Skip to content

Dementia

Close-up shows inflammation and yellowish white patches of roof and back of the mouth caused by candidiasis. Uvula is greatly swollen, hanging near the level of the tongue. Courtesy: Wikipedia.
Close-up shows inflammation and infected patches on roof and back of the mouth caused by candidiasis. Uvula is swollen, hanging near the tongue. Courtesy: Wikimedia.

What Is Candida Albicans Infection?

[dropcap]C andida albicans infection, called candidosis or candidiasis, is an opportunistic invasion of mucous membrane or skin by candida albicans, an endogenous yeast found in 40 to 80% of normal human beings. A former name for this small, budding fungus is monilia albicans.

Opportunistic means that yeast living on mucosal and skin surfaces does not invade (infect) unless these tissues become unhealthy and therefore cannot protect themselves.

Q: How does candida albicans cause infection?

A: Candida albicans lives on the mucosal surfaces and skin in most people without causing infection (colonizes) because of our normal defenses against invasion. In fact, candida albicans is a very effective colonizer of humans. For example, Russell and Lay found that 47% of 1-month-old infants were orally colonized with candida albicans, and 49% were colonized with other fungi.

During growth within the intestinal tract, the organism senses pH (acidity), oxygen, carbon sources, and the presence of surfaces allowing it to optimize gene expression for a particular environment. With these mechanisms for sensing, candida albicans is able to efficiently colonize humans in infancy.1

Candida Infection Of The Esophagus on X-ray. Courtesy Radiology Assistant.nl
Candida Infection Of The Esophagus (White Area) On X-ray. Courtesy Radiology Assistant.nl

Lowered host defenses allow yeast already present on mucosal and skin surfaces to take advantage and can grow rapidly, becoming pathogenic (disease producing) so that infection results.

Infection is characterized by superficial, irregular white patches on mucosal surfaces and possible invasion of the bloodstream by a filamentous form (thread-like structures) that can rapidly develop.

Candida albicans is unique among oral pathogens in its ability to invade cornified layers of stratified squamous epithelium of the tongue, mouth surfaces, hard and soft palate, esophagus, and gut. Stratified squamous epithelium is the tough surface cells that ordinarily protect underlying tissues from damage or invasion by microbes.

Candida albicans is also capable of invading the lungs and causing pneumonia and septicemia, which is the spread of infection into the bloodstream.

Here is a time honored simple do-it-youself test for infection of the mouth or throat: First thing in the morning before brushing your teeth or eating, fill a small see through glass with water then gently spit onto the surface. If after an hour the spit remains on the water surface, it is unlikely you have candida in the mouth. If it grows legs downward, it indicates that yeast is growing. If the spit sinks to the bottom, you have this problem. Yeast in the mouth can quickly travel down the esophagus and into the gut.

Medical diagnosis. Difinitive diagnosis for the oral cavity is made by your clinician by swabbing the areas of your mouth and/or throat and viewing under a microscope for evidence of candida.

Infections of the esophagus and gut require inspection by gastroscopy or endoscopy procedure and the taking of samples to be examined under microscope. This examination also give the opportunity to rule out other problems. Barium swallow can show the extent of infection and any disfiguration of the esophagus that results.

What Is Candida Albicans Infection In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Rosenbach A, Dignard D, Pierce JV, Whiteway M, Kumamoto CA. Adaptations of Candida albicans for growth in the mammalian intestinal tract. Eukaryot Cell. 2010 Jul;9(7):1075-86. doi: 10.1128/EC.00034-10. Epub 2010 Apr 30. [↩]

Osteoporosis

Woman with long standing osteoporosis. Courtesy of Wikimedia.
Woman with long standing osteoporosis. Courtesy of Wikimedia.

What Is Osteoporosis?

[dropcap]O[/dropcap]steoporosis is a metabolic bone disorder characterized by diminished bone mass (density) with normal cell appearance but fragile bone strength that prediposes to broken bones, and with high bone turnover.

This condition usually goes undetected until late when loss of height or a bone fracture occurs. In fact, each year  1.5 million fractures mainly of the hip, spine and wrist are attributed to osteoporosis. Compression fractures of vertebrae bones are the most common, accounting for 700,000 cases.

Bone is composed of specialized connective tissue called osseous tissue. Osseous tissue is made up of living bone cells (osteocytes) that are embedded in a hard matrix (framework) of calcified substance.

Bone matrix contains collagen fibers and the minerals calcium phosphate and calcium carbonate, which provide strength to bone. The copper enzyme, lysyl oxidase, is involved in the cross-linking of collagen in forming the framework for depositing calcium and other minerals to build and repair bone.

Q: How do osteocytes function in bone?

A: Osteocytes maintain the health of bone by their metabolic activity in regulating normal bone turnover. Bone turnover is the breaking down and removal of old or damaged bone and rebuilding or remodeling of healthy bone that is ongoing throughout life. The bone formation process takes about 3 months to complete.

