue transglutaminase autoantibodies of the IgA class, circulating levels of IgA and adrenal cortex antibodies. Two (1.8%) of the patients were affected by already diagnosed celiac disease and were already on a gluten-free diet. Out of the remaining 107 patients, four (3.7%) were found to be positive for IgA antibodies to human tissue transglutaminase. Three of the four patients who were positive for tissue transglutaminase autoantibodies agreed to undergo endoscopy and duodenal biopsies and, in one, a latent form of celiac disease was identified. 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%.<\/p>\n<p style=\"text-align: justify\">Specifically, celiac disease was present in 12.5% of the\u00a0autoimmune polyglandular syndrome\u00a0(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 AAD 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.<a href=\"#footnote_25_469\" id=\"identifier_32_469\" class=\"footnote-link footnote-identifier-link\" title=\"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&rsquo;s disease. Eur J Endocrinol. 2006 Feb;154(2):275-9.\">25<\/a><b>\u00a0<\/b><\/p>\n<h4 style=\"text-align: justify\"><strong>CASE REPORT SUMMARIES<\/strong><\/h4>\n<p style=\"text-align: justify\"><strong>\u201cMultiple Disease Associations in Autoimmune Polyglandular Syndrome Type II. \u201c<\/strong> This case report describes the course of a patient with autoimmune polyglandular syndrome type II (APS II) \u00a0with a dramatic development of eight autoimmune diseases over the course of ten years. She developed Addison&#8217;s disease, hypothyroidism, type 1 diabetes, Hashimoto&#8217;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.<\/p>\n<p style=\"text-align: justify\">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&#8217;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&#8217;s disease, vitiligo, sero-negative arthritis, and hypothyroidism.<a href=\"#footnote_26_469\" id=\"identifier_33_469\" class=\"footnote-link footnote-identifier-link\" title=\"Maturu A, Michels A, Draznin B. Multiple Disease Associations in Autoimmune Polyglandular Syndrome Type II. Endocr Pract. 2014 Aug 22:1-13.\">26<\/a><\/p>\n<p style=\"text-align: justify\"><b>\u201cDermatitis herpetiformis co-localised with vitiligo in a patient with autoimmune polyglandular syndrome.\u201d\u00a0<\/b>This case report describes the unusual presentation of dermatitis herpetiformis co-localised with segmental\u00a0vitiligo\u00a0in a 37-year-old woman with a background history of autoimmune polyglandular syndrome type 2.<\/p>\n<p style=\"text-align: justify\">The patient presented with a 3-day history of a severe, itchy, bullous eruption on the trunk and limbs associated with malaise. Her past medical history included Addison\u2019s disease, autoimmune hypothyroidism, type 1 diabetes mellitus, coeliac disease and vitiligo. Coeliac disease was diagnosed following distal duodenal biopsy which demonstrated subtotal villous atrophy. The patient reported strict adherence to a gluten-free diet. Vitiligo on the limbs, trunk, and neck was treated with moderate potency topical corticosteroids fourteen years prior to this acute presentation.<\/p>\n<p style=\"text-align: justify\">On examination, multiple, well-demarcated, segmental areas of depigmentation were present on the forearms, neck, groin, and upper thighs. There were vesicles and bullae of up to 20 mm in diameter with adjacent crusted, erythematous papules exclusively within the depigmented areas but not within the\u00a0pigmented patches. She was managed with a gluten-free diet and hydroxyzine 25 mg when required. We propose genetic mosaicism as a possible mechanism. There has only been one previous case report in which dermatitis hepetiformis co-localised in close proximity but not exclusively within vilitigo in a patient with autoimmune thyroiditis.<a href=\"#footnote_27_469\" id=\"identifier_34_469\" class=\"footnote-link footnote-identifier-link\" title=\"Macbeth AE, Lee KY, Levell NJ, Igali L, Millington GW. Photoletter to the editor: Dermatitis herpetiformis co-localised with vitiligo in a patient with autoimmune polyglandular syndrome.