Selenium is a mineral that is required by the body in trace amounts for a healthy immune system, normal thyroid function, and antioxidant protection.
Selenium is absolutely required in the production of at least 30 selenoproteins in the body. First, selenium is joined to the amino acids cysteine as selenocysteine and to methionine as selenomethionine before being used as components for selenoproteins. Many selenoproteins are important antioxidant enzymes such as glutathione peroxidase.
Q: How does glutathione peroxidase work?
A: Glutathione peroxidase activity helps the recycling of vitamins C and E in optimizing the performance of the antioxidant system. The antioxidant properties of selenoproteins help prevent cellular damage from free radicals. Free radicals are natural by-products of oxygen metabolism that may contribute to the development of chronic diseases such as cancer and heart disease.
In the immune system, selenium stimulates immune properties of lymphocytes (white blood cells) by contributing to higher natural killer lymphocyte activity. Natural killer lymphocytes have the ability to destroy cancer cells and bacterial and viral agents.
Other selenoproteins help protect the thyroid gland from anti-oxidants and regulate thyroid function. Specifically, selenium plays an integral role in thyroid gland metabolism.1 Functions are more fully described below.
According to the Food and Agriculture Organization, United Nations, approximately 30 percent of tissue selenium is contained in the liver, 15 percent in kidney, 30 percent in muscle, and 10 percent in blood plasma.
What Is Selenium Deficiency In Celiac Disease and/or Gluten Sensitivity?
Sources:
Stazi AV, Trinti B. Selenium status and over-expression of interleukin-15 in celiac disease and autoimmune thyroid diseases. Ann Ist Super Sanita. 2010;46(4):389-99.DOI: 10.4415/ANN_10_04_06. [↩]
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
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. [↩]
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. [↩]
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. [↩]
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. [↩]
Robinson BL, Davis SC, Vess J, Lebel, J. Primary care management of celiac disease. Nurse Practitioner. February 2015: Vol 40 – Issue 2; 28–34. [↩]
This is a stained liver biopsy sample showing advanced cellular changes in non-alcoholic fatty liver disease. Blue is fibrosis. White is fat accumulation in degenerated cells. Courtesy of Nephron’s work.
What Is Non-Alcoholic Fatty Liver Disease?
N on-alcoholic fatty liver is a non-inflammatory liver disorder characterized by degenerative changes in the liver caused by excessive accumulation of lipid (fat) in hepatocytes (liver cells) that is called free fatty acid-generated lipotoxicity.
Non-alcoholic fatty liver shows an increase in liver enzymes called transaminases.
Q: What are the enzymes that increase?
A: The transaminases that increase are ALT and AST. ALT is the abbreviation for alanine aminotransferase enzyme and AST is the abbreviation for aspartate aminotransferase enzyme. They are commonly measured in blood tests to determine liver function and when elevated indicate inflammation.
What Is Non-Alcoholic Fatty Liver In Celiac Disease and/or Gluten Sensitivity?
P rurigo nodularis is a chronic dermatitis characterized by hard, dry, deep seated, intensely itchy papules (small bumps like pimples) and/or nodules (large bumps) that erupt most commonly on the arms, legs, and back.
Papules and nodules vary in number and may become infected after picking or scratching.
Q: Does the itching go away?
A: New nodules develop from time to time, and existing nodules may remain itchy indefinitely, although some may regress spontaneously and leave scars. In most cases, the disease runs a very protracted course with exacerbations and remissions.1
Prurigo nodularis is an unusual disorder of unknown etiology, which is notoriously resistant to therapy. A variety of systemic conditions have been reported to be associated with prurigo nodularis. However, the mechanism by which these disorders may trigger prurigo nodularis is unknown.2
It has been shown to be associated with malnutriton and infection such as tonsillitis, which resolved after removal of tonsils.3
What Is Prurigo Nodularis In Celiac Disease and/or Gluten Sensitivity?
