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Hypocalciuria (Low Urine Calcium)

IgA Molecule.
Depiction of the IgA Molecule

What Is IgA Deficiency?

[dropcap]I gA deficiency (IgAD) is an immunodeficiency disease characterized by lack of immunoglobulin A type antibody production, called IgA antibody, with no detectable levels in blood or secretions.

Q: What is an IgA antibody?

A: IgA is an antibody of the immune system that is secreted by plasma cells (specialized white blood cells) through epithelial cell linings of mucosal surfaces into mucosa secretions to protect the lining from microbe invasion.

In fact, immunoglobulin class A is the main protein of the mucosal immune system. This includes mucosa of the eye surface, digestive tract, respiratory tract, urinary tract, and genital tract.

Both major histocompatibility complex (MHC) and non-MHC genes contribute to susceptibility to the disease. The former genes appear to be located in different parts of the MHC region depending on the HLA haplotype. The latter show a marked overlap with genes associated with a variety of autoimmune disorders including Graves’ disease, systemic lupus erythematosus, type 1 diabetes and celiac disease, suggesting common pathophysiological mechanisms. The involvement of genes associated with autoimmunity may suggest that IgAD in itself is an autoimmune disease.1

IgA deficiency may progress into a common variable immunodeficiency (CVID).2

What Is IgA Deficiency (IgAD) In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Wang N, Hammarström L. IgA deficiency: what is new? Curr Opin Allergy Clin Immunol. 2012 Dec;12(6):602-8. doi: 10.1097/ACI.0b013e3283594219. [↩]
  2. Binek A, Jarosz-Chobot P.Selective immunoglobulin A deficiency. Pediatr Endocrinol Diabetes Metab. 2012;18(2):76-8. [↩]

Night Blindness – Nyctalopia

What Is Steatorrhea?

[dropcap]S teatorrhea is a condition of abnormal stool composition and consistency that is due to high fat content because fat from food is not  digested and absorbed into the body but rather passes out with stool.1

Q: How does fatty stool look?

A: The stool in steatorrhea appears pale, bulky and may float in the toilet. If stool is loose, it varies from a pudding consistency to whipped cream. If it is solid, it can vary from thin sqiggles to big turds that smear the sides of the toilet bowl. All types have a foul smell.

Fat of any kind must be digested, or broken down, by enzymes into fatty acids and glycerol and then these parts only are absorbed through the small intestinal lining into the body. The failure to digest or absorb fats deprives the body of these foodstuffs needed for many functions such as blood clotting and vital cell parts such as eye and brain structure.

Fat malabsorption produces malabsorption of vitamins A, D, E, and K because these vitamins can only be absorbed along with fatty acids.

What Is Steatorrhea In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Murray JA, The widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999;69 (3):354-365. [↩]

IgA Nephropathy

X-ray of lungs in sacroidosis showing honeycoming. Courtesy Wikimedia.
X-ray of Lungs in Sacroidosis Showing Honeycoming. Courtesy Wikimedia.

What Is Sarcoidosis?

[dropcap]S arcoidosis is a multisystem granulomatous disease characterized by hard granulomas and inflammation of the alveoli in lungs that occurrs in 80% of patients.

Alveoli are the tiny one cell thick round structures that are clustered at the ends of air passages in the lungs where oxygen from air inhaled is exchanged for carbon dioxide from blood which is breathed out.

Q: What are granulomas?

A: Granulomas are collections of macrophages (white blood cells) that targeted and enclosed but failed to destroy a foreign substance that entered the body.  In turn, the macrophages become encased by other immune cells and fibroblasts and collagen. They can occur in any organ.

Presently, the etiology, or cause, of sarcoidosis is unknown, although it is thought the predisposition is genetic with a local immune mechanism. This disease has flares when active and remissions when symptoms subside.

Referral to a specialist is important for proper treatment and monitoring. The main treatment for severe active sarcoidosis is prednisone, a type of steroid that reduces inflammation in the body. In most people, prednisone relieves symptoms within a couple of months, although most people need to take prednisone for 12 months or longer. Long-term use of prednisone, especially at high doses, can cause serious side effects. Side effects include bone loss, elevated blood sugar, and high blood pressure.