&nbsp;J Dermatol Case Rep.&nbsp;2013 Sep 30;7(3):101-2. doi: 10.3315\/jdcr.2013.1153.\">27<\/a><\/p>\n<p style=\"text-align: justify\"><strong>&#8220;Treatment-refractory hypothyroidism.&#8221;<\/strong> This case report describes diagnosing celiac disease and subsequent 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\u2019s 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\u20134.5) mU\/L, and the dose of levothyroxine he was prescribed had been increased to 225 \u03bcg per day, or 2.7 (usual recommended dose 1.6) \u03bcg\/kg daily.<\/p>\n<p style=\"text-align: justify\">The patient\u2019s 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.<\/p>\n<p style=\"text-align: justify\">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 &lt; 9.0, borderline 9\u201316, positive &gt; 16.0) units\/mL. A subsequent endoscopic biopsy of the patient\u2019s bowel was consistent with a diagnosis of celiac disease. The patient was directed to follow a low-gluten diet. The patient\u2019s histological abnormalities resolved, and his serum level of TSH normalized with his usual dose of thyroxine (225 \u03bcg daily).<\/p>\n<p style=\"text-align: justify\">Because of the patient\u2019s previous Grave\u2019s 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.<a href=\"#footnote_28_469\" id=\"identifier_35_469\" class=\"footnote-link footnote-identifier-link\" title=\"Ramadhan A, Tamilia M. Treatment-refractory hypothyroidism. CMAJ. 2012 Feb 7;184(2):205-9. doi: 10.1503\/cmaj.110994.\">28<\/a><\/p>\n<p style=\"text-align: justify\">&#8220;<strong>Multiple immune disorders in unrecognized celiac disease: a case report<\/strong>.&#8221; This case report describes the course of a 34 year old female patient with unrecognized celiac disease and multiple extra intestinal manifestations, mainly related to a deranged immune function, including macroamilasemia, macrolipasemia, IgA nephropathy, thyroiditis, and anti-b2-glicoprotein-1 antibodies, that disappeared or improved after the implementation of a gluten-free diet.<\/p>\n<p style=\"text-align: justify\">After six months of controlled gluten free diet, the patient&#8217;s body weight increased 12 kg; laboratory investigations demonstrated normalization of serum amylase, serum lipase and immunoglobulin levels; antigliadin, anti-\uf0622-glicoprotein-1 and anti-thyreoglobulin antibodies were no longer detectable, but antiendomysial antibodies were still present. Endoscopy showed a normal appearance of duodenal mucosa, and duodenal biopsy revealed a partial recovery of duodenal morphology. Due to the persistence of proteinuria (2.3 g\/day), microscopic hematuria and hyaline and granular casts, a kidney biopsy showed that it was IgA nephropathy.\u00a0After 18 months of gluten-free diet, antiendomysial antibodies disappeared; creatinine clearance increased, but proteinuria further worsened (2.9 g\/day, Table 1), and albumin levels were still low.\u00a0After 24 months of gluten-free diet, a new duodenal biopsy showed complete recovery of villous architecture. Renal function further improved and proteinuria markedly decreased (Table 1). Amylase, lipase, and immunoglobulin levels were within the normal range. Anti-\uf0622-glicoprotein-1, anti-thyreoglobulin, antigliadin, antiendomysial and anti-TTG antibodies were undetectable. A coagulation study was normal.<\/p>\n<p style=\"text-align: justify\">&#8220;Although both celiac disease and the other manifestations of a deranged immunity might be explained on the basis of a common genetic predisposition to this kind of disorders, some findings suggest that celiac disease itself is responsible for the initiation of the immunological response. Indeed, persistent stimulation by some proinflammatory cytokines, such as interferon \uf067 and tumor necrosis factor \uf061, could induce further processing of autoantigens and their presentation to T lymphocytes by macrophage-type immunocompetent cells. As a matter of fact, the prevalence of immune diseases among patients with\u00a0celiac disease\u00a0seems proportional to the time of exposure to gluten, and many immune alterations disappear following the recognition of\u00a0celiac disease\u00a0and appropriate treatment, just as it occurred in this patient.