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Occipital Lobe Epilepsy With Cerebral Calcifications

Close-up Slice of a Small Intestinal Villus Showing How Enterocytes Appear Tightly Lining the Entire Outside Surface Of A Villus. Courtesy Cleo Libonati

What Is Increased Intestinal Permeability?

I ncreased intestinal permeability is characterized by dysfunctional intestinal permeability (leakiness) allowing for the penetration of harmful entities from the gut into the bloodstream such as undigested proteins and microbes. The popular name is “leaky gut.”

Q: Why does intestinal permeability increase?

A: Intestinal permeability is an essential function of the small intestinal mucosal lining by which wanted substances such as properly digested foodstuffs are allowed to permeate through the lining to enter the body via the bloodstream and lymphatics. At the same time unwanted substances are kept out.

The mucosal lining is one cell thick and makes up the surface between the digested foodstuffs inside the hollow of the intestine and the underlying tissues.

The mucosal lining is covered by millions of microscopic finger-like structures called villi that project toward the inside of the intestine giving the appearance of a shag rug.

Each one, called a villus, contains a capillary bringing blood to absorb nutrients, a vein to take away nutrients, and a lacteal to absorb and take away digested fat. Its wall is made up of a single layer of tightly connecting cells, called enterocytes.

This single layer of cells separates the contents of our small intestine from the lamina propria (underlying tissues of the small intestine) and the rest of our body. Breaching of this single layer of cells by leakiness can expose lymphocytes (immune cells) located in the lamina propria to a myriad of microorganisms and food antigens, leading to immune reactions.1

To protect the body from unwanted substances, a gatekeeping barrier system operates to regulate the passage of nutrients, or permeation, through the surface mucosal lining. This system acts to seal the inside body from the gut.

The integrity of intestinal permeability is determined by interactions among several barrier components including the unstirred water layer, mucosal surface hydrophobicity, the surface mucous coat, and cell factors (especially tight junctions).

Tight junctions hold cells tightly together side-by-side to prevent unwanted substances from passing through the lining. Tight junctions are complex structures comprising over 50 proteins, such as the claudin proteins which are considered to be the structural backbone of tight junctions.

Tight junctions include a series of special proteins forming fibrils (springy like proteins) that cross the plasma membrane and interact with proteins in the adjoining cells. Tight junctions are regulated by the protein zonulin.2

If zonulin deregulates from the action of substances such as gliadin (gluten in wheat) and bacteria, the tight junction barrier fails which results in increased intestinal permeability. Dysfunction of the barrier system allows unwanted substances to enter the body where they are damaging to many tissues.

Tight junction dysfunction has been shown to be a part of certain autoimmune diseases such as celiac disease, type I diabetes mellitus, multiple sclerosis, and rheumatoid arthritis. Other diseases associated are cancer, allergies, and infections.3

Important gastrointestinal infections that cause leaky gut include rotavirus, parasites, pathogenic bacteria (escherichia coli, clostridium difficile), and mycotoxins produced by fungi found in stored grain and dried fruit.4

Fortunately, the presence of some commensal (friendly intestinal bacteria) and probiotic strains leads to an increase in tight junctions  proteins at the cell boundaries and in some cases prevents or reverses the adverse effects of pathogens, food and stress. Various dietary components are also known to regulate epithelial permeability by modifying expression and localization of  tight junctions proteins.2

What Is Increased Intestinal Permeability In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Fahardi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease. Journal of Gastroenterology and Hepatology. 2003; 18: 479-497. [↩]
  2. Ulluwishewa D, Anderson RC, McNabb WC, Moughan PJ, Wells JM, Roy NC. Regulation of tight junction permeability by intestinal bacteria and dietary components. J Nutr. 2011 May;141(5):769-76. doi: 10.3945/jn.110.135657. [↩] [↩]
  3. Fasano A. Zonulin and Its Regulation of Intestinal Barrier Function: The Biological Door to Inflammation, Autoimmunity, and Cancer. Physiological Reviews. January 2011Vol. 91no. 151-175DOI: 10.1152/physrev.00003.2008 [↩]
  4. Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease. Journal of Gastroenterology and Hepatology. 2003;18:479-91. [↩]

Allergic Rhinitis

hypomagnesemiaWhat Is Hypomagnesemia?