Osteoporosis develops from failure of the body to maintain health and to provide bone tissue with adequate nutrition for proper function. Risk factors that can be modified include: low calcium intake, sedentary lifestyle, smoking, drinking alcohol excessively, eating a diet with excessive caffeine, protein, and phosphate, and taking certain medications over a long time such as steroids, thyroid preparations, the anti-convulsive drug phenytoin, aspirin, antacids, anticoagulants, some diuretics, and some chemotherapeutic drugs. See below for a fuller description.

In addition to celiac disease, osteoporosis is associated with advancing age, family history, nulliparity (no pregnancies) and post-menopause in females, certain disorders such as hyperthyroidism, hypogonadism, inflammatory bowel disease like Crohn’s disease, multiple myeloma, anorexia nervosa, and Cushing’s disease.

Bone strength is easily measured by testing bone mineral density (BMD). BMD is evaluated by DEXA scan (dual-energy X-ray absorptiometry).  DEXA at the femoral neck and lumbar spine is considered the gold standard to confirm the diagnosis of osteoporosis.  Results are expressed as T and Z scores. T scores compare the result with a 20 to 40 year old helathy person while  Z scores compare the result with persons in the same age group. Both are measured in standard deviations (SD).

According to WHO criteria (World Health Organization), a T-score of -1 SD or greater denotes normal bone, a T-score between −1 to −2.5 SD denotes osteopenia, and a T-score of −2.5 or more denotes osteoporosis.1

Treatment is aimed to preserve and increase bone density, minimize symptoms for better quality of life and reduce risk of bone fractures.

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

The cumulative effects of gluten-induced inflammation, treatment delay, and malabsorption result in lower bone density and bone fragility.2

Sources:
  1. Pantaleoni S, Luchino M, Adriani A, Pellicano R, Stradella D, Ribaldone DG, Sapone N, Isaia GC, Di Stefano M, Astegiano M. Bone mineral density at diagnosis of celiac disease and after 1 year of gluten-free diet. ScientificWorldJournal. 2014;2014:173082. doi: 10.1155/2014/173082. [↩]
  2. Grace-Farfaglia P. Bones of Contention: Bone Mineral Density Recovery in Celiac Disease-A Systematic Review. Nutrients. 2015 May 7;7(5):3347-3369. [↩]

Apathy

Cows Milk enteropathyWhat Is Milk Intolerance (Bovine Beta Casein Enteropathy)?

[dropcap]B ovine beta casein enteropathy is characterized by raised serum IgA antibodies to bovine beta casein found by blood testing and damage to mucosa of the jejunum found by biopsy.

The jejunum is the second section of the small intestine, between the duodenum and the ileum.

Mucosa damage is similar to damage caused by gluten.

Q: What is bovine beta casein?

A: Bovine beta casein is a protein found in cow’s milk.

An immune reaction to protein in milk is totally different from lactose intolerance. Lactose intolerance develops from deficiency of an intestinal enzyme called lactase which is required to digest lactose, the sugar in milk.

What Is Milk Intolerance In Celiac Disease and/or Gluten Sensitivity?

Bone Fractures 

Proptosis and lid retraction are features of Grave's disease, or hyperthyroidism. Courtesy of Wikimedia.
Proptosis and Lid Retraction are Features of Grave’s Disease, or Hyperthyroidism.

What Is Grave’s Disease (Hyperthyroidism)?

[dropcap]G rave’s disease, or hyperthyroidism, is an autoimmune thyroid disease characterized by diffuse nontender goiter, elevated thyroxine hormone levels (T4, T3), suppressed thyroid stimulating hormone (TSH), and presence of thyroid receptor antibodies in the blood.

The autoantibodies involved are anti-thyroid peroxidase and anti-thyroglobulin antibodies. They bind to the thyroid stimulating hormone receptors, causing thyroid stimulation. These antibodies are detected by blood tests.

Q: What happens to the thyroid gland in Grave’s disease?

A: The thyroid gland is located in the front of the neck. This butterfly shaped 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

Thyroxine molecule, chemical structure. Thyroid gland hormone that plays a role in energy metabolism regulation. It is a iodine containing derivative of thyrosine. Atoms are represented as spheres with conventional color coding: hydrogen (white), carbon (grey), oxygen (red), nitrogen (blue), iodine (purple).
Thyroxine molecule. Atoms are represented as spheres with conventional color coding: hydrogen (white), carbon (grey), oxygen (red), nitrogen (blue), iodine (purple).