&#8221;<a href=\"#footnote_29_469\" id=\"identifier_36_469\" class=\"footnote-link footnote-identifier-link\" title=\"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.&nbsp;World J Gastroenterol&nbsp;2003; 9(6): 1377-1380.\">29<\/a><\/p>\n<p style=\"text-align: justify\"><strong>\u201cWe report on a 19-year-old woman with\u00a0polyglandular\u00a0autoimmune\u00a0syndrome\u00a0type II (APS II).\u201d<\/strong>\u00a0This case report describes diagnosing autoimmune polyglandular syndrome type-2 in a patient who was diagnosed with Addison&#8217;s\u00a0disease\u00a0and hypothyroidism due to chronic\u00a0autoimmune\u00a0thyroiditis. Her mother had\u00a0celiac disease\u00a0and her brother had diabetes mellitus type 1. Chronic autoimmune\u00a0thyroiditis was diagnosed in her mother, subsequently. In patients and their relatives, who have\u00a0autoimmune\u00a0disorders, a search for autoimmune polyglandular syndrome\u00a0is crucial. Consequently, it would be appropriate that the patient and all family members are asked for clinical signs and symptoms of\u00a0autoimmune\u00a0disorders.<\/p>\n<p style=\"text-align: justify\">Annual measurement of morning cortisol, TSH and fasting plasma glucose may useful. Screening of affected individuals as well as their first-degree relatives for\u00a0celiac disease\u00a0is recommended. Therapy of APS II consists of hormone replacement therapy, but thyroxin replacement may induce life-threatening adrenal failure in a patient with untreated Addison&#8217;s\u00a0disease. Thus, in case of doubt hydrocortisone should be given before the thyroxine administration is started.<a href=\"#footnote_10_469\" id=\"identifier_37_469\" class=\"footnote-link footnote-identifier-link\" title=\"Lipowsky C, Schorl-Schweikardt BA, Kehl O, Br&auml;ndle M. 19-year-old patient with adrenal cortex insufficiency&ndash;only the tip of the iceberg. Polyendocrine autoimmune syndrome type II (Schmidt syndrome). Praxis (Bern 1994). 2008 Jan 23;97(2):77-81.\">10<\/a><\/p>\n<p style=\"text-align: justify\"><b>\u201cCoeliac disease associated with Sjogren&#8217;s syndrome, renal tubular acidosis, primary biliary cirrhosis and autoimmune hyperthyroidism.\u201d<\/b>\u00a0This case report of a patient diagnosed with biliary cirrhosis, Sjogren&#8217;s syndrome, and renal tubular acidosis who developed diarrhea and weight loss, describes subsequent diagnosis of celiac disease.\u00a0She went on to develop autoimmune hyperthyroidism despite a gluten free diet.<a href=\"#footnote_30_469\" id=\"identifier_38_469\" class=\"footnote-link footnote-identifier-link\" title=\"Fracchia M, Galatola G, Corradi F, et al. Coeliac disease associated with Sjogren&rsquo;s syndrome, renal tubular acidosis, primary biliary cirrhosis and autoimmune hyperthyroidism.&nbsp;Digestive and Liver Disease: Official Journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver. Jul 2004;36(7):489-91.\">30<\/a><\/p>\n<ol class=\"footnotes\"><li id=\"footnote_1_469\" class=\"footnote\">W\u00e9meau JL, Proust-Lemoine E, Ryndak A, Vanhove L. Thyroid autoimmunity and polyglandular endocrine syndromes. <em>Hormones (Athens)<\/em>. 2013 Jan-Mar;12(1):39-45.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_1_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_2_469\" class=\"footnote\">Femiano P, Castaldo V, Iossa C. Complex family association in autoimmune polyendocrine syndrome.\u00a0<\/span><i style=\"line-height: 1.5em\">Minerva Pediatrica<\/i><span style=\"line-height: 1.5em\">. Apr 2003;55(2):163-70.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_2_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_3_469\" class=\"footnote\">W\u00e9meau JL, Proust-Lemoine E, Ryndak A, Vanhove L. Thyroid autoimmunity and polyglandular endocrine syndromes. <\/span><i style=\"line-height: 1.5em\">Hormones (Athens)<\/i><span style=\"line-height: 1.5em\">. 