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Abnormal Blood Values in Childhood

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Illustration Showing Skin Anatomy.

What Is Pruritic Skin?

P ruritic skin is a symptom of a primary disease that may involve only the skin or a systemic disorder with other features and is characterized by chronic itching.

Q: What part of skin is affected by itchiness?

A: Itching may arise from any layer of skin, depending on the cause.

In the image to the right, the outermost protective surface layer, or stratum cornem, is shown as a thin tan line. It is the top dead layer of the epidermis that normally sloughs off as new cells move up to replace it. The epidermis is shown as a dark pink layer. It is composed of five layers of keratinocytes that flatten as they move upward.

The pink layer under the epidermis is the dermis, or true skin, which is composed of collagen and elastin tissue. It contains oil glands that lubricate skin, sweat glands, blood vessels, nerve endings, lymphatics, and hair follicles. Under the dermis is subcutaneous tissue containing fat cells here colored yellow on the bottom of the image.

What Is Pruritic Skin In Celiac Disease and/or Gluten Sensitivity?

Adenocarcinoma Of Small Intestine (Cancer)

Section of small bowel surgically removed for adenocarcinoma that grew through the wall. By: CDC/ Dr. Edwin P. Ewing, Jr.
Section of small bowel surgically removed for adenocarcinoma that grew through the wall. By: CDC/ Dr. Edwin P. Ewing, Jr.

What Is Adenocarcinoma Of Small Intestine?

Adenocarcinomas are malignant tumors, or cancer, of the small bowel arising out of glandular tissue. They fall in the category of rare neoplasm, comprising only 3% of all gastrointestinal malignancies.

Primary adenocarcinoma is the most common histological (cell) subtype constituting 35–50% of cases.1 

Q: What does adenocarcinoma look like?

A: Adenocarcinoma may manifest as strictures, nodules, excavating masses, or annular lesions.2

What Is Adenocarcinoma Of Small Intestine In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Benhammane H, El M’rabet FZ, Serhouchni KI, El yousfi M, Charif I, Toughray I, et al. Small Bowel Adenocarcinoma Complicating Coeliac Disease: A Report of Three Cases and the Literature Review. Case Rep Oncol Med. 2012; 2012: 935183. Published online 2012 December 1. doi: 10.1155/2012/935183 [↩]
  2. Ramachandran I, Sinha R, Rajesh A, Verma R. Multidetector row CT of small bowel tumors.  Clinical Radiology. 2007; 62:607-614. [↩]

Tongue – Beefy Red, Smooth, Burning 

tongue in B12 deficiencyWhat Is Beefy Red, Smooth, Burning Tongue?

Beefy, red, smooth, burning tongue is an inflammatory alteration in tongue tissue characteristic of vitamin B12 deficiency.

Inflammation makes the tongue red and sore which, when untreated, progresses to atrophied papillae (shrunken taste buds) that makes the tongue smooth.

Q: Why does vitamin B12 alter the tongue?

A: Vitamin B12 is essential for the metabolism of all cells, especially for those of the digestive tract of which the tongue is an organ.1

These easily seen changes to tongue tissue are an important diagnostic feature of deficient vitamin B12, which causes other devastating unseen damage, because the discomfort generally causes the individual to seek medical care.

What Is Beefy Red, Smooth, Burning Tongue In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Krause’s Food, Nutrition, & Diet Therapy. 10th Edition. Kathleen Mahan, Sylvia Escott-Stump. 2000. W.B. Saunders Company. [↩]

Schizophrenia

Collagenous Colitis.
Microscopic Image Showing a Pink Collagen Band in Collagenous Colitis.

What Is Collagenous Colitis?

C ollagenous colitis is a disease of the large intestine (colon) that is characterized by microscopic inflammation of the surface mucosal lining and an abnormally thickened collagen band of tissue that develops wthin the lining of the colon.

The thicker than normal layer of collagen of at least 10 µm (reference value: 2–7 µm) can vary in different locations. Inflammation occurs with increased numbers of lymphocytes (white blood cells) and plasma cells and epithelial (surface cell) damage. These changes can only be seen under microscopic examination of multiple biopsied tissue samples taken during a colonoscopy procedure.

Q: What is collagen?

