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Anemia, Folic Acid Deficiency  

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

What Is Folic Acid Or Folate Deficiency Anemia?

Folic 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. [↩]

Prolonged Prothrombin Time

bloodvialWhat Is Prolonged Prothrombin Time?

Prolonged 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?

Anti-Endomysium Antibodies (EMA) Present In Blood

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

What Are Anti-Endomysium Antibodies?

Anti-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. [↩]

Anti-Gliadin Antibodies Present

This is a model of Immunoglobulin-G Antibody (IgG)
This is a model of Immunoglobulin-G Antibody (IgG)

What Are Anti-Gliadin Antibodies?

Anti-gliadin antibodies (AGA) are produced by the body as an immune response against partially digested gliadin peptides (fragments) that have abnormally entered the body from the intestinal tract. Gliadin is a protein in wheat grain.

Anti-gliadin antibodies circulating in blood are measured by laboratory testing on blood that is drawn. The antibodies are both immunoglobulin A (IgA) and immunoglobulin G (IgG) types, which are termed AGA-IgA and AGA-IgG.

The presence of anti-gliadin antibodies in blood is an abnormal laboratory finding. That is, when the intestinal lining is healthy and able to keep out undigested matter from the body, there are no molecules of gliadin present to trigger the immune system for defense.

Q: Who produces anti-gliadin antibodies?

A: Persons, with or without celiac disease, can produce anti-gliadin antibodies if and when leaky gut (increased intestinal permeability) develops that then allow gliadin peptides to get into the bloodstream.

Gliadin itself causes leaky gut, but there are other causes such as various foods, intestinal infections, medications, and other diseases of the gastrointestinal tract. Whatever the cause of leaky gut, if poorly digested gliadin is present, it can slip through the leaky lining and enter the bloodstream where it can trigger an antibody response by anti-gliadin antibodies.

What Are Anti-Gliadin Antibodies In Celiac Disease and/or Gluten Sensitivity Or Non-Celiac Gluten Sensitivity?

Hypokalemia (Low Potassium Blood Level)

hypokalemia gluten celiac disease symptomWhat Is Hypokalemia?

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:
  1. 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. [↩]

Anti-tissue Transglutaminase Antibodies (tTG) Present In Blood

Image depicts tissue transglutaminase (tTg).
Image Depicts Tissue Transglutaminase (tTG).

What Are Anti-tissue Transglutaminase Antibodies?

Anti-tissue transglutaminase antibodies (anti-tTG) are connective tissue autoantibodies and can be detected in blood samples from affected persons who are reacting to gluten in the diet.

Autoantibodies are abnormal because they attack the body’s own tissue, which in the case of these antibodies is tissue transglutaminase 2 (TG2).

Q: What is tissue transglutaminase 2 (TG2)?

A: Tissue transglutaminase 2 (TG2) is an enzyme that appears in many cell locations and is particularly abundant in endothelial cells that line the small intestine. It has been implicated in a variety of cellular processes, such as differentiation, cell death, inflammation, cell migration and wound healing.

The cell appears to adapt the dynamics of this enzyme to meet specific sub-cellular needs or to respond to stress or other stimuli. Substantial evidence indicates that the location of TG2 within cells is critical for the regulation of its various biochemical activities, which subsequently trigger diverse downstream events,1

Although initially studied as an enzyme within cells, TG2 is now known to be secreted also into the extracellular space (between cells) or onto the cell surface.1

Abnormal activation of TG2 or deregulation of its function(s) is involved in a variety of human diseases, such as celiac disease, diabetes, neurodegenerative diseases, multiple sclerosis and rheumatoid arthritis. A role in inflammatory disorders and septic shock has also been shown. Moreover, multiple studies have revealed elevated TG2 expression in many types of cancer cells.1

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

Sources:
  1. Piacentini M, D’Eletto M, Farrace MG, Rodolfo C, Del Nonno F, Ippolito G, Falasca L. Characterization of distinct sub-cellular location of transglutaminase type II: changes in intracellular distribution in physiological and pathological states. Cell Tissue Res. 2014 Dec;358(3):793-805. doi: 10.1007/s00441-014-1990-x. [↩] [↩] [↩]

Bone Alkaline Phosphatase (BALP), Elevated

Vertebrae. Courtesy FreePik.com
Vertebrae. Courtesy FreePik.com

What Is Elevated Bone Alkaline Phosphatase?

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?

Vitamin B12 Deficiency Anemia

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… 

Anemia, Severe Iron Deficiency In Pregnancy 

Dermatitis Herpetiformis. Blisters Opened Giving Relief From Pain and Itching.
Dermatitis Herpetiformis On Forearm. Skin Is Darkened Where Old Blisters Healed.

What Is Dermatitis Herpetiformis?

D ermatitis herpetiformis (DH) is an autoimmune extremely itchy, painful bullous skin rash (blistering eruptions) arising from the underlying dermis layer of skin as a consequence of gluten sensitivity.