When wheezing and coughing are a problem, inhaler devices are used to deliver medicine into the lungs in order to help open the airways.1

Ibuprofen is prescribed if sarcoidosis is causing joint pain. Steroid creams are prescribed for skin problems.

Sarcoidosis affects 10 to 20 person per 100,000.

What Is Sarcoidosis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. National Heart, Lung, and Blood Institute [↩]

Ocular Myopathy

What Is Primary Hyperparathyroidism?

Tissue changes in hyperparathyroidism. Courtesy Quizlet.com
Tissue Changes in Hyperparathyroidism Causing Brown Tumor. Courtesy Quizlet.com

[dropcap]P rimary hyperparathyroidism is a parathyroid disorder characterized by excessive secretion of parathyroid hormone by one or more parathyroid glands for more than 6 months.

In primary hyperparathyroidism, blood calcium levels are high while phosphorus levels are decreased due to the action of parathyroid hormone.

Parathyroid hormone is produced by the four pea sized parathyroid glands that are located on the thyroid gland in the front of the neck. Partly because the thyroid and parathyroid glands share the same anatomic place in the body and partly because they have similar names, they are often confused although they have completely different actions.

Parathyroid hormone normally keeps calcium and the opposing mineral phosphorus levels in balance by drawing calcium as needed from bones to increase it in blood and releasing excess phosphorus through the kidneys to decrease blood levels.

Primary hyperparathyroidism is commonly caused by an adenoma (tumor) in a parathyroid gland (80%) or 15% due to hyperplasia of gland tissue (overgrowth). It is seldom associated with autoimmune disorders. However, cancer is a  possibility.

Q: What is a parathyroid adenoma?

A: A parathyroid adenoma is usually a solitary, well circumscribed, soft, tan reddish-brown nodule with a capsule. Gland tissues outside of the adenoma are normal or slightly shrunken (not needed anymore).1

Untreated, primary hyperparathyroidism results in cyst formations in bone marrow (osteitis fibrosa cystica) and brown tumors in bone tissue. Cysts contain large amounts of fibrous tissue with areas of hemorrhage. Brown tumors contain aggregates of osteoclasts (bone cells), hemorrhage and giant cells resembling neoplasms.2

Here is the symptomatolgy: “Painful Bones, Renal Stones, Abdominal Groans, and Mental Moans.”

What Is Primary Hyperparathyroidism In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. http://quizlet.com/32428692/pathology-of-parathyroid-and-bone-flash-cards [↩]
  2. http://quizlet.com/32428692/pathology-of-parathyroid-and-bone-flash-cards/ [↩]

Kidney Stones (Renal Calculi)

Testing the Eyes for Sjogren's Syndrome.
Testing the Eye for Tear Production (L) and Damage to Conjunctiva from Dryness (R).

What Is Sjögren’s Syndrome?

[dropcap]S jögren’s syndrome is a systemic inflammatory autoimmune disease with a chronic, progressive course that primarily attacks the lacrimal glands of the eye and the salivary glands of the mouth, which are exocrine glands. Exocrine glands secrete the substances they produce through a duct.

Sjögren’s syndrome is ordinarily characterized by dysfunction of the lacrimal glands to produce tears causing dry eye and the salivary glands to produce saliva causing dry mouth, but is not limited by or to these features.

Besides involvement of these exocrine glands, there may be involvement of other parts of the body, termed extraglandular, which may be more severe than eye or mouth features.

There is not yet agreement on classifying Sjögren’s syndrome. Primary and secondary are the two forms generally accepted.1 Both forms can cause mild to severe disease, called the spectrum:

  • Primary Sjögren syndrome. Disease occurs without involvement of other linked autoimmune disorders. In addition to the eyes and mouth, the nose, throat and skin may also be affected and joints, lungs, kidneys, blood vessels, digestive organs and nerves as well.2 Systemic manifestations (other than eyes and mouth) concern a third of patients, including lymphoma in 5% of the patients.3
  • Secondary Sjögren’s syndrome. Disease complicates other autoimmune disease such as systemic lupus erythematosus, rheumatoid arthritis, primary biliary cirrhosis, and celiac disease.

