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Inflammation

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inflammation-post-4What Is Inflammation?

[dropcap]I[/dropcap]nflammation is our body’s necessary self-defense response and repair mechanism for these assaults:

1) injuries such as cuts, scrapes, sprains, broken bones, burns, insect bites, toxins; 2) invading organisms such as bacteria; and 3) allergens and food sensitivities such as gluten.

Inflammation can be immediate (acute) or persistent (chronic).

Acute inflammation is marked by increased blood flow, migration of white blood cells, and release of defensive proteins and chemicals to the site of injured tissue. Among these chemicals are free radicals in the immune response to injury that are beneficial yet require the activity of anti-oxidants such as vitamin E and vitamin C to control.

Free radicals are chemical particles containing one or more unpaired electrons, which may be part of the molecule. They cause the molecule to become highly reactive.1

The majority of this response takes place in the first 12 to 24 hours after the assault. The inflammatory process continues until all the damaged tissue or invading germs are removed (usually about 5 days).2

Chronic inflammation is marked by persistence weeks to months or longer after tissue damage. Note: high concentrations of free radicals generated in chronic inflammation may be important causes of damage to cell structures. The defensive activity of anti-oxidants such as vitamin E and vitamin C are required to remove free radicals.

Chronic inflammation increases the risk for systemic diseases such as type II diabetes, obesity, heart disease, high blood pressure, arthritis, osteoporosis, chronic fatigue, migraine, autoimmune disease, and vasculitis which may cause stroke, heart attack or deep vein thrombosis (DVT).

Importantly, chronic inflammation is a risk factor for the onset of cancer.3

Q: Are there blood tests available for detecting inflammation?

A: Yes. Your medical health practitioner can order either or both of the following blood tests that measure the amount of inflammation present although not the source of inflammation. Abnormal is an elevation in blood levels.

  1. C-reactive protein (CRP). This test measure C-reactive proteins that are released into the bloodstream within a few hours of tissue injury or infection. CRPs are cytokines called ‘acute phase reactants,’ meaning first on the scene. The CRP test is also useful to monitor treatment response and flare-ups of chronic inflammatory disease such as vasculitis, systemic lupus, and inflammatory bowel disease.
  2. Erythrocyte sedimentation rate (ESR or sed rate). This test measures the rate of fall of blood cells in a sample tube of blood. An increase in the rate of fall shows inflammation due to an increase of C-reactive proteins in the blood specimen. Alone or with the CRP test, the ESR is especially useful for monitoring inflammation of veins and arteries.

In regards to celiac disease, disappearance of blood antibody levels of tissue transglutaminase IgA (tTG-IgA) indicate that inflammation has also subsided. These antibodies should be checked at 3 months, 6 months if indicated, and one year after diagnosis to monitor healing. On the other hand, raised antibodies indicate that there is definitely ongoing inflammation in the small intestine.

In regards to non-celiac gluten sensitivity, disappearance of blood antibody levels of anti-gliadin IgA and IgG at 3 months, 6 months if indicated, and one year after diagnosis indicate that inflammation has also subsided. On the other hand, raised antibodies indicate that there is definitely ongoing inflammation caused by gluten within the body.

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

Sources:
  1. Ruttkay-Nedecky B, Nejdl L , Gumulec J. The Role of Metallothionein in Oxidative Stress. Int. J. Mol. Sci. 2013, 14(3), 6044-6066; doi:10.3390/ijms14036044. [↩]
  2. Taber’s Cyclopedic Medical Dictionary. 19th ed. F A Davis Company. Philadelphia, PA. [↩]
  3. Brighenti E, Giannone FA, Fornari F, Onofrillo C, Govoni M, Montanaro L, Treré D, Derenzini M. Therapeutic dosages of aspirin counteract the IL-6 induced pro-tumorigenic effects by slowing-down the ribosome biogenesis rate. Oncotarget. 2016 Aug 20. doi: 10.18632/oncotarget.11441. [↩]

Tuberculosis – Increased Susceptibility 

Bacteria that causes tuberculosis. Courtesy Wikimedia.
Bacteria that causes tuberculosis. Courtesy Wikimedia.

What Is Increased Susceptibility To Tuberculosis?

[dropcap]T[/dropcap]uberculosis (TB), is an infectious disease caused by a bacteria called mycobacterium tuberculosis. It is characterized by chronic bacterial infection most commonly affecting lungs that develops in stages.

Increased susceptibility to tuberculosis menas the person’s defense mechanisms against developing infection are inadequate. Tuberculosis may be dormant or active.

Q: What happens in active tuberculosis?

A: Active tuberculosis  produces inflammation and formation of tubercles, necrosis (death of tissues), abcess, fibrosis, and calcification. Calcification is the body’s action to encapsulate the bacterial invasion. Active tuberculosis is life-threatening and may result in death.

