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Vitamin C Deficiency

vitamin c gluten celiac disease symptomWhat Is Vitamin C?

[dropcap]V[/dropcap]itamin C, also called ascorbic acid or ascorbate, is an essential water soluble vitamin.

Fresh supplies of vitamin C are required every day to perform vital roles throughout the body among which are the production of connective tissue such as skin, blood vessels and bone, anti-inflammatory responses and anti-oxidant performance. See below for all roles.

Vitamin C fights for us! It has an anti-cancer effect stemming from its role as a potent anti-oxidant in blood plasma and within cells. It also protects nucleic acids (DNA) from oxidative damage and inhibits the formation of nitrosamines (carcinogenic compounds formed in the digestive tract).

Importantly, vitamin C can regenerate vitamin E from an oxidized state after vitamin E performs its own anti-oxidant role against free radicals and vitamin C works together with other anti-oxidants, such as beta-carotene and glutathione, to increase their overall anti-oxidant effect.

A study investigating the specific anti-inflammatory and anti-oxidant micronutrients that reduce oxidative stress found that in adolescents with metabolic syndrome (MetS) the lower the vitamin C level in blood the worse the MetS status and blood uric acid level.  MetS prevalence was estimated at 7% among boys and 3% among girls.1

Vitamin C reverses osteoporosis by reducing or preventing oxidative stress that destroys living bone tissue. Osteoporosis is a disorder of bone inflammation that results in thin, weak bones that may easily fracture. In normal bone structure, vitamin C is required to form collagen, which is living bone tissue.

In humans, vitamin C reduces the duration of common cold symptoms, even if its effect is not clear.2

Vitamin C must be obtained from food daily because our bodies, unlike monkeys and other animals, cannot produce it.

Urinary excretion of vitamin C cannot be detected when vitamin intake is below the required levels. On the other hand, when intake exceeds saturation in the body, the vitamin and/or its metabolites are actively excreted into urine to prevent excessive toxicity of the vitamins.3

What Is Vitamin C Deficiency In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. TGBeydoun MA, Canas JA, Beydoun HA, Chen X, Shroff MR, Zonderman AB. Serum antioxidant concentrations and metabolic syndrome are associated among U.S. adolescents in recent national surveys. J Nutr. 2012 Sep;142(9):1693-704. doi: 10.3945/jn.112.160416. [↩]
  2. Shaik-Dasthagirisaheb YB, Varvara G, Murmura G, Saggini A, Caraffa A, Antinolfi P, Tete’ S, Tripodi D, Conti F, Cianchetti E, Toniato E, Rosati M, Speranza L,Pantalone A, Saggini R, Tei M, Speziali A, Conti P, Theoharides TC, Pandolfi F. Role of vitamins D, E and C in immunity and inflammation. J Biol Regul Homeost Agents. 2013 Apr-Jun;27(2):291-5. [↩]
  3. Shibata K, Hirose J, Fukuwatari T. Relationship Between Urinary Concentrations of Nine Water-soluble Vitamins and their Vitamin Intakes in Japanese Adult Males. Nutr Metab Insights. 2014 Aug 5;7:61-75. doi: 10.4137/NMI.S17245. eCollection 2014. [↩]

Systemic Lupus Erythematosus 

bruiseWhat Is Hypoprothrombinemia?

[dropcap]H ypoprothrombinemia is a deficiency of prothrombin (clotting factor II) in the blood that is characterized by impaired hemostasis in response to trauma or a laceration.

Q: What is hemostasis and how is it altered by a deficiency of prothrombin?

A: Hemostasis encompasses the tightly regulated processes of blood clotting, platelet activation, and blood vessel repair.1

Prothrombin is a protein clotting factor present in blood that is involved in the first part of hemostasis, which is blood clotting or coagulation. Vitamin K is required for prothrombin production.

When a laceration or wound is sustained, prothrombin is converted to the enzyme thrombin. Thrombin in turn acts on fibrinogen to convert it to fibrin which then forms the framework of a clot to stop bleeding. Deficiency of prothrombin prevents this series of events and bleeding is not properly stopped.

After the clotting process of hemostasis would come the second part, platelet activation. Eventually, coagulation and platelet activation are switched off by blood-borne inhibitors.

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

Sources:
  1. Versteeg HH, Heemskerk JWM, Levi M,  Reitsma PH. New Fundamentals in Hemostasis. Physiological Reviews Published 1 January 2013Vol. 93no. 327-358DOI: 10.1152/physrev.00016.2011 [↩]

Sjögren’s Syndrome 

Hemochromatosis
Microscopic View of Hemochromatosis Stained Blue. Courtesy Wikimedia

What Is Hemochromatosis?

[dropcap]H emochromatosis, also called iron overload liver disease, is a common inherited disease in the Caucasian population that is characterized by increased iron deposition within the tissues (overload) associated with injury to them.

