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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?

Erythema Elevatum Diutinum (EED)

unexpected weight loss celiac disease symptomWhat Is Unexpected Weight Loss?

[dropcap]U nexpected weight loss is unintentional loss of body mass composition or inability to gain weight marked by decreased serum proteins and increased stool fat.1

What Is Unexpected Weight Loss 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. [↩]

Erythema Nodosum 

anorexia nervosa celiac disease gluten symptomWhat Is Anorexia?

[dropcap]A norexia or loss of appetite is a reduced desire to eat which can cause unintentional weight loss.

Anorexia is a feature of many disorders caused by malutrition such as celiac disease and aging or gastrointestinal problems such as chronic gastroenteritis, and dysgeusia (loss of taste).

Q: Are there other conditions that cause anorexia?

A: Other underlying problem include medication side effects, infection, chronic pain, depression, grief, dehydration, hormonal dysfunction such as thyroid disease, primary hyperparathyroidism, or Addison’s disease, autoimmune mechanisms such as sarcoidosis,  and cancer growth.

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

Hangnail

Aphthous_ulcer[1]What Are Aphthous Ulcers?

[dropcap]A phthous ulcers, also called canker sores, are a chronic disorder of soft mouth tissue characterized by small, painful purpuric, papular, or erosive lesions that are often surrounded by erythematous (red) margins.1

Q: What soft mouth tissues develop canker sores?

A: Canker sores can erupt on the mucosal surface of the inside lip, sides of mouth, under the tongue and along the side of the tongue. When they are forming, the area swells into a papule, or small bump. Later, the surface erodes and a crater forms with firm pus.

What Are Aphthous Ulcers In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Lahteenoja H, Toivanen A, Viander M, Maki M, Irjala K, Raiha I, Syrjanen S. Oral mucosal changes in coeliac patients on a gluten-free diet. European Journal of Oral Sciences. Oct 1998;106(5):899,8p. [↩]

Ichthyosis, Acquired  

cheilosisWhat Is Cheilosis?

[dropcap]C heilosis is a painful feature of nutritional deficiencies, especially riboflavin and/or pyridoxine deficiency, and less frequently, from vitamin B12, folic acid, and iron. It is characterized by redness of the lips with cracking and weeping in the corner of the mouth.

Q: What is the consequence of weeping at the corners of the mouth?

A: The open sores that develop at the corners of the mouth invite infection by candida albicans, a yeast organism, and less commonly by bacteria normally present on the skin such as staphylococcus aureus.

These sores make opening the mouth very painful and so restrict eating, talking, socializing, and dental care.

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

Melanoma

Enamel_celiac[1]What Are Dental Enamel Defects?

[dropcap]D ental enamel defects (DED) comprise a variety of abnormalities in the dental enamel of the second or permanent teeth and of primary or baby teeth.

Teeth may appear with pits, thin or missing enamel, non-white enamel (yellow, orange, or gray colored teeth), and demarcated opacities (very white spots) even if teeth are white.

Q: What is enamel?

A: Dental enamel is the shiny, hard, white, dense, inorganic substance covering the crowns of the teeth. The crown is the tooth portion above the gum. Under the enamel is hard dentin which surround the living pulp. In teeth with missing enamel, the areas with exposed dentin appear dull and tan colored.

What Are Dental Enamel Defects In Celiac Disease and/or Gluten Sensitivity?

Pityriasis Rubra Pilaris

Vitamin C Deficiency: Clean Teeth with Swollen Gums.
Vitamin C Deficiency: Swollen Gums.

What Are Bleeding / Swollen Gums?

[dropcap]B leeding and/or swollen gums is  an inflammatory disorder characterized by changes in gum integrity that may result in tooth loss.

Sponginess of the gum (swelling) indicates inflammation, called gingivitis. 

Q: What causes gingivitis?

A: Gingivitis that is caused by inadequate dental hygiene shows as pockets of swollen gum between or along the base of teeth where sticky plaque was allowed to build up. Plaque holds bacteria that inflames the gums where it occurs.

Gingivitis that is caused by vitamin C deficiency, pregnancy, certain drugs such as the anti-epileptic drug phenytoin, and leukemia affects the whole gum irrespective of mouth care.

What Are Bleeding / Swollen Gums In Celiac Disease and/or Gluten Sensitivity?

Itchy (Pruritic) Skin  

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

[dropcap]B eefy, 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. [↩]

Immune Thrombocytopenic Purpura

Photo of Skin Rash in ITP Courtesy Wikipedia.
Photo of Skin Rash in ITP Courtesy Wikipedia.

What Is Immune Thrombocytopenic Purpura?

[dropcap]I[/dropcap]mmune thrombocytopenia purpura (ITP), formerly called idiopathic, is an immune mediated bleeding disorder characterized by destruction of circulating platelets (thrombocytes) by autoantibodies in the presence of normal bone marrow and without other conditions that cause bleeding problems including many medications.

Q: How do autoantibodies destroy platelets?

A: Autoantibodies bind to normal platelet surface antigens (targets) which forms a complex that is cleared from blood by the reticuloendothelial system. Consequently, this condition results in an abnormal decrease in the number of platelets circulating in blood plasma.

Platelets are cells that are needed to stop bleeding. A normal platelet count is in the range of 150,000 to 450,000. With ITP, the platelet count is less than 100,000. By the time significant bleeding occurs, the patient may have a platelet count of less than 10,000. The lower the platelet count, the greater the risk of bleeding. 

Because of inability of blood to properly clot due to lack of sufficient platelets, a distinctive purplish rash develops under the skin from blood leakage and an appearance of many small red spots of varying size can cover the skin. Depending on the number of platelets, there may be minimal to extensive bleeding in various parts of the body.  Bleeding in the brain is the worst complication, causing death in approximately 1% of affected children and 5% of affected adults.

Immune thrombocytopenic purpura is common in childhood, on average 50 cases per 1,000,000 per year with same incidence in boys as girls. It may follow a viral infection or immunization and is caused by an inappropriate response of the immune system to cross react against the body’s platelets.1

The incidence of immune thrombocytopenic purpura in adults is approximately 66 cases per 1,000,000 per year.  Older persons and persons with a previous history of hemorrhage are at increased risk of severe bleeding in adult ITP.  

Spontaneous remission occurs in most children (80%).  Remission in adults usually requires treatment. 

What Is Immune Thrombocytopenic Purpura In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Dogan M, Sal E, Akbayram S, Peker E, Cesur Y, Oner AF. Concurrent celiac disease, idiopathic thrombocytopenic purpura and autoimmune thyroiditis. Clin Appl Thromb Hemost. 2011 Nov-Dec;17(6):E13-6. doi: 10.1177/1076029610378502. Epub 2010 Aug 3. [↩]