T3 is the active hormone and is made from T4. Thyroid hormones are released into the bloodstream as needed to control 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 in response to stimulation by the nearby hypothalamus which is continually monitoring levels of thyroxin. When thyroid hormone levels are high, the pituitary decreases TSH production. So in Grave’s disease, release of TSH by the pituitary gland is suppressed by the hypothalamus because thyroid hormone is elevated. Goiter develops from growth stimulation by thyroid stimulating autoantibodies.

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

Sources:
  1. Taber’s Cyclopedic Medical Dictionary. 19th ed. F.A. Davis Company. Philadelphia, PA. [↩]

Abnormal Blood Values in Childhood

canstockphoto18551453
Illustration Showing Skin Anatomy.

What Is Pruritic Skin?

[dropcap]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?

Osteopenia In Childhood 

sclerodermaWhat Is Scleroderma?

[dropcap]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:
  1. 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. [↩]
  2. http://www.rheumatology.org [↩]

Cutis Laxa, Acquired

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)?

[dropcap]C oronary 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. [↩]

Edema

Cachexia with Wasted Muscles, Weakness, and That Developed over 3 Years Time.
Cachexia with Wasted Muscles, Weakness, Weight Loss, Anemia, Skin Hemorrhages, Anorexia. GFW

What Is Cachexia?

[dropcap]C achexia is a state of ill health involving deteriorating body composition that is characterized by general malnutrition and loss of lean tissue such as muscle.

Q: What are typical findings in cachexia?

A: Arm muscle triceps (the muscles at the back of the upper arm), skin folds, subscapular skin folds, fat area index, and bone mineral content are significantly lower than normal.

Cachexia may develop in protein-losing enteropathy such as celiac disease, chronic or severe infection such as pneumonia, tuberculosis, malaria, or many chronic diseases such as heart failure and cancer.

Cachexia can develop in persons of any age.

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

Ataxia, Gait

Normal Liver Lobule. Courtesy almostadoctor.com
Figure 1: Normal Liver Lobule. Courtesy almostadoctor.com

What Is Autoimmune Cholangitis?

[dropcap]A utoimmune cholangitis is a rare inflammatory self-targeted disease of the biliary tract produced by high levels of immunoglobulin G (IgG) antibodies and antinuclear antibodies (ANA).

Autoimmune cholangitis is characterized by progressive inflammation and scarring that leads to narrowing and destruction of the bile ducts and development of biliary cirrhosis of the liver.

Autoimmune cholangitis is also termed anti-mitochondrial antibody-negative primary biliary cirrhosis because there is no production of anti-mitochondrial antibodies.

Q: What happens when bile ducts can no longer transport bile out of the liver?

A: Bile that cannot be removed from the liver by the biliary tract backs up and damages the liver, causing cirrhosis. In Figure 1, bile back up would directly damage the hepatic (liver) cells seen here as grey “blocks.” 

Bile is a greenish brown liquid continually made by the liver cells (hepatocytes) from phospholipids salt, cholesterol, and aging blood cells that it removes from circulation. 

Bile also carries away waste products produced by normal metabolism and toxic substances that are removed by the liver for eventual elimination in stool. As such, bile must continually flow out of the liver to prevent build-up in the liver. 

Bile from the hepatic cells drains into small tubes called canniculi and then into larger bile ducts to be carried out of the liver to the gall bladder for storage until needed to aid in the digestion and absorption of fat from the small intestine.   Bile emulsifies fat eaten in the diet so that the pancreatic enzyme called lypase can break it down into its fatty acid and glycerol components. 

Unfortunately, autoimmune cholangitis is difficult to diagnose because it mimics many other diseases such as primary sclerosing cholangitis, sarcoidosis, cancer and lymphoma.

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

Neutropenia 

neutrophilWhat Is Neutropenia?

[dropcap]N[/dropcap]eutropenia  is a blood disorder characterized by presence of an abnormally low number of neutrophils.

Neutrophils are white blood cells (leukocytes) that serves as the primary defense against infections by destroying bacteria in the blood. 

Specfically, neutrophils are a type of granulocyte that contain granules filled with potent chemicals to break down the microbes they ingest. Some of these chemicals, such as histamine, also contribute to inflammation and allergy.

The process of eating and digesting microbes is called phagocytosis. Neutrophils are phagocytes.1

Q: How do neutrophils eat microbes?

A: Segmented neutrophils  are the mature phagocytes that migrate through tissues to destroy microbes and respond to inflammatory stimuli. Segmented neutrophils comprise 40-75 % of the peripheral leukocytes. They are usually 9 to 16 µm in diameter. The nuclear lobes, normally numbering from 2 to 5, may be spread out so that the connecting filaments are clearly visible, or the lobes may overlap or twist. The chromatin pattern is coarse and clumped. The cytoplasm is abundant with a few nonspecific granules and a full complement of rose-violet specific granules.1

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

Sources:
  1. http://www.wadsworth.org/chemheme/heme/microscope/seg.htm [↩] [↩]