Sources:
Katotomichelakis M, Balatsouras DG, Bassioukas K, Kontogiannis N, Simopoulos K, Danielides V. Recurrent prurigo nodularis related to infected tonsils: a case report. J Med Case Rep. 2008 Jul 24;2:243. doi: 10.1186/1752-1947-2-243. [↩]
Lee MR, Shumack S. Prurigo nodularis: a review. Australas J Dermatol. 2005 Nov;46(4):211-18; quiz 219-20. [↩]
Katotomichelakis M, Balatsouras DG, Bassioukas K, Kontogiannis N, Simopoulos K, Danielides V. Recurrent prurigo nodularis related to infected tonsils: a case report. J Med Case Rep. 2008 Jul 24;2:243. doi: 10.1186/1752-1947-2-243. [↩]
P soriasis is a chronic, autommune relapsing skin disorder characterized by scaling, erythema (redness), and less commonly, pustulation.1
The body surface area affected and the degree to which psoriasis is a problem varies considerably among patients and over time.2 Often there are additional manifestations in the nails and in joints.3
Q: Are there different forms of psoriasis?
A: There are five forms of psoriasis. The lesions in all forms are itchy and red but vary in appearance and severity. Plaque psoriasis is the most common form observed in more than 80% of patients. Atypical forms include guttate, inverse, pustular, and erythrodermic psoriasis.4
Plaque psoriasis features thickened or raised red areas that have a distinct edge and are covered with silvery white buildup of flaky skin typically on elbows, knees, scalp and buttocks.
Gutate psoriasis appears as small, flat red patches with shiny buildup that are not usually painful, just itchy. There may be a few or many patches and they can group together.
Inverse psoriasis affects folds of skin, armpits and the groin area. Lesions are deep red with shiny buildup. It can be a thin red area along a crease line or involve, for example, the whole armpit.
Pustular psoriasis features an itchy, red base followed by blisters of white, non-infectious pus that appears glossy after a day or two and then sloughs in cycles. These areas may be limited to certain areas such as the hands and feet or be more widespread.
Erythrodermic psoriasis involves large areas of the body’s surface, inflaming normal skin and changing it into very red, raw looking flesh that is painful, swollen and itchy. This form requires extensive treatment, and complications can be life-threatening. Fortunately, this form of psoriasis is the least common.
Psoriasis in children has been reported to differ from that among adults being more frequently itchy and plaque lesions are relatively thinner, softer, and less scaly, face and flexural involvement is common and guttate type is the characteristic presentation.5
In children, psoriasis is a common skin disorder with about one third of all patients having onset of disease in the first or second decade of life. A chronic disfiguring skin disease, such as psoriasis, in childhood is likely to have profound emotional and psychological effects, and hence requires special attention.6
What Is Psoriasis In Celiac Disease and/or Gluten Sensitivity?
Sources:
Addolorato G, Parente A, de Lorenzi G, et al. Rapid regression of psoriasis in a coeliac patient after gluten-free diet. A case report and review of the literature. Digestion. 2003;68(1):9-12. [↩]
Stern, R. S., Nijsten, T., Feldman, S. R., Margolis, D. J. and Rolstad, T.
Psoriasis is common, carries a substantial burden even when not extensive, and is associated with widespread treatment dissatisfaction. J. Invest. Dermatol. Symp.. 2004 Mar;9(2):136-9.. [↩]
Weigle N, McBane S. Psoriasis. Am Fam Physician. 2013 May 1;87(9):626-33. [↩]
Weigle N, McBane S. Psoriasis. Am Fam Physician. 2013 May 1;87(9):626-33. [↩]
Dogra S, Kaur I. Childhood psoriasis. Indian J Dermatol Venereol Leprol. 2010 Jul-Aug;76(4):357-65. doi: 10.4103/0378-6323.66580. [↩]
Dogra S, Kaur I. Childhood psoriasis. Indian J Dermatol Venereol Leprol. 2010 Jul-Aug;76(4):357-65. doi: 10.4103/0378-6323.66580. [↩]
S cleroderma is a chronic skin manifestation of progressive systemic sclerosis characterized by generalized thickened, edematous skin firmly bound to subcutaneous tissue which causes limited movement.