Hemochromatosis is an autosomal recessive disease, meaning a pair of abnormal genes are inherited from each parent. Parents are unaffected because they carry only one gene.

Q: Where is iron deposited?

A: In hemochromatosis, more iron is absorbed from the small intestine than is needed by the body. Subsequently, because the body has no satisfactory means to release iron overload, excess iron is deposited in various organs such as the liver causing cirrhosis, joints causing arthritis, and the pancreas causing diabetes mellitus.1

Consumption of alcoholic drinks with food should be avoided because alcohol increases leaky gut and greatly increases the absorption of iron. On the flip side, eggs and foods containing calcium such as milk and cheese are beneficial for hemochromatosis because they impair the absorption of iron. Another iron inhibitor is food that contains phytic acid which includes the bran and outer layer of grains, seeds, nuts, peas, beans, and lentils.

Iron overloading, as measured by a random (non-fasting) elevated transferrin saturation value, is estimated to occur in 1 to 6 people per 100 in the United States according to the CDC (Center for Disease Control and Prevention). Too much iron increases the risk for metabolic syndrome, type 2 diabetes mellitus, cancer, liver disease, and osteoporosis.

Medical treatment to remove excess iron from the body uses phlebotomy that draws blood through a vein and/or certain injectable drugs (deferoxamine and deferairox) that bind to iron.

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

Sources:
  1. www.irondisorders.org [↩]

Sarcoidosis

What Is Vitamin B12 Deficiency Anemia? [dropcap]V itamin 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… 

Autoimmune Disorders In Celiac Disease

Lipase Enzyme. Courtesy johnsonmatthey.
Lipase Enzyme. Courtesy Johnson Matthey Catalysts.

What Is Macrolipasemia?

[dropcap]M acrolipasemia is a rare enzyme disorder characterized by altered molecules of lipase, a pancreatic enzyme needed to digest fats, that are abnormally bound with serum antibody proteins. These antibodies are commonly immunoglobulin G (IgG) and/or less likely immunoglobulin A (IgA).

Q: What happens when lipase is bound to immunoglobulins (IgA and/or IgG)?

A: The resulting molecule is too large to be filtered by the kidneys and excreted in the urine, consequently these abnormal molecules build up in the plasma causing sustained elevation of lipase levels called macrolipasemia.

Macrolipasemia occurs with or without macroamylasemia, which is the binding of immunoglobulin A and/or G to amylase, a pancreatic enzyme needed to digest starches.1

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

Sources:
  1. La Villa G, Pantaleo P, Tarquini R, Cirami L, Perfetto F, Mancuso F, Laffi G. Multiple immune disorders in unrecognized celiac disease: a case report. World J Gastroenterol. 2003;9(6):1377-1380, Available at: http://www.wjgnet.com/1007-9327/9/1377.asp. Accessed Jan 3, 2005. [↩]

Asthma

Depiction of pancreatic amylase molecule.
Depiction of pancreatic amylase molecule.

What Is Macroamylasemia?

[dropcap]M acroamylasemia is an acquired enzyme disorder that causes elevated levels of the enzyme amylase (hyperamylasaemia) in the bloodstream. It is characterized by altered amylase molecules that have become abnormally bound with plasma proteins in the bloodstream, commonly IgG (immunoglobulin G) and/or IgA (immunoglobulin A).

The resulting molecule is too large to be properly filtered by the kidneys and excreted in the urine as would be normal unbound amylase, causing sustained elevation of amylase levels in the plasma.

With normal kidney function, a hyperamylasemia without an increase in urine amylase suggests the diagnosis of macroamylasemia, and is confirmed by identifying the macromolecular components.1

Amylase is a an enzyme produced by the pancreas and the parotid glands to digest starch in the diet. Comparatively small amounts are also produced by other organs.

Q: How do the pancreas and parotid glands deliver their amylase for digestion of starch?

A: The parotid glands deliver their amylase into the mouth. The action of amylase in the mouth starts the breakdown of starch as it is chewed and moistened with saliva.

After the starchy food is liquified in the stomach, the mass empties into the duodenum. Here pancreatic amylase is delivered through the common bile duct into the duodenum where it turns starch into maltose sugar. The next step to final digestion of starch is carried out by enzymes in the small intestinal lining that split maltose into its component sugar which is glucose.

Glucose is a simple sugar that can be absorbed into the bloodstream for use in the body. Humans cannot live without adequate glucose.

Distinquishing macroamylasemia from hyperamylasemia due to pancreatic disease is necessary to prevent needless treatment and investigation for pancreatitis.2

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

Sources:
  1. Torrent Vernetta A, Segarra Cantón O, Soler Palacín P, Segura Cardona RM, Infante Pina D. Macroamylasaemia in paediatrics. An Pediatr (Barc). 2008 Nov;69(5):439-41. [↩]
  2. Isham CA, Ridgeway NA, Hedrick R, Cate JC 4th. Screening for macroamylase in a community hospital. Clin Chem. 1984 May;30(5):741-2. [↩]

Urticaria or Hives, Chronic

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

What Is Immune Thrombocytopenic Purpura?