Diagnosis  of Sjögren’s syndrome is made by most doctors based on Schimer’s test for tears and unstimulated whole salivary flow to assess objective eye and oral involvement, since these are the tests most physicians use in clinical practice.4 Specific antibody tests would be  positive for anti-Ro (SSA)/anti-La (SSB) autoantibodies. Sjögren’s syndrome should also be considered when extraglandular manifestations such as vasculitis, polyneuropathy or arthritis occur, even when the patients do not complain of dry eyes and mouth.5

There is no cure for Sjögren’s syndrome. Treatment is aimed to diminish symptoms. For example, steroids and Ibupropen are used to decrease inflammation and pain in joints. Artificial tears and ointments are used for dry eye.

Most people who develop Sjogren’s syndrome are older than 40 years. Nine of ten people with Sjögren’s syndrome are women.2

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

Sources:
  1. Huang YF, Cheng Q, Jiang CM, An S, Xiao L, Gou YC, Yu WJ, Lei L, Chen QM, Wang Y, Wang J. The immune factors involved in the pathogenesis, diagnosis, and treatment of Sjogren’s syndrome. Clin Dev Immunol. 2013;2013:160491. doi: 10.1155/2013/160491. Epub 2013 Jul 9. [↩]
  2. nlm.nih.gov [↩] [↩]
  3. Fazaa A, Bourcier T, Chatelus E, Sordet C, Theulin A, Sibilia J, Gottenberg JE. Classification criteria and treatment modalities in primary Sjögren’s syndrome. Expert Rev Clin Immunol. 2014 Apr;10(4):543-51. doi: 10.1586/1744666X.2014.897230. [↩]
  4. Cornec D, Saraux A, Cochener B, Pers JO, Jousse-Joulin S, Renaudineau Y, Marhadour T, Devauchelle-Pensec V. Level of agreement between 2002 American-European Consensus Group and 2012 American College of Rheumatology classification criteria for Sjogren’s syndrome and reasons for discrepancies. Arthritis Res Ther. 2014 Mar 19;16(2):R74. [↩]
  5. Witte T. Pathogenesis and diagnosis of Sjögren’s syndrome. Z  Rheumatol. 2010 Feb;69(1):50-6. doi: 10.1007/s00393-009-0519-2. [↩]

Bronchoalveolitis Leading to Bronchitis and Pneumonia

Constipation in a young child as seen on X-ray. Lowest circle shows hard feces in the pelvis. Source, James Heilman, MD.

What Is Chronic Constipation?

[dropcap]C hronic constipation is an intestinal motility disorder characterized by abnormal stool formation, consistency, and evacuation.

Motility disorder means the normal rhythmic movement of intestinal muscles, called peristalsis, that moves food matter through the gut is hampered or dysfunctional.

Studies show that methane gas present in the colon induces constipation by delaying transit time, which is the time it takes for stool to pass through the colon.

Researchers investigating the relationship between methane and constipation found that methane positivity was detected in 75% of patients with slow transit, 44% of patients with normal transit and and 28% of the patients who were controls. However, methane positivity was not related with stool consistency.1

Other researchers investigating the total amount of methane produced found that there was significantly more methane production in patients with constipation (21.1 ppm vs. 6.1 ppm, respectively) than in controls without constipation.2

Q. How does methane get into the colon?

A. Methane is produced in the colon by intestinal methanogens (microbes) that metabolize hydrogen, one of the end products of normal anaerobic (meaning without oxygen) bacterial fermentation.  Fermentation of the undigested starchy part of carbohydrates produces hydrogen in the intestine which is the substrate (food) for methane production by intestinal methanogens.

Hydrogen and methane are excreted in the flatus and in breath giving the opportunity to indirectly measure their production using breath testing. Methane is detected in 30%-50% of the healthy adult population worldwide.3

Other common causes of constipation include not getting enough exercise, not drinking enough fluids, not eating enough fiber in the diet, not eating foods that supply microbes needed by the colon (probiotics), not eating foods that nourish the good microbe population (prebiotics) and supply minerals needed for healthy movement of stool, and food sensitivities. Too much cows milk is a common cause of stool that forms into balls.

