Elevated bone alkaline phosphatase (BALP) is a laboratory result that indicates an abnormal blood level of this bone enzyme.
A bone alkaline phosphatase blood level is one of the most frequently used biochemical markers of bone formation.
Q: Why is the purpose of bone alkaline phosphatase?
A: Bone alkaline phosphatase is produced by bone cells called osteoclasts in normal bone maintenance for the purpose of breaking down old or damaged bone so that other bone cells called osteoblasts can fill in the excavated areas with new bone. This process keeps bone stong and healthy.
Elevated bone alkaline phosphatase shows that more bone is being broken down than is being replaced. It can be caused by hyperparathyroidism, bone tumors from cancer, and malnutrition.
What Is Elevated Bone Alkaline Phosphatase (BALP) In Celiac Disease and/or Gluten Sensitivity?
Hypokalemia means the level of potassium in the bloodstream is too low to meet metabolic needs of the body for this mineral and is characterized by metabolic acidosis, altered nerve conduction and muscle contraction.
Rapid potassium loss can result in life-threatening hypokalemic rhabdomyolysis which is destruction of muscle tissue that results in kidney damage.1
Q: What are metabolic needs of the body for potassium?
A: The metabolic needs of the body for potassium are great because this mineral is crucial for life and especially for normal nerve and muscle function.
Most potassium is intracellular, meaning it is found within cells while sodium, its opposing mineral (both electrolytes), is found in the fluid surrounding cells. In muscle contraction, exchange of potassium and sodium takes place so that potassium moves out of muscle cells and sodium moves into them. With muscle relaxation, potassium moves back into the cells and sodium moves out.
What Is Hypokalemia In Celiac Disease and/or Gluten Sensitivity?
Sources:
Williams SG, Davison AG, Glynn MJ. Hypokalaemic rhabdomyolsis: an unusual presentation of celiac disease. European Journal of Gastroenterology and Hepatology. Feb 1995;7(2):183-4. [↩]
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, 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?
H ypertransaminasemia is a chronic condition of elevated blood liver transaminase enzymes, commonly called “liver enzymes,” that signifies hepatocellular (liver) injury.
Q: What are serum transaminases?
A: Transaminases are the liver enzymes ALT and AST. ALT is the abbreviation for alanine aminotransferase enzyme and AST is the abbreviation for aspartate aminotransferase enzyme.
Transaminases are commonly measured in routine blood tests to determine liver function. Elevated ALT and AST transaminases indicate inflammation of the liver. Other specific tests must follow to determine the cause of inflammation.
What Is Hypertransaminasemia In Celiac Disease and/or Gluten Sensitivity?
Drawing of Biopsy Showing Muscle Fibers Invaded by Immune Cells. Courtesy MDA.org
What Is Polymyositis?
P olymyositis is a body-wide connective tissue disease resulting from autoimmune attack of skeletal muscles that is characterized by inflammatory and degeneratory changes. The course is unpredictable being marked by spontaneous flare-ups and remissions.
Polymyositis can begin slowly or abruptly according to the factor that is triggering the onset such as infection, medications like phenytoin, and autoimmune disease.
Progressive muscle weakness starts in the proximal skeletal muscles (muscles closest to the trunk of the body).
Skeletal muscles, also called voluntary, are muscles that move the body as we want, such as walking and lifting objects, as opposed to those we cannot voluntarily control, such as the muscles of digestion.
Q: What are the degeneratory changes in skeletal muscles?
A: In polymyositis, degeneratory changes in skeletal muscles means that muscles are being destroyed (called necrosis), resulting in fibrosis, or scarring. When scar tissue takes the place of lost muscle tissue, it cannot act like muscle to contract and relax. Muscle destruction is what causes muscle pain and weakness.
After the clinical work-up of exams and blood studies to determine muscle damage, the diagnosis of polymyositis is confirmed by muscle biopsy. See image at above left. The black dots are inflammatory cells. Edema (fluid) between cells caused by inflammation pushes muscle fibers apart.
There is no cure for polymyositis, but the symptoms can be treated. Options include medication, physical therapy, exercise, heat therapy (including microwave and ultrasound), orthotics and assistive devices, and rest. The standard treatment for polymyositis is a corticosteroid drug, given either in pill form or intravenously. Immunosuppressant drugs, such as azathioprine and methotrexate, may reduce inflammation in people who do not respond well to prednisone.
Periodic treatment using intravenous immunoglobulin can also improve recovery. Other immunosuppressive agents used to treat the inflammation associated with polymyositis include cyclosporine A, cyclophosphamide, and tacrolimus. Physical therapy is usually recommended to prevent muscle atrophy and to regain muscle strength and range of motion.1
Diagnosis is based on elevated muscles enzymes, increased urinary creatine level, and electromyograph abnormalities.
Polymyositis can affect people at any age. It is most common in adults between ages 50 and 70, and in children ages 5 to 15. It affects women twice as often as men and is more common in African Americans than Caucasians.2 The major causes of death from polymyositis are cancer and lung disease, including pneumonia. The 5-year mortality rate can be as high as 1 in 5 patients.2
What Is Polymyositis In Celiac Disease and/or Gluten Sensitivity?
Sources:
National Institute of Neurological Disorders and Stroke [↩]
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. [↩] [↩]
A utoimmune disorders refer to those conditions that involve an abnormal attack on the body’s own tissues perpetuated by the production of autoantibodies directed against self.
Q: What happens when autoantibodies attack the body’s own tissues?
A: This abnormal immune activity by autoantibodies causes inflammation and damage to targeted body tissues.
Dermatitis herpetiformis is a skin manifestation of celiac disease characterized by extremely itchy blisters that commonly erupt on forearms and knees but may appear on the face, scalp or buttocks.
Autoimmune diseases as a group affect approximately 8.5% of people worldwide.
What Are Autoimmune Disorders In Dermatitis Herpetiformis?
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?