A: Collagen is a strong, fibrous protein found in connective tissue of the colon and many other tissues such as tendons. The normal basement membrane in the bowel consists mainly of collagen type IV, laminin, and fibronectin. The increased collagen band observed in collagenous colitis consists basically of collagen type I and III, which are the subtypes produced by repair functions, indicating a reactive origin to some irritant or drug.1

The biopsies should preferably be taken from the ascending colon, since the pathological hallmarks may be absent in the descending colon, and in the normally occurring thicker collagen layer in the rectosigmoid region.1 Inflammation of the ileum (last segment of the small intestine next to colon) is common.2

Endoscopy and radiological (x-ray) examinations are usually normal.3

Autoimmune disorders are frequently seen in adult patients with collagenous colitis.4 In the study below by Koskela et al. concomittent autoimmune diseases were present in 53% of patients with collagenous colitis.5

Importantly, the finding of collagenous colitis in patients with autoimmune diseases may reflect the treatment with NSAIDs (non-steroidal anti-inflammatory drugs), such as Ibuprofin and aspirin, PPIs (proton pump inhibitors), and other drugs. However, if secondary forms of collagenous colitis are not taken into consideration, underlying, treatable diseases may be overlooked, while only the gastrointestinal symptoms are treated symptomatically or with budesonide (a steroid).6

Treatment with budesonide steroid is efficacious irrespective of bile acid malabsorption.7

Budesonide at a mean dose of 4.5 mg/day maintained clinical remission for at least 1 year in the majority of patients with collagenous colitis and preserved health-related quality of life without safety concerns. Treatment extension with low-dose budesonide beyond 1 year may be beneficial given the high relapse rate after budesonide discontinuation.8

See below for nutritional deficiency problems caused by steroid usage and steps to be taken for correction.

What Is Collagenous Colitis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Ohlsson B. New insights and challenges in microscopic colitis. Therap Adv Gastroenterol. 2015 Jan;8(1):37-47. doi: 10.1177/1756283X14550134. [↩] [↩]
  2. Bjørnbak C, Engel PJ, Nielsen PL, Munck LK. Microscopic colitis: clinical findings, topography and persistence of histopathological subgroups. Aliment Pharmacol Ther. 2011 Nov;34(10):1225-34. doi: 10.1111/j.1365-2036.2011.04865.x. [↩]
  3. Abdo AA, Urbanski SJ, Beck PL. Lymphotcytic and collagenous colitis: the emerging entity of microscopic colitis. An update on pathophysiology, diagnosis and management. Canadian Journal of Gastroenterology. Jul 2003;17(7):425-32. [↩]
  4. Leung ST, Chandan VS, Murray JA, Wu TT. Collagenous gastritis: histopathologic features and association with other gastrointestinal diseases. Am J Surg Pathol. 2009 May;33(5):788-98. doi: 10.1097/PAS.0b013e318196a67f. [↩]
  5. Koskela RM, Niemela SE, Karttunen TJ, Lehtola JK. Clinical characteristics of collagenous and lymphocytic colitis. Scandanavian Journal of Gastroenterology. Sep 2004;39(9):837-45. [↩]
  6. Ohlsson B. New insights and challenges in microscopic colitis. Therap Adv Gastroenterol. 2015 Jan;8(1):37-47. doi: 10.1177/1756283X14550134. [↩]
  7. Bjørnbak C, Engel PJ, Nielsen PL, Munck LK. Microscopic colitis: clinical findings, topography and persistence of histopathological subgroups. Aliment Pharmacol Ther. 2011 Nov;34(10):1225-34. doi: 10.1111/j.1365-2036.2011.04865.x. [↩]
  8. Münch A, Bohr J, Miehlke S, et al. Low-dose budesonide for maintenance of clinical remission in collagenous colitis: a randomised, placebo-controlled, 12-month trial. Gut. 2014 Nov 25. pii: gutjnl-2014-308363. doi: 10.1136/gutjnl-2014-308363. [↩]

Vitamin B12 Deficiency Anemia

What Is Vitamin B12 Deficiency Anemia? Vitamin B12 deficiency anemia is a megaloblastic anemia that is characterized by defective DNA synthesis of red blood cells due to a lack of vitamin B12. Vitamin B12 is essential… 

Angina Pectoris

What Is Angina Pectoris?Coronary Artery Lesion

Angina pectoris, or simply angina, is a coronary syndrome characterized by an oppressive substernal pain (pain under breastbone) or pressure brought on by exertion and relieved by rest that results from failure of coronary arteries to deliver adequate oxygen to heart tissue due to ischemic heart disease.

Q: Why do coronary arteries fail to deliver adequate oxygen to heart tissue?