Systemic sclerosis a connective tissue disease that involves destructive changes in the skin, blood vessels, muscles, and internal organs. The course can be mild or it can be fatal. Cardiopulmonary complications from fibrosis are the most common cause of death.
Gastrointestinal problems mainly due to fibrosis affect 50 to 90% of patients.1
Q: Is there a cure for scleroderma?
A: There is no cure for scleroderma. Treatment is aimed at improving symptoms.
Heartburn (acid reflux) can be treated with antacid drugs.
Scleroderma kidney disease can be treated with blood pressure medications called “angiotensin converting enzyme inhibitors” (ACE inhibitors). These can often effectively control kidney damage if started early and use of these drugs has been a major advance for treating scleroderma.
Muscle pain and weakness can be treated with anti-inflammatory drugs such as prednisone, intravenous immunoglobin (IVIg), and/or immunosuppressive medications. Physical therapy may be useful to maintain joint and skin flexibility.2
What Is Scleroderma In Celiac Disease and/or Gluten Sensitivity?
Sources:
Forbes A, Marie I. Gastrointestinal complications: the most frequent internal complications of systemic sclerosis. Rheumatology (Oxford). 2009 Jun;48 Suppl 3:iii36-9. doi: 10.1093/rheumatology/ ken485. [↩]
The spleen is the darkish oval organ in the lower middle of this photo.
What Is Hyposplenism?
H yposplenism is the condition resulting from having lost spleen tissue, called atrophy of the spleen. Spleen atrophy impairs splenic functions or activities because there are insufficient tissues to do the work required.
Q: What splenic functions are impaired?
A: The spleen, apart from acting as a phagocytic filter, thus removing aging and damaged cells, is crucial in regulating immune homeostasis by linking innate and adaptive immunity, and in protecting against infections by encapsulated bacteria.1
Impaired function of the spleen therefore increases risk of infections with encapsulated bacteria because of inability to mount a proper defense and to filter and remove bacteria from the circulation.
The spleen is a highly vascular and solid organ about the size of a fist. It has a delicate structure inside that is enclosed by fibrous, elastic layers consisting of connective tissue.
The tissues within are made up of two different types of tissues, called white pulp and red pulp. White pulp carries out lymphoid functions. Red pulp filters and cleanses the blood. The spleen is situated above the stomach on the left side of the upper abdomen and firmly fixed in place by ligaments and ribs.
The spleen is an important organ of the lymph system, having the largest collection of lymph tissue in the body. It functions to produce antibodies (immunoglobulins) and white blood cells (T-cells and B-cells), help control the amount of blood in the body, keep body fluids in balance, destroy and filter out old and damaged cells2 and salvage the iron needed for producing new blood cells, and lastly, clear bacteria through production of substances that enable phagocytosis (engulfing bacteria and other unwanted particles, such as antigens, from blood).
Children and adults with hyposplenism are at risk for overwhelming infections. Management of hypospenism is directed towards preventing pneumonia by immununization against pneumonia and meningitis and treating bacterial infections as they arise, which may require hospitalization. For some patients, life-long treatment with antibiotics, such as erythromycin and penicillin, are recommended.
What Is Hyposplenism In Celiac Disease and/or Gluten Sensitivity?
Sources:
Di Sabatino A, Brunetti L, Carnevale Maffè G, Giuffrida P, Corazza GR. Is it worth investigating splenic function in patients with celiac disease? World J Gastroenterol. 2013 Apr 21;19(15):2313-8. doi: 10.3748/wjg.v19.i15.2313. [↩]
H ypokalemic rhabdomyolysis is an acute and sometimes fatal disease due to its rapid progression of muscle destruction when untreated.
It is characterized by the accumulation of by-products of skeletal muscle destruction in the renal (kidney) tubules and producing acute kidney failure caused by rapid potassium loss.
This condition puts you in bed because the legs muscles cannot support the body and arms are too weak to move.
