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:
Takeda E, Ikeda S, Nakahashi O. Lack of phosphorus intake and nutrition. Clin Calcium. 2012 Oct;22(10):1487-91. [↩]
What Is Plummer-Vinson Syndrome Affecting the Esophagus?
Plummer-Vinson syndrome is a manifestation of severe, long-term, iron deficiency anemia that is characterized by post-cricoid esophageal webs and dysphagia.
Q: What are esophageal webs?
A: Esophageal webs are one or more thin horizontal membranes consisting of squamous epithelium (cells that line the surface of the esophagus) and submucosa. They usually protrude from the anterior (front) wall, extending laterally across the inside esophagus but not to the posterior (rear) wall, which means that they rarely encircle the lumen.1
Dysphagia, or difficulty swallowing, from these webs is commonly painless and intermittent or progressive and may cause obstruction.
Webs can be detected by barium swallow X-ray, but the best way for demonstration is videofluoroscopy and by upper gastrointestinal endoscopy. They appear smooth, thin, and gray with eccentric or central lumen space. The webs typically occur in the upper part of the esophagus and may be missed and accidentally ruptured unless the endoscope is introduced under direct visualization.1
Iron deficiency is believed to decrease the contraction amplitude or force of the esophageal muscle resulting in motility impairment. Slower transit times have been recorded at the proximal and middle parts of the esophagus of Plummer-Vinson syndrome patients compared to healthy volunteers.2 Transit time is how fast ingested food and fluids travel through the esophagus.
Gude et al, report that iron replacement does not necessarily reverse the dysphagia in all the cases of Plummer-Vinson syndrome and that close monitoring of the web is mandated to watch for malignant change. In fact, 3 to 15 per cent of the patients with Plummer-Vinson syndrome, mostly women between 15 and 50 years of age, have been reported to develop esophageal or pharyngeal cancer.2
What Is Plummer-Vinson Syndrome Affecting the Esophagus In Celiac Disease and/or Gluten Sensitivity?
Sources:
Novacek G. Plummer-Vinson syndrome. Orphanet J Rare Dis. 2006; 1: 36. Published online 2006 September 15. doi: 10.1186/1750-1172-1-36. [↩] [↩]
Gude D, Bansal DP, and Malu A. Revisiting Plummer Vinson Syndrome. Annals of Medical and Health Sciences Research. 2013 Jan-Mar;3(1):119-121. [↩] [↩]
Bristol Stool Chart Showing Normal and Abnormal Stool.
What Is Chronic Constipation Alternating With Diarrhea?
C hronic constipation alternating with diarrhea is an intestinal motility disorder, or irregularity, characterized by alteration in stool formation, consistency, and evacuation which results in a bowel movement that consists of some hard or balled stool along with some loose stool that can cause leakage.
Q: How do irregular movement patterns develop in the colon?
A: The colon produces irregular movements as a result of problems that originate in the colon (large intestine) itself and/or the small intestine which then affects function of the colon.
Here are listed the many types of problems or diseases that cause these abnormal bowel movements:
Disorders that adversely affect the colon, an organ which must propel stool, remove excess water, absorb electrolytes, ferment undigested food material that passes into it, and produce nutrients from the fermentation process:
Poor diet that does not contain adequate nutrition, fiber, probiotics, prebiotics, and water to form normal stool.
Diet that contains irritating, toxic or allergenic food that cause spasms.
Diseases that inflame the mucosa lining such as collagenous colitis, altering the proper absorption of water and electrolytes.
Diseases that damage and swell the colon walls, such as Crohn’s disease, ulcerative colitis, and diverticulitis.
Diseases that obstruct the lumen or passageway so that stool passes with difficulty.
Diseases that hamper normal peristalsis (muscle action), such as irritable bowel syndrome (IBS), diabetes and thyroid disease.
Disorders that adversely affect the small intestine, an organ which must digest and absorb nutrients needed by the body while passing unabsorbed food material to the colon:
Diet that conatins too much fat, sugar or artifical sweeteners, causing diarrhea.