A: Coronary arteries are the blood vessels that serve the heart. In angina, these vessels fail to deliver adequate oxygen to heart tissue because they are narrowed or blocked by fatty buildups, called atherosclerotic plaques or by a blood clot which impair their ability to carry adequate blood that carries the oxygen. Diseased coronary arteries cannot deliver adequate oxygenated blood pumped by the heart to its own muscle cells.

The heart is a muscular organ that is working all the time without rest, so it needs a constant supply of oxygen. When heart muscle has to work harder, it needs more oxygen. Lack of oxygen causes pain which makes the affected person stop activity and rest.

Angina can be stable or unstable. Unstable angina is much more serious and can be life-threatening.

  • Stable angina produces predictable pain and responds to rest and/or medication. It is less serious than unstable angina but can be very painful or uncomfortable. Anything that makes the heart muscle need more oxygen can cause an angina attack in someone with heart disease, including: smoking, cold weather, exercise, emotional stress, obesity, and large meals. Other causes of angina include: abnormal heart rhythms (usually ones that cause the heart to beat quickly), anemia, coronary artery spasm, heart failure, heart valve disease, and hyperthyroidism (overactive thyroid).1
  • Unstable angina produces unpredictable pain that may occur at rest, lasting more than 20 minutes. It is more severe than stable angina and less responsive to medication. Atherosclerosis is by far the most common cause of unstable angina. Oxidized low-density lipoprotein, so-called bad cholesterol, and oxysterols play an important role in atherogenesis, the development of atherosclerosis. Coronary arteries that are narrowed by atherosclerotic plaques can rupture causing injury to the coronary blood vessel resulting in blood clotting which blocks the flow of blood to the heart muscle. Blood clots may form, partially dissolve, and later form again and angina can occur each time a clot blocks blood flow in an artery. People with unstable angina are at increased risk of having a heart attack.2

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

Sources:
  1. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001247/ [↩]
  2. http://www.heart.org/HEARTORG/Conditions/HeartAttack/SymptomsDiagnosisofHeartAttack/Unstable-Angina_UCM_437513_Article.jsp# [↩]

Antiphospholipid Syndrome

Testing Thigh Strength. Courtesy Charlie Goldberg, M.D., UCSD School of Medicine
Testing Thigh Strength. Courtesy Charlie Goldberg, M.D., UCSD School of Medicine

What Is Hypophosphatemia?

H ypophosphatemia means the level of phosphates in the bloodstream is too low to meet metabolic needs of the body for this mineral.

Q: How important is phosphorus in metabolism?

A: Phosphorus is crucial to  life, being present in every cell of the body and constitutes 45% of skeletal bone weight along with 40% calcium needed to support the body as a framework.

A low blood phosphate level is characterized by alterations in blood acid-alkaline balance and serious neuromuscular, hematologic, renal, skeletal, and dental abnormalities.

Symptoms result primarily from decreased production of adenosine triphosphate (ATP), the main energy source in cells, and phosphocreatine, a secondary energy source for muscle contraction.

  • Acute phosphorus deficiency may precipitate rhabdomyolysis which is destruction of muscle.
  • Nervous system dysfunction is observed in severe hypophosphatemia.
  • Chronic phosphorus deficiency causes proximal myopathy (upper arms and thighs).1
  • Severe phosphorus deficiency has widespread and ultimately fatal consequences.

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

Sources:
  1. Takeda E, Ikeda S, Nakahashi O. Lack of phosphorus intake and nutrition. Clin Calcium. 2012 Oct;22(10):1487-91. [↩]

Coronary Artery Disease

Image on left shows how atherosclerosis impedes blood flow through coronary arteries while blood clots block blood flow. Courtesy Google.
Figure on right shows how atherosclerosis impedes blood flow through coronary arteries while blood clots block blood flow. Courtesy Google.

What Is Coronary Artery Disease (CAD)?

Coronary artery disease (CAD), also called ischemic heart disease, is a gradual narrowing of medium and large arteries of the heart by fatty buildups, called atherosclerotic plaques.

It is characterized by slowly developing interference with blood flow to heart tissue itself, resulting in oppressive chest pain called angina and, ultimately, thrombosis (clot) causing heart attack.  

The heart is a muscular organ that is working all the time, so it needs a constant supply of oxygen. Oxygen is brought to the working heart tissue by the coronary arteries with each beat of the heart. When heart muscle has to work harder, it needs more oxygen delivered to itself. Lack of oxygen causes pain.