H ypomagnesemia means the level of magnesium in the bloodstream is too low to meet metabolic needs of the body for this mineral.

Q: What are the metabolic needs of the body for magnesium?

A: The metabolic needs of the body for magnesium are numerous which gives rise to very many distressing symptoms when this mineral is deficient.

A major function of magnesium is to stabilize the structure of an enzyme called adenosine triphosphate (ATP) within cells for the production of energy. In the brain, magnesium plays important roles in all the major metabolisms such as oxidation-reduction and regulation of ions (charged minerals).1

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

Sources:
  1. Bourre JM. Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients. J Nutr Health Aging. 2006 Sep-Oct;10(5):377-85. [↩]

Itchy (Pruritic) Skin  

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

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. [↩]

Autoimmune Disorders In Dermatitis Herpetiformis

bloodvialWhat Is Prolonged Prothrombin Time?

P rolonged prothrombin time (PT) is a laboratory blood test result showing that blood clots too slowly which makes the patient subject to abnormal bleeding.

Q: What does the prothrombin time (PT) test measure?

A: The prothrombin test measures the clotting ability of blood protein factors I, II (prothrombin), V, VII, and X. If any of these factors are too low, it takes longer than normal for the blood to clot. Prothrombin is a vitamin K dependent factor meaning a deficiency of vitamin K will cause low prothrombin.

Blood is drawn into a blood collection tube with a light blue stopper which has a buffering additive. Tubes must be completely filled.

What Is Prolonged Prothrombin Time In Celiac Disease and/or Gluten Sensitivity?

Lymphoma, B-Cell Non-Hodgkin’s

e3343bf0a689b5f974a852fa2e84a718What Is Laryngospasm?

L aryngospasm is an acute disorder of the larynx that is characterized by life-threatening spasms of the muscles of the larynx located in the throat.

Laryngospasm is a rare feature of hypocalcemia (low blood calcium level) characterized by severe alteration in nerve conduction and muscle contraction.

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

Common Variable Immunodeficiency 

Folic acid deficiency anemia gluten celiac disease symptom
Red Blood Cells.

What Is Folic Acid Or Folate Deficiency Anemia?

F olic acid deficiency anemia, also called folate deficiency anemia, is a macrocytic anemia characterized by defective DNA synthesis of red blood cells that results from a lack of folate in the body.

Q: How does folate deficiency cause anemia?

A: Folates are a family of B vitamins and folic acid is an active form.

Folate is required for the formation of both red and white blood cells in the bone marrow and for their maturation.

Also, folate serves as a carrier in the formation of heme, which contains iron, and is the non-protein part of the hemoglobin molecule.1

Red blood cells provide oxygen to body tissues. When there are not enough red blood cells or when they cannot properly carry oxygen, the condition is called anemia. In folic acid deficiency anemia, the red blood cells are abnormally large. Such cells are called macrocytes (macro size cells). They are also called megaloblasts (mega size cells) as seen in the bone marrow where they are produced. This is why this macrocytic anemia is also called megaloblastic anemia.2

Tests that may be done to determine folate adequacy are complete blood count (CBC), red blood cell folate level, methylmalonic acid level, and homocysteine level. Folic acid deficiency anemia shows a decrease in red blood cell folate and/or serum folate levels and normal plasma methylmalonic acid level with elevated homocysteine blood level. These levels distinguish folic acid deficiency anemia from vitamin B12 deficiency anemia.3

What Is Folate Deficiency Anemia In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Kathleen Mahan and Sylvia Escott-Stump, ed. Krause’s Food, Nutrition & Diet Therapy, 10th Edition. Philadelphia, PA. USA: W.B. Saunders Company, 2000. [↩]
  2. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001578/ [↩]
  3. Mark Beers and Robert Berkow. The Merck Manual, 17th Edition. Whitehouse Station, N.J. USA: Merck Research Laboratories, 1999. [↩]

Celiac Disease, Refractory

Anatomy of Upper Airway and Throat. Courtesy Wikipedia.org
Anatomy of Upper Airway and Throat. Courtesy Wikipedia.org

What Is Post-Cricoid Carcinoma?

P ost-cricoid carcinoma is a rare malignancy arising in the hypopharynx.

Q: What is the hypopharynx?

