Skip to content

Tuberculosis – Increased Susceptibility 

What Is Irritable Bowel Syndrome? I rritable bowel syndrome (IBS) is a motility disorder without anatomic cause involving the entire gastrointestinal tract that is characterized by these four features: 1) Abdominal pain usually relieved by… 

Osteoporosis

Woman with long standing osteoporosis. Courtesy of Wikimedia.
Woman with long standing osteoporosis. Courtesy of Wikimedia.

What Is Osteoporosis?

Osteoporosis is a metabolic bone disorder characterized by diminished bone mass (density) with normal cell appearance but fragile bone strength that prediposes to broken bones, and with high bone turnover.

This condition usually goes undetected until late when loss of height or a bone fracture occurs. In fact, each year  1.5 million fractures mainly of the hip, spine and wrist are attributed to osteoporosis. Compression fractures of vertebrae bones are the most common, accounting for 700,000 cases.

Bone is composed of specialized connective tissue called osseous tissue. Osseous tissue is made up of living bone cells (osteocytes) that are embedded in a hard matrix (framework) of calcified substance.

Bone matrix contains collagen fibers and the minerals calcium phosphate and calcium carbonate, which provide strength to bone. The copper enzyme, lysyl oxidase, is involved in the cross-linking of collagen in forming the framework for depositing calcium and other minerals to build and repair bone.

Q: How do osteocytes function in bone?

A: Osteocytes maintain the health of bone by their metabolic activity in regulating normal bone turnover. Bone turnover is the breaking down and removal of old or damaged bone and rebuilding or remodeling of healthy bone that is ongoing throughout life. The bone formation process takes about 3 months to complete.

Osteoporosis develops from failure of the body to maintain health and to provide bone tissue with adequate nutrition for proper function. Risk factors that can be modified include: low calcium intake, sedentary lifestyle, smoking, drinking alcohol excessively, eating a diet with excessive caffeine, protein, and phosphate, and taking certain medications over a long time such as steroids, thyroid preparations, the anti-convulsive drug phenytoin, aspirin, antacids, anticoagulants, some diuretics, and some chemotherapeutic drugs. See below for a fuller description.

In addition to celiac disease, osteoporosis is associated with advancing age, family history, nulliparity (no pregnancies) and post-menopause in females, certain disorders such as hyperthyroidism, hypogonadism, inflammatory bowel disease like Crohn’s disease, multiple myeloma, anorexia nervosa, and Cushing’s disease.

Bone strength is easily measured by testing bone mineral density (BMD). BMD is evaluated by DEXA scan (dual-energy X-ray absorptiometry).  DEXA at the femoral neck and lumbar spine is considered the gold standard to confirm the diagnosis of osteoporosis.  Results are expressed as T and Z scores. T scores compare the result with a 20 to 40 year old helathy person while  Z scores compare the result with persons in the same age group. Both are measured in standard deviations (SD).

According to WHO criteria (World Health Organization), a T-score of -1 SD or greater denotes normal bone, a T-score between −1 to −2.5 SD denotes osteopenia, and a T-score of −2.5 or more denotes osteoporosis.1

Treatment is aimed to preserve and increase bone density, minimize symptoms for better quality of life and reduce risk of bone fractures.

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

The cumulative effects of gluten-induced inflammation, treatment delay, and malabsorption result in lower bone density and bone fragility.2

Sources:
  1. Pantaleoni S, Luchino M, Adriani A, Pellicano R, Stradella D, Ribaldone DG, Sapone N, Isaia GC, Di Stefano M, Astegiano M. Bone mineral density at diagnosis of celiac disease and after 1 year of gluten-free diet. ScientificWorldJournal. 2014;2014:173082. doi: 10.1155/2014/173082. []
  2. Grace-Farfaglia P. Bones of Contention: Bone Mineral Density Recovery in Celiac Disease-A Systematic Review. Nutrients. 2015 May 7;7(5):3347-3369. []

Non-Alcoholic Fatty Liver Disease

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

What Are Anti-Endomysium Antibodies?

A 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. []

Cataracts

Glucose Meter Reading Showing Hypoglycemia. Courtesy Abbott.
Glucose Meter Reading.Courtesy Abbott.

What Is Diabetic Instability?

D iabetic instability, also called brittle diabetes, is poor control of blood sugar characterized by frequent rise (hyperglycemia) and fall (hypoglycemia). These