About one third of the world’s population is infected with tuberculosis bacteria. In 2012 the number reached a staggering 8.6 million people. Of these, 1.3 million people died from tuberulosis.  About 95% of tuberulosis deaths occur in low- and middle-income countries and it is among the top three causes of death among women aged 15 to 44.1

People with weakened immune systems have a much greater risk of falling ill from tuberculosis. For example, a person living with HIV is about 20 to 30 times more likely to develop active tuberculosis.2 The combination of tuberculosis, HIV coinfection, and malnutrition has been commonly termed as “triple trouble.”3

What Is Increased Susceptibility To Tuberculosis In Celiac Disease and/or Gluten Sensitivity?

Sources:

  1. http://www.who.int/features/factfiles/tb_facts/en/index.html [↩]
  2. http://www.who.int/features/factfiles/tuberculosis/en/ [↩]
  3. Steinbrenner H, Al-Quraishy S, Dkhil MA, Wunderlich F, Sies H. Dietary selenium in adjuvant therapy of viral and bacterial infections. Adv Nutr. 2015 Jan 15;6(1):73-82. doi: 10.3945/an.114.007575. Print 2015 Jan. [↩]

Progressive Multifocal Leukoencephalopathy

View of Progressive Leukoencephalopathy. Courtesy quizlet.com.
View of Progressive Multifocal Leukoencephalopathy. Courtesy quizlet.com.

What Is Progressive Multifocal Leukoencephalopathy?

[dropcap]P[/dropcap]rogressive multifocal leukoencephalopathy is a progressive demyelinating disorder of the central nervous system (brain) caused by JC virus that leads to rapid death.

Progressive multifocal leukoencephalopathy usually occurs as an opportunistic infection in patients with underlying depression of cell-mediated immunity. It has been recognized that the JC virus is highly prevalent in the adult population, with 50–90% of healthy individuals having been exposed to the virus. Approximately 85% of the population has antibodies to JC virus. The virus’ purported site of latency in the human body is currently under debate.1

Progressive multifocal leukoencephalopathy is characterized by tissue loss of subcortical white matter (brain tissue) and active perivascular inflammatory foci (locations in blood vessels) with numerous eosinophilic granulocytes (white blood cells).

Q: What is demyelinating?

A: Demyelinating means there is damage to the myelin sheath of nerve cells called oligodendrites in the brain. In this disorder the damaged, irregular areas caused by the infection get progressively bigger.

The myelin sheath is a fatty substance that surrounds and protects nerve cells and enhances the transmission of nerve impulses much like the covering of a lamp cord keeps the electricity flowing within it from the plug to the light bulb. Damage to the myelin sheath impairs transmission of nerve impulses in the way that fraying an electric cord impairs the flow of electricity. 

What Is Progressive Multifocal Leukoencephalopathy In Celiac Disease and/or Gluten Sensitivity?

Sources:

  1. Gourineni VC, Juvet T, Kumar Y, Bordea D, Sena KN. Progressive multifocal leukoencephalopathy in a 62-year-old immunocompetent woman. Case Rep Neurol Med. 2014;2014:549271. doi: 10.1155/2014/549271. [↩]

Erythema Nodosum 

Crohnie_sores_4[1]What Is Erythema Nodosum?

[dropcap]E[/dropcap]rythema nodosum is an inflammatory disorder involving the deep dermis layer of skin and subcutaneous fat septa that underlies the skin. It is characterized by eruptions of recurrent or persistent multiple painful, red nodules under the skin that leave a bruised appearance when healing and do not scar.

The lower legs are most affected, but sores can appear anywhere there is subcutaneous fat.

Q: How do the nodules develop in erythema nodosum?

A: The edges of nodules are poorly defined, and the nodules vary from 2-6 cm.

During the first week of eruption, nodules become tense, hard, and painful. During the second week, they change color from bright red to bluish or livid and may become soft, but do not ulcerate. As absorption progresses, the color gradually fades to a yellowish hue, resembling a bruise. This disappears in 1 or 2 weeks as the overlying skin sloughs off and is replaced.1

The eruptive phase of erythema nodosum begins with flulike symptoms of fever and generalized aching followed by a painful rash within 1-2 days.  Aching legs and swelling ankles may occur and precede the eruption or appear during the eruptive phase and may persist for weeks.2

Currently, the most common cause of erythema nodosum is streptococcal infection in children and streptococcal infection and sarcoidosis in adults.3 Most sores in infection-induced erythema nodosum heal within 7 weeks, but active disease may last up to 18 weeks.

In contrast, 30% of idiopathic erythema nodosum cases may last more than 6 months. Idiopathic means that the cause is not known.

What Is Erythema Nodosum In Celiac Disease and/or Gluten Sensitivity?

Sources:

  1. http://emedicine.medscape.com/article/1081633-clinical#a0217 [↩]
  2. http://emedicine.medscape.com/article/1081633-clinical [↩]
  3. http://emedicine.medscape.com/article/1081633-overview#a0199 [↩]