2013 Jan-Mar;12(1):39-45.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_3_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_4_469\" class=\"footnote\">http:\/\/autoimmune.pathology.jhmi.edu\/diseases.cfm?systemID=3&amp;DiseaseID=66<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_4_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_5_469\" class=\"footnote\">W\u00e9meau JL, Proust-Lemoine E, Ryndak A, Vanhove L. Thyroid autoimmunity and polyglandular endocrine syndromes. <i>Hormones (Athens)<\/i>. 2013 Jan-Mar;12(1):39-45.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_5_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_6_469\" class=\"footnote\">W\u00e9meau JL, Proust-Lemoine E, Ryndak A, Vanhove L. Thyroid autoimmunity and polyglandular endocrine syndromes.\u00a0<i>Hormones (Athens)<\/i>. 2013 Jan-Mar;12(1):39-45.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_6_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_7_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_7_469\" class=\"footnote\">http:\/\/autoimmune.pathology.jhmi.edu\/diseases.cfm?systemID=3&amp;DiseaseID=67<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_8_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_14_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_8_469\" class=\"footnote\"><\/span><span style=\"line-height: 1.5em\"><a href=\"http:\/\/www.dundee.ac.uk\/medther\/tayendoweb\/images\/polyglandular.htm)\">http:\/\/www.dundee.ac.uk\/medther\/tayendoweb\/images\/polyglandular.htm<\/a><span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_9_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_9_469\" class=\"footnote\">MAJERONI BA and PATEL P. Autoimmune Polyglandular Syndrome, Type II. <i>Am Fam Physician<\/i>. 2007 Mar 1;75(5):667-670.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_10_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_10_469\" class=\"footnote\">Lipowsky C, Schorl-Schweikardt BA, Kehl O, Br\u00e4ndle M. 19-year-old patient with adrenal cortex insufficiency&#8211;only the tip of the iceberg. Polyendocrine autoimmune syndrome type II (Schmidt syndrome). <i>Praxis<\/i> (Bern 1994). 2008 Jan 23;97(2):77-81.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_11_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_37_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_11_469\" class=\"footnote\"><a href=\"http:\/\/autoimmune.pathology.jhmi.edu\/diseases.cfm?systemID=3&amp;DiseaseID=68)\">http:\/\/autoimmune.pathology.jhmi.edu\/diseases.cfm?systemID=3&amp;DiseaseID=68<\/a><span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_12_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_12_469\" class=\"footnote\">Van den Driessche A, Eenkhoorn V, Van Gaal L, De Block C. Type 1 diabetes and autoimmune polyglandular syndrome: a clinical review. <em>Neth J Med<\/em>. 2009 Dec;67(11):376-87.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_13_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_13_469\" class=\"footnote\">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.\u00a0<em>World J Gastroenterol<\/em>.\u00a02003;9(6):1377-1380.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_15_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_14_469\" class=\"footnote\">Iughetti L, Bulgarelli S, Forese S, Lorini R, Balli F, Bernasconi S. Endocrine aspects of coeliac disease.\u00a0<em>Journal of Pediatric Endocrinology &amp; Metabolism : JPEM<\/em>. Jul-Aug 2003;16(6):805-18.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_16_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_15_469\" class=\"footnote\">Femiano P, Castaldo V, Iossa C. Complex family association in autoimmune polyendocrine syndrome.\u00a0<em>Minerva Pediatrica<\/em>. Apr 2003;55(2):163-70.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_17_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_16_469\" class=\"footnote\">Lipowsky C, Schorl-Schweikardt BA, Kehl O, Br\u00e4ndle M. 19-year-old patient with adrenal cortex insufficiency&#8211;only the tip of the iceberg. Polyendocrine autoimmune syndrome type II (Schmidt syndrome).