Dermatitis herpetiformis is characterized by multiple intensely itchy, red blisters appearing on the elbows which can extend down the forearm to the wrist and the knees. Less usual areas involve the back, buttocks, scalp, and abdomen.

Q: Do the blisters leave a mark when healed?

A: Crops of skin eruptions begin with itching or a burning sensation in reddened papules. There are grouped vesicles and tense blisters. The blister contents may be serous or bloody, with symmetrical distribution (eg, both knees or both elbows). Fluid filled elements rupture leaving denuded areas of sore skin and crust. Subsequently, there is residual hypopigmentation (a white area) or hyperpigmentation (dark area).1

Rupture of blisters begins relief from intense burning and itching.

Dermatitis Herpetiformis Eruptions On Knees.
Dermatitis Herpetiformis Eruptions On Knees. Notice White Areas Showing Loss of Pigmentation From Healed Blisters.

What Is Dermatitis Herpetiformis In Celiac Disease and/or Gluten Sensitivity?

Primary care providers should be aware of this skin condition, as they are more likely than a gastroenterologist to be confronted with this type of presentation of celiac disease.2

Sources:
  1. Mendes FB, Hissa-Elian A, de Abreu MA, Gonçalves VS. Review: dermatitis herpetiformis. An Bras Dermatol. 2013 Jul-Aug;88(4):594-9. [↩]
  2. Robinson BL, Davis SC, Vess J, Lebel, J. Primary care management of celiac disease. Autoimmune Disorders. Nurse Practitioner. February 2015: Vol 40 – Issue 2; 28–34. [↩]

Anemia, Refractory Iron Deficiency In Childhood (Unresponsive To Iron)

Psoriasis_on_back[1]

 What Is Psoriasis?

P soriasis is a chronic, autommune relapsing skin disorder characterized by scaling, erythema (redness), and less commonly, pustulation.1 

The body surface area affected and the degree to which psoriasis is a problem varies considerably among patients and over time.2 Often there are additional manifestations in the nails and in joints.3

Q: Are there different forms of psoriasis?

A: There are five forms of psoriasis. The lesions in all forms are itchy and red but vary in appearance and severity. Plaque psoriasis is the most common form observed in more than 80% of patients. Atypical forms include guttate, inverse, pustular, and erythrodermic psoriasis.4

  • Plaque psoriasis features thickened or raised red areas that have a distinct edge and are covered with silvery white buildup of flaky skin typically on elbows, knees, scalp and buttocks.
  • Gutate psoriasis appears as small, flat red patches with shiny buildup that are not usually painful, just itchy. There may be a few or many patches and they can group together.
  • Inverse psoriasis affects folds of skin, armpits and the groin area. Lesions are deep red with shiny buildup. It can be a thin red area along a crease line or involve, for example, the whole armpit.
  • Pustular psoriasis features an itchy, red base followed by blisters of white, non-infectious pus that appears glossy after a day or two and then sloughs in cycles. These areas may be limited to certain areas such as the hands and feet or be more widespread.
  • Erythrodermic psoriasis involves large areas of the body’s surface, inflaming normal skin and changing it into very red, raw looking flesh that is painful, swollen and itchy. This form requires extensive treatment, and complications can be life-threatening. Fortunately, this form of psoriasis is the least common.

Psoriasis in children has been reported to differ from that among adults being more frequently itchy and plaque lesions are relatively thinner, softer, and less scaly, face and flexural involvement is common and guttate type is the characteristic presentation.5

In children, psoriasis is a common skin disorder with about one third of all patients having onset of disease in the first or second decade of life. A chronic disfiguring skin disease, such as psoriasis, in childhood is likely to have profound emotional and psychological effects, and hence requires special attention.6

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

Sources:
  1. Addolorato G, Parente A, de Lorenzi G, et al. Rapid regression of psoriasis in a coeliac patient after gluten-free diet. A case report and review of the literature. Digestion. 2003;68(1):9-12. [↩]
  2. Stern, R. S., Nijsten, T., Feldman, S. R., Margolis, D. J. and Rolstad, T.

    Psoriasis is common, carries a substantial burden even when not extensive, and is associated with widespread treatment dissatisfaction. J. Invest. Dermatol. Symp.. 2004 Mar;9(2):136-9.. [↩]

  3. Weigle N, McBane S. Psoriasis. Am Fam Physician. 2013 May 1;87(9):626-33. [↩]
  4. Weigle N, McBane S. Psoriasis. Am Fam Physician. 2013 May 1;87(9):626-33. [↩]
  5. Dogra S, Kaur I. Childhood psoriasis. Indian J Dermatol Venereol Leprol. 2010 Jul-Aug;76(4):357-65. doi: 10.4103/0378-6323.66580. [↩]
  6. Dogra S, Kaur I. Childhood psoriasis. Indian J Dermatol Venereol Leprol. 2010 Jul-Aug;76(4):357-65. doi: 10.4103/0378-6323.66580. [↩]