In fact, failure of diseased coronary arteries to deliver adequate oxygen to heart tissue is the most common cause of angina pectoris – substernal pain (under breastbone) or pressure brought on by exertion and relieved by rest. 

Thrombosis, or clot formation, occurs when blood cells within a narrowed artery can no longer get through. Trapped, blood cells pile up and block the artery thus triggering a cascade of events called heart attack. Coronary arteries that are narrowed by atherosclerotic plaques can rupture causing injury to the coronary blood vessel resulting in blood clotting which blocks the flow of blood to the heart muscle. Blood clots may form, partially dissolve, and later form again and angina can occur each time a clot blocks blood flow in an artery.1

Q: How does coronary artery disease develop?

A: Coronary artery disease slowly develops from this combination of events:

  • Dysfunction of epithelial cells that line the inside of arteries cause the vessels to stiffen, and subsequently

  • Accumulation of lipid (fat) in smooth muscle cells beneath the inside lining of arteries and in foam cells cause buildup of fatty deposits on the inside walls progressing to fibrous plaque formation.

Oxidized low-density lipoprotein (oxLDL), so-called bad cholesterol, and oxysterols play important roles in the development of  atherosclerosis. OxLDL triggers the immune system to produce autoantibodies against oxLDL that are detectable in serum. These antibodies are called anti-oxLDL. Anti-oxLDL antibody and oxysterol concentrations are associated with coronary artery stenosis. Oxidative stress may be greatly increased in unstable angina.2 and Chronic inflammation in the general population is a major risk factor for ischemic heart disease.

The pathophysiology of atherosclerosis is, clearly, different in women when compared to the men. The women have a higher risk of blood coagulability making them at high risk for the blood clot formation. In a large number of women endothelial dysfunction, small vessel size and diffuse atherosclerosis have been identified as causes of ischemia without evidence of blockade in the coronary arteries.3

Also, atherosclerotic plaque in women is less fibrotic and contains more lipid filled foam cells, implying greater potential for reversibility but also potentially greater vulnerability for plaque rupture and thrombosis.4

Who is Affected in the General Population?

  • Coronary artery disease remains the leading cause of death in developed countries despite significant progress in primary prevention and treatment strategies.

  • It is the leading cause of death in women, as well as an important cause of disability.

  • Older patients are at particularly high risk of poor outcomes following acute coronary syndrome.5

What Is Coronary Artery Disease In Celiac Disease and/or Gluten Sensitivity?

Ischemic heart disease is the leading cause of death in the United States, making cardiovascular risk assessments and potential interventions or treatments imperative for patients with celiac disease.6

Sources:
  1. http://www.heart.org/HEARTORG/Conditions/HeartAttack/SymptomsDiagnosisofHeartAttack/Unstable-Angina_UCM_437513_Article.jsp# [↩]
  2. Yasunobu Y, Hayashi K, Shingu T, Yamagata T, Kajiyama G, Kambe M. Coronary atherosclerosis and oxidative stress as reflected by autoantibodies against oxidized low-density lipoprotein and oxysterosis. Atherosclerosis. Apr 2001;155(2):445-53. [↩]
  3. Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. Epub 2013 Dec 19. [↩]
  4. Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. Epub 2013 Dec 19. [↩]
  5. Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. [↩]
  6. Robinson BL, Davis SC, Vess J, Lebel, J. Primary care management of celiac disease. Nurse Practitioner. February 2015: Vol 40 – Issue 2; 28–34. [↩]

Dysgeusia (Impaired Taste)

DyspareuniaWhat Is Autoimmune Thyroiditis (Hypothyroidism)?

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. [↩]

Impotence

This White Spot Is A Feature of Zinc Deficiency.
This White Spot Is A Feature of Zinc Deficiency.

What Are White Spots And White Bands In Nails?

W hite spots in the nails is a feature of zinc deficiency and white bands signify protein deficiency characterized by abnormal appearance anywhere in one or more nails.

White spots and bands can appear separately or together in nails. There may be just one mark or many marks depending on the level of deficiency.

Q: What part of the nail is affected by zinc and/or protein deficiency?

A: Zinc and protein deficiencies affect the nail plate.

The nail plate is the hard keratin cover of the finger tip and toe tip, simply called “the nail.” The nail plate is produced by the living nail tissue at its base. Here is an illustration of the parts that make up a fingernail:

Nail Anatomy. Nail Anatomy. A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikipedia.org.

A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikipedia.

What Are White Spots And White Bands In Nails In Celiac Disease and/or Gluten Sensitivity?