A: The hypopharynx is the lower portion of the pharynx that opens into the larynx. It is comprised of the postcricoid region, pyriform sinus, and posterior hypopharyngeal wall.

Tumors rarely appear in the posterior pharyngeal wall or postcricoid region without also involving the pyriform sinus. The lack of anatomic barriers between these sites and a propensity for these tumors to develop in the pyriform sinus and spread outward account for this phenomenon.

Overall prognosis for these tumors is poor. Because of the rich organic lymphatic and vascular networks, aggressive growth and early cervical metastases (compared with cancers at other head and neck sites) characterize these cancers.

A study investigating the clinical course of 21 patients with post-cricoid carcinoma found the 5-year cause-specific survival rate was 52%. All the patients who eventually died did so within 3 years of the treatment. Seven patients had distant metastases, representing a higher frequency as compared with that of patients with recurrence of the primary focus and cervical lymph node metastasis. All of these patients who had been treated by surgery died of the cancer.1

Unfortunately, hypopharyngeal cancers are discovered at a later stage than other head and neck cancers. The delay in diagnosis from symptom onset averages 10 months.2

What Is Post-Cricoid Carcinoma In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Asakage T, Nakao K, Ebihara Y, Fujishiro Y, Watanabe K. A clinical study of post-cricoid carcinoma. Acta Otolaryngol Suppl. 2007 Dec;(559):118-22. doi: 10.1080/03655230701599354. [↩]
  2. http://emedicine.medscape.com/article/848359-overview [↩]

IgA Deficiency

Red Blood Cell Comparison. Courtesy medindia.com
Red Blood Cell Comparison. Courtesy medindia.com

What Is Iron Deficiency Anemia?

I ron deficiency anemia is a blood cell disorder that is characterized by formation of small, pale red blood cells, causing tissue hypoxia. Hypoxia is the inability to meet the demands of the body for oxygen.

Q: Why do small, pale red blood cells cause tissue hypoxia?

A: Small, pale red blood cells (erythrocytes) cause tissue hypoxia because they are not able, as do normal erythrocytes, to pick up adequate oxygen from the lungs and carry it to cells that use oxygen.

Red blood cell production and function are dependent on a sufficient level of iron in the body and also the ability to use available iron to make hemoglobin in red blood cells.

Hemoglobin is a protein that binds oxygen in red blood cells to be carried by the bloodstream to cells throughout the body. In iron deficiency anemia,  hemoglobin in females is below 12.5g/dl (normal range is 12.5 to 16g/dl) and in males it is below 13.5g/dl (normal range is 13.5 to 17.5g/dl).

Iron must be obtained from the diet, since the body cannot make it, but there are various factors that can interfere with absorption and use in the body, causing anemia. Iron absorption from the gut first requires ionization, or gaining a positive electrical charge, in the strongly acidic environment of stomach juice. Ionized iron, only, can be absorbed in the duodenum, which receives the acidic contents of the stomach before it is neutralized further along.

Dietary iron can be heme or non-heme depending on the food source. Heme iron obtained only from animal food sources is absorbed into the bloodstream by active transport across the brush border (microvilli) which cover the multitudinous villi of the small intestinal lining.

Non-heme iron obtained from plants must bind with apoprotein after entering the enterocyte (surface cell of small intestinal lining) to be ferried to the underlying basolateral membrane and exited by active transport into the bloodstream.

Frequently, chronic anemia due to iron deficiency is accompanied by increased platelets, and this thrombocytosis resolves with iron repletion (normal iron level). Conversely, in severe iron deficiency anemia, patients may have thrombocytopenia (low platelets), which also resolves with iron therapy.1

What Is Iron Deficiency Anemia In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Koury M and Rhodes M. How to approach chronic anemia. Hematology Am Soc Hematol Educ Program. 2012;2012:183-90. doi: 10.1182/asheducation-2012.1.183. [↩]

Lymphomas, Extraintestinal

What Is Dysphagia? D ysphagia is a functional upper digestive disorder characterized by difficulty in swallowing or food getting stuck and swallowing that takes longer than 10 seconds to complete. Q: What determines the symptoms?… 

Constipation Alternating with Diarrhea

Bristol Stool Chart Showing Normal and Abnormal Stool.
Bristol Stool Chart Showing Normal and Abnormal Stool.

What Is Chronic Constipation Alternating With Diarrhea?

Chronic 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?