What Is Hypokalemic Rhabdomyolysis In Celiac Disease and/or Gluten Sensitivity and Dermatitis Herpetiformis?
M uscle weakness is the impaired status of muscle function characterized by decreased or low muscle strength and inability to perform normal work such as lifting a pot off the stove.
Q: How do muscles work?
A: Muscles do their work by contracting or shortening. For example, to move the foot up and down at the ankle, muscles attached to the foot by tendons must contract to shorten or relax to return to their resting length. Calf muscles contract to point the foot down (flexion) while the shin muscles relax (extension). For the foot to point up, calf muscles relax while the opposing shin muscles contract.
Each muscle is made up of individual muscle fibers. A muscle fiber is a long cylindrical cell that contains many nuclei, mitochondria, and sarcomeres. Each muscle fiber is surrounded by a thin layer of connective tissue called the endomysium.
Approximately 20–80 of these muscle fibers are grouped together in a parallel arrangement called a muscle fascicle or fiber bundle that is encapsulated by a perimysium. A distinct muscle is formed by enveloping a large number of muscle fascicles in a thick collagenous external sheath extending from the tendons called the epimysium.1
Muscles fall into three types:
Voluntary muscles. These muscles, also called skeletal, we can control by will. Voluntary muscles function by contracting their fibers to draw one part of the body toward another in flexion while opposing muscles that extend or pull a body part away from another. They move our bones to perform activities such as walking to get somewhere, chewing to eat food, lifting to do work, and moving the eyeball to look at something.
Involuntary muscles. These muscles work independently of our conscious control. They are needed for internal organs, sphincters, and other parts to do their work, such as peristalsis in the gut that must function at all times to digest and move food, the squirting of bile juice into the duodenum by the Sphincter of Odi in the presence of fat eaten, and action of the pupil to see.
Cardiac muscles. These muscles are specialized to keep the heart functioning at all times.
Muscle weakness can involve all types of muscles.
What Is Muscle Weakness In Celiac Disease and/or Gluten Sensitivity?
Dermatitis Herpetiformis On Forearm. Skin Is Darkened Where Old Blisters Healed.
What Is Dermatitis Herpetiformis?
D ermatitis herpetiformis (DH) is an autoimmune extremely itchy, painful bullous skin rash (blistering eruptions) arising from the underlying dermis layer of skin as a consequence of gluten sensitivity.
Dermatitis herpetiformis is characterized by multiple intensely itchy, red blisters appearing on the elbows which can extend down the forearm to the wrist and the knees. Less usual areas involve the back, buttocks, scalp, and abdomen.
Q: Do the blisters leave a mark when healed?
A: Crops of skin eruptions begin with itching or a burning sensation in reddened papules. There are grouped vesicles and tense blisters. The blister contents may be serous or bloody, with symmetrical distribution (eg, both knees or both elbows). Fluid filled elements rupture leaving denuded areas of sore skin and crust. Subsequently, there is residual hypopigmentation (a white area) or hyperpigmentation (dark area).1
Rupture of blisters begins relief from intense burning and itching.
Dermatitis Herpetiformis Eruptions On Knees. Notice White Areas Showing Loss of Pigmentation From Healed Blisters.
What Is Dermatitis Herpetiformis In Celiac Disease and/or Gluten Sensitivity?
Primary care providers should be aware of this skin condition, as they are more likely than a gastroenterologist to be confronted with this type of presentation of celiac disease.2
Sources:
Mendes FB, Hissa-Elian A, de Abreu MA, Gonçalves VS. Review: dermatitis herpetiformis. An Bras Dermatol. 2013 Jul-Aug;88(4):594-9. [↩]
Robinson BL, Davis SC, Vess J, Lebel, J. Primary care management of celiac disease. Autoimmune Disorders. Nurse Practitioner. February 2015: Vol 40 – Issue 2; 28–34. [↩]
What Is Selenium?
![Psoriasis_on_back[1]](https://glutenfreeworks.com/health/wp-content/uploads/sites/10/Psoriasis_on_back1.jpg)