Disorders that result in malabsorption, such as gluten enteropathy, milk enteropathy, steatorrhea (fat malabsorption), lactose intolerance, sucrose intolerance, maltose intolerance, and bacterial overgrowth, passing abnormal amounts of undigested food material to the colon where it is fermented producing excessive gas, diarrhea and spasm.
Disorders that impair peristalsis, such as active celiac disease, diabetes, scleroderma, and thyroid disease.
Tumors like cancer and lymphoma impair regular passage of material to colon.
Drugs that impair peristalsis, such as iron supplements, aluminum containing antacids, narcotics, some anti-depressants, some anti-seizure, and some diuretics.
What Is Chronic Constipation Alternating With Diarrhea In Celiac Disease and/or Gluten Sensitivity?
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. [↩]
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. [↩]
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?
E rythema nodosum is an inflammatory disorder involving the deep dermis layer of skin and subcutaneous fat septa that underlies the skin. It is characterized by eruptions of recurrent or persistent multiple painful, red nodules under the skin that leave a bruised appearance when healing and do not scar.
The lower legs are most affected, but sores can appear anywhere there is subcutaneous fat.
Q: How do the nodules develop in erythema nodosum?
A: The edges of nodules are poorly defined, and the nodules vary from 2-6 cm.
During the first week of eruption, nodules become tense, hard, and painful. During the second week, they change color from bright red to bluish or livid and may become soft, but do not ulcerate. As absorption progresses, the color gradually fades to a yellowish hue, resembling a bruise. This disappears in 1 or 2 weeks as the overlying skin sloughs off and is replaced.1
The eruptive phase of erythema nodosum begins with flulike symptoms of fever and generalized aching followed by a painful rash within 1-2 days. Aching legs and swelling ankles may occur and precede the eruption or appear during the eruptive phase and may persist for weeks.2
Currently, the most common cause of erythema nodosum is streptococcal infection in children and streptococcal infection and sarcoidosis in adults.3Most sores in infection-induced erythema nodosum heal within 7 weeks, but active disease may last up to 18 weeks.
In contrast, 30% of idiopathic erythema nodosum cases may last more than 6 months. Idiopathic means that the cause is not known.
What Is Erythema Nodosum In Celiac Disease and/or Gluten Sensitivity?
H angnail is a broken strip of epidermis (piece of skin) at root or lateral (side) edge of fingernail or toenail that causes sharp pain.
A hangnail develops because the skin around the nail is unhealthy due to inadequate nutrition. Injury from trauma including biting the skin and pushing back the cuticles or exposure to excessive detergents and water that remove protective oils promote the development of hangnail.
All ages and both sexes can be affected.
Q: Can a hangnail become infected?
A: Infection, called paronychia, may develop from invasion of sore skin by any of these pathogens: bacteria, fungus, or yeast (Candida). Infected skin is red, swollen, and painful. Topical ointment is required to treat the infection.1
What Is Hangnail In Celiac Disease and/or Gluten Sensitivity?
P ityriasis rubra pilaris (PRP) is a chronic generalized exfoliative dermatitis (sloughing skin) characterized by erythema (redness), scaling, dilated plugged hair follicles, and keratoderma (thickened skin) of the hands and feet that is often associated with anemia and low serum albumin.
It may manifest either as Type I classical adult onset PRP, Type II atypical adult (onset) PRP, or Type VI PRP (HIV-associated PRP pityriasis rubra pilaris) in contrast to classical juvenile (Type III) and circumscribed juvenile (Type IV) encountered among children.1
Q: Who is affected in the general population?
A: All ages are affected. Pityriasis rubra pilaris occurs all over the world but with racial variations – it is 1 in 5,000 in Great Britainand 1 in 50,000 in India.2
What Is Pityriasis Rubra Pilaris In Celiac Disease and/or Gluten Sensitivity?
Sources:
Sehgal VN, Srivastava G, Dogra S. Adult onset pityriasis rubra pilaris. Indian J Dermatol Venereol Leprol. 2008 Jul-Aug;74(4):311-21. [↩]
Sehgal VN, Srivastava G, Dogra S. Adult onset pityriasis rubra pilaris. Indian J Dermatol Venereol Leprol. 2008 Jul-Aug;74(4):311-21. [↩]
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