Who is Affected in the General Population? Chronic constipation is a remarkably common and costly condition that can negatively impact the quality of life and result in a major social and economic burden. Based on the definition, either self-reported or using Rome criteria, chronic constipation can affect up to 27% of the population. There is strong evidence that constipation occurs more frequently in women.4

What Is Chronic Constipation In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Triantafyllou K, Chang C, Pimentel M. Methanogens, Methane and Gastrointestinal Motility. J Neurogastroenterol Motil. 2014 Jan;20(1):31-40. Epub 2013 Dec 30. [↩]
  2. Triantafyllou K, Chang C, Pimentel M. Methanogens, Methane and Gastrointestinal Motility. J Neurogastroenterol Motil. 2014 Jan;20(1):31-40. Epub 2013 Dec 30. [↩]
  3. Triantafyllou K, Chang C, Pimentel M. Methanogens, Methane and Gastrointestinal Motility. J Neurogastroenterol Motil. 2014 Jan;20(1):31-40. Epub 2013 Dec 30. [↩]
  4. Sanchez MI, Bercik P. Epidemiology and burden of chronic constipation. Can J Gastroenterol. 2011 Oct;25 Suppl B:11B-15B. [↩]

Pneumococcal Septicemia 

Endoscopic image of Crohn'sDisease showing deep ulceration in sigmoid colon.
Endoscopic Image of Crohn’s Disease Showing Deep Ulceration in the Sigmoid Colon.

What Is Crohn’s Disease?

[dropcap]C rohn’s disease is an inflammatory bowel disease characterized by patchy inflamed areas involving the full thickness of the intestinal wall that can occur anywhere in the intestinal tract, in addition to, mucosal disease.

In Crohn’s disease there is ongoing immune activation which produces inflammation and ulceration but the cause is not known and the severity varies among patients. At diagnosis of Crohn’s disease, factors predictive of subsequent 5-year aggressive disease are an age below 40 years, the presence of perianal disease, and the initial requirement for steroids.1

Dysbiosis is a factor that develops in and worsens Crohn’s disease and stress is a factor in both of these conditions. Psychological stress activates multiple physiological processes aimed at maintaining balance within the body. These physiological processes also have the capacity to influence the composition of microbial communities in the digestive tract, and research now indicates that exposure to stressful stimuli leads to gut microbiota dysbiosis.2

While the relative abundance of many different bacterial types can be altered during stressor exposure, findings in nonhuman primates and laboratory rodents, as well as humans, indicate that bacteria in the genus Lactobacillus are consistently reduced in the gut during stress.2

Q: Is there a cure for Crohn’s disease?

A: Presently, Crohn’s disease cannot be cured. This condition has a course of remissions, when symptoms subside, and flares, when symtpoms get worse. Treatment is aimed to reduce flares and promote remission.

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

Sources:
  1. Beaugerie L, Seksik P, Nion-Larmurier I, Gendre JP, Cosnes J. Predictors of Crohn’s disease. Gastroenterology. 2006;130:650–656. [↩]
  2. Galley JD, Bailey MT. Impact of stressor exposure on the interplay between commensal microbiota and host inflammation. Gut Microbes. 2014 May 1;5(3):390-396. Epub 2014 Apr 1. [↩] [↩]

Late Menarche (Start of Periods)

Courtesy quizlet.com
Courtesy quizlet.com

What Is Diffuse Alopecia?

[dropcap]D iffuse alopecia is characterized by abnormal hair loss or baldness.

Hair loss usually develops gradually and may be patchy or all over (diffuse). The average scalp contains about 100,000 hairs. Roughly 100 hairs are shed from the head every day.

Diffuse baldness not related to male pattern or heredity can be related to aging, nutritional deficiencies, some froms of dermatitis, radiation, endocrine disorders, especially thyroid hormone imbalance and diabetes, and undue stress.

Q: Can sudden stress cause hair loss?

A: A sudden physical or emotional stress may cause one-half to three-quarters of the hair throughout the scalp to shed. Other causes that need to be evaluated include use of common medications such as birth control pills, blood thinners, and anti-inflammatory pain drugs, and continued exposure to environmental chemicals such cleaning products.