[dropcap]I 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. [↩]

Arachidonic Acid (AA) Deficiency

QueijoFresco.
QueijoFresco.

What Is Arachidonic Acid?

[dropcap]A[/dropcap]rachidonic acid is a major essential (must have/can’t make) omega-6 fatty acid.

Structurally, arachidonic acid is a key component of nerve membranes, together with docosahexaenoic acid (DHA), a major opposing omega-3 fatty acid, making up 15-20% of the brain’s dry mass and more than 30% of the retina.

In healthy human volunteers, positron emission tomography (PET) has shown that the normal human brain consumes 17.8 mg/day of arachidonic acid.1

Arachidonic acid is particularly concentrated in highly active membranes such as nerve synapses (junctions) and in photoreceptors in the eye retina.2

Arachidonic acid is an important building substance for the eicosanoids.

Q: What function do the eicosanoids have that are derived from arachidonic acid?

A: Eicosanoids are a large group of highly bioactive hormone-like substances including prostaglandins, leukotrienes, and thromboxanes that are involved in blood clotting, inflammation, and vasoconstriction. Eicosanoids derived from arachidonic acid are pro-inflammatory, pro-blood clotting, and constrict blood vessels in opposition to those derived from the omega-3 fatty acids which do the opposite in order to keep a balance in the body.

What Is Arachidonic Acid Deficiency In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Rapoport SI. Brain arachidonic and docosahexaenoic acid cascades are selectively altered by drugs, diet and disease. Prostaglandins Leukot Essent Fatty Acids. 2008 Sep-Nov;79(3-5):153-6. Epub 2008 Oct 29. [↩]
  2. Richardson AJ. The importance of omega-3 fatty acids for behavior, cognition, and mood. Scandinavian Journal of Nutrition. 2003;47(2):92-8. [↩]

Anti-Endomysium Antibodies (EMA) Present In Blood

Smooth muscle. Courtesy pathguy.com
Smooth Muscle. Courtesy pathguy.com

What Are Anti-Endomysium Antibodies?

[dropcap]A[/dropcap]nti-endomysium antibodies (EmA) are connective tissue autoantibodies produced in persons who have inherited the genes for celiac disease, an autoimmune disease, and are reacting to gluten in their diet.

Autoantibodies are abnormal in that they attack the body’s own tissue.

Q: What is endomysium?

A: Endomysium is the delicate connective tissue that surrounds individual muscle fibers. The autoantigen, or target, that stimulates the autoimmune response is the naturally occuring enzyme in endomysium called tissue transglutaminase (tTG), or more specifically tranglutaminase-2 (TG2). Anti-tissue transglutaminase antibodies recognize the same antigen as EmA, from which they differ in terms of detection method.

Anti-endomysium antibodies (EmA) are tested by the indirect immunofluorescence method and directed against “reticulin-like” fibres in connective tissue around smooth muscle fibres in the esophagus, liver, stomach, and bladder of monkeys, in the sections of the jejunum and kidneys of rats and in sections of the human umbilical cord. In comparison, for the determination of anti-tissue transglutaminase IgA and IgG antibodies, ELISA with human extractive or recombinant transglutaminase is recommended.1

EmA‐binding patterns in serum samples from patients with celiac disease have proved to be exclusively TG2‐targeted and the correlation between EmA and TG2 antibodies is therefore good. Evidence shows that celiac autoantibodies are produced in the small‐bowel mucosa.2

What Are Anti-Endomysium Antibodies In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Trigoni E, Tsirogianni A, Pipi E, Mantzaris G, Papasteriades C. Celiac disease in adult patients: specific autoantibodies in the diagnosis, monitoring, and screening. Autoimmune Dis. 2014;2014:623514. doi: 10.1155/2014/623514. [↩]
  2. Salmi TT, Collin P, Korponay-Szabó IR, Laurila K, Partanen J, Huhtala H, Király R, Lorand L, Reunala T, Mäki M, Kaukinen K. Endomysial antibody‐negative coeliac disease: clinical characteristics and intestinal autoantibody deposits.Gut. 2006 Dec;55(12):1746-53. [↩]

Autoimmune Polyglandular Syndromes 

Zincemia low zinc level symptom of celiac disease and glutenWhat Is Zincemia?

[dropcap]Z incemia means the zinc level in blood plasma is too low to meet metabolic needs of the body for this mineral.

Q: How important is a normal blood level of zinc?

A: A low blood level of zinc is characterized by widespread alterations in energy metabolism, growth, hemoglobin, carbon dioxide transport, hormone activity, insulin storage, many enzyme activities, prostaglandin function, collagen production, male fertility, protein synthesis, and vitamin A metabolism.

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