\u00a0<i>Praxis<\/i>\u00a0(Bern 1994). 2008 Jan 23;97(2):77-81.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_18_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_17_469\" class=\"footnote\">Iughetti L, Bulgarelli S, Forese S, Lorini R, Balli F, Bernasconi S. Endocrine aspects of coeliac disease.\u00a0<i>Journal of Pediatric Endocrinology &amp; Metabolism : JPEM.<\/i>\u00a0Jul-Aug 2003;16(6):805-18.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_19_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_18_469\" class=\"footnote\">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&#8217;s disease. <em>Eur J Endocrinol<\/em>. 2006 Feb;154(2):275-9.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_20_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_19_469\" class=\"footnote\">Fracchia M, Galatola G, Corradi F, et al. Coeliac disease associated with Sjogren&#8217;s syndrome, renal tubular acidosis, primary biliary cirrhosis and autoimmune hyperthyroidism.\u00a0<i>Digestive and Liver Disease: Official Journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver.<\/i>\u00a0Jul 2004;36(7):489-91.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_21_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_20_469\" class=\"footnote\">Femiano P, Castaldo V, Iossa C. Complex family association in autoimmune polyendocrine syndrome.\u00a0<i>Minerva Pediatrica<\/i>. Apr 2003;55(2):163-70.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_22_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_21_469\" class=\"footnote\">Cummins AG, Thompson FM, Butler RN, et al. Improvement in intestinal permeability precedes morphometric recovery of the small intestine in coeliac disease.\u00a0<em>Clinical Science<\/em>. Apr 2001;100(4):379-86.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_23_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_22_469\" class=\"footnote\">Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease.\u00a0<em>Journal of Gastroenterology and Hepatology<\/em>. 2003;18:479-91.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_24_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_25_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_26_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_27_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_28_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_29_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_23_469\" class=\"footnote\">Gouveia S, Gomes L, Ribeiro C, Carrilho F. Screening for autoimmune polyglandular syndrome in a cohort of patients with type 1 diabetes mellitus. <i>Arq Bras Endocrinol Metabol.<\/i> 2013 Dec;57(9):733-8.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_30_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_24_469\" class=\"footnote\">Kota SK, Meher LK, Jammula S, Kota SK, Modi KD. Clinical profile of coexisting conditions in type 1 diabetes mellitus patients. <i>Diabetes Metab Syndr<\/i>. 2012 Apr-Jun;6(2):70-6. doi: 10.1016\/j.dsx.2012.08.006.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_31_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_25_469\" class=\"footnote\">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&#8217;s disease. <em>Eur J Endocrinol.<\/em> 2006 Feb;154(2):275-9.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_32_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_26_469\" class=\"footnote\">Maturu A, Michels A, Draznin B. Multiple Disease Associations in Autoimmune Polyglandular Syndrome Type II.<em> Endocr Pract<\/em>. 2014 Aug 22:1-13.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_33_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_27_469\" class=\"footnote\">Macbeth AE, Lee KY, Levell NJ, Igali L, Millington GW. Photoletter to the editor: Dermatitis herpetiformis co-localised with vitiligo in a patient with autoimmune polyglandular syndrome.