What Is Diffuse Alopecia In Celiac Disease and/or Gluten Sensitivity?

Dysgeusia (Impaired Taste)

DyspareuniaWhat Is Autoimmune Thyroiditis (Hypothyroidism)?

[dropcap]A utoimmune thyroiditis, also called Hashimoto’s thyroiditis or Hashimoto’s Disease, is an autoimmune destruction of thyroid tissue characterized by insufficient thyroid hormone circulating in the body that causes formation of a goiter (enlarged thyroid gland) and hypothyroidism.

Hypothroidism refers to the condition of markedly reduced secretion of thyroid hormone. There are other causes of hypothyroidism besides Hashimoto’s thyroiditis.

Hashimoto’s thyroiditis is often associated with other autoimmune diseases such as celiac disease.

In Hashimoto’s thyroiditis, a profusion of antibodies are produced, which build up in the blood. Left untreated so that much of the thyroid gland is destroyed, this condition may progress to the very serious and life-threatening condition called myxedema.

Note: In myxedema, protein, electrolytes, and water abnormally accumulate in between cells which produce firm, inelastic puffy skin that is cool, dry, rough, scaly, and may appear yellow; in some people, areas such as the ankles become crusty with a look of tree bark. Many systemic changes develop shown by significant slowing of mental and physical functions. Please see below.

Q: What thyroid tissue is targeted for destruction?

A: In Hashimoto’s thyroiditis, high levels of autoantibodies target thyroglobulin and thyroid peroxidase, leading to inflammation and destruction of the thyroid gland. The resulting fibrosis or scarring of the gland results in lack of thyroid hormone production.

The thyroid gland consists of a large number of closed vesicles that contain a homogenous substance called colloid, which contains the thyroglobulin. Thyroglobulin is an iodine-containing protein secreted by the thyroid gland and stored within its colloid, from which the thyroid hormones thyroxine (T4) and triiodothyroinine (T3) are derived.1

T3 is the active hormone and is made from T4. Thyroid hormones affect metabolism, brain development, breathing, heart and nervous system functions, body temperature, muscle strength, skin dryness, menstrual cycles, weight, and cholesterol levels.

Thyroid hormone production is regulated by thyroid-stimulating hormone (TSH), which is made by the pituitary gland in the brain. Normally, when thyroid hormone levels in the blood are low, the pituitary releases more TSH. When thyroid hormone levels are high, the pituitary decreases TSH production.

Hashimoto’s disease, with or without the development of hypothyroidism, is treated with synthetic thyroxine, which is man-made T4. Health care providers prefer to use synthetic T4, such as Synthroid® (Levothyroxine), rather than synthetic T3, because T4 stays in the body longer, ensuring a steady supply of thyroid hormone throughout the day. The thyroid preparations made with animal thyroid are not considered as consistent as synthetic thyroid.2

What Is Autoimmune Thyroiditis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Taber’s Cyclopedic Medical Dictionary. 19th ed. F.A. Davis Company. Philadelphia, PA. [↩]
  2. National Endocrine and Metabolic Diseases Information Service. [↩]

Early Menopause or Ovarian Failure

Hair Follicles.
Hair Follicles.

What Is Fine Hair With Rough Texture?

[dropcap]F ine hair (lower diameter across the width) with rough texture is an abnormal hair shaft feature altered from the normal diameter and smooth quality of hair.

Q: What is the normal diameter and smooth quality of hair?

A: Although hair may appear to be a simple structure, it is actually a complex part of the anatomy whose biology is only partially understood. Hair grows from small organs (follicles) located within the complex microenvironment of the skin which has multiple layers of tissue, three glands whose secretions bathe hair, and multiple vascular systems.1

An individual hair is a thread-like shaft made up of cornified cells. It consists of the outermost layer, or cuticle, the cortex which is a horny component, and the medulla which is the central part.

Hairs receive nourishment from capillaries via the papilla at the base of their follicles (roots). Since the number of hair follicles are determined at birth, it is important to properly nourish them so they remain healthy.

What Is Fine Hair with Rough Texture In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Harkey MR. Anatomy and physiology of hair. Forensic Sci Int. 1993 Dec;63(1-3):9-18. [↩]