\u00a0<i>J Dermatol Case Rep.<\/i>\u00a02013 Sep 30;7(3):101-2. doi: 10.3315\/jdcr.2013.1153.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_34_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_28_469\" class=\"footnote\">Ramadhan A, Tamilia M. Treatment-refractory hypothyroidism. <em>CMAJ<\/em>. 2012 Feb 7;184(2):205-9. doi: 10.1503\/cmaj.110994.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_35_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_29_469\" class=\"footnote\">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.\u00a0<em>World J Gastroenterol<\/em>\u00a02003; 9(6): 1377-1380.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_36_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><li id=\"footnote_30_469\" class=\"footnote\">Fracchia M, Galatola G, Corradi F, et al. Coeliac disease associated with Sjogren&#8217;s syndrome, renal tubular acidosis, primary biliary cirrhosis and autoimmune hyperthyroidism.<i>\u00a0Digestive and Liver Disease: Official Journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver<\/i>. Jul 2004;36(7):489-91.<span class=\"footnote-back-link-wrapper\"> [<a href=\"#identifier_38_469\" class=\"footnote-link footnote-back-link\">&#8617;<\/a>]<\/span><\/li><\/ol>","protected":false},"excerpt":{"rendered":"<p>What Are Autoimmune Polyglandular Syndromes? Autoimmune polyglandular syndromes (APS) are rare clusterings of two or more endocrine and non-endocrine autoimmune disorders in the same affected person. Polyglandular is somewhat of a misnomer since many of the manifestations of the diseases do not concern endocrine glands.1 Endocrine autoimmune disorders involve the abnormal production of autoantibodies that\u00a0target &#8230;<\/p>\n","protected":false},"author":29,"featured_media":6496,"comment_status":"open","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_monsterinsights_skip_tracking":false,"_monsterinsights_sitenote_active":false,"_monsterinsights_sitenote_note":"","_monsterinsights_sitenote_category":0,"footnotes":""},"categories":[4,173,779,408,969,55],"tags":[831,1027,101,79,832,844,508,1265,235,776,1266,1264,1263,1267,848,1499,1138,871],"class_list":["post-469","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-health-conditions-2","category-antibodies","category-associated-disorder","category-autoimmune","category-genetic","category-immune-2","tag-addisons-disease","tag-alopecia","tag-associated-disorders","tag-autoantibodies","tag-autoimmune-hepatitis","tag-autoimmune-polyglandular-syndromes","tag-autoimmune-thyroiditis","tag-chronic-candida-infection","tag-exocrine-glands","tag-health-conditions","tag-hypoparathyroidism","tag-myasthenia-gravis","tag-pernicious-anemia","tag-premature-menopause","tag-sjogrens-syndrome","tag-system-immune","tag-type1-diabetes-mellitus","tag-vitiligo"],"_links":{"self":[{"href":"https:\/\/glutenfreeworks.com\/health\/wp-json\/wp\/v2\/posts\/469","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/glutenfreeworks.com\/health\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/glutenfreeworks.com\/health\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/glutenfreeworks.com\/health\/wp-json\/wp\/v2\/users\/29"}],"replies":[{"embeddable":true,"href":"https:\/\/glutenfreeworks.com\/health\/wp-json\/wp\/v2\/comments?post=469"}],"version-history":[{"count":41,"href":"https:\/\/glutenfreeworks.com\/health\/wp-json\/wp\/v2\/posts\/469\/revisions"}],"predecessor-version":[{"id":18816,"href":"https:\/\/glutenfreeworks.com\/health\/wp-json\/wp\/v2\/posts\/469\/revisions\/18816"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/glutenfreeworks.com\/health\/wp-json\/wp\/v2\/media\/6496"}],"wp:attachment":[{"href":"https:\/\/glutenfreeworks.com\/health\/wp-json\/wp\/v2\/media?parent=469"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/glutenfreeworks.com\/health\/wp-json\/wp\/v2\/categories?post=469"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/glutenfreeworks.com\/health\/wp-json\/wp\/v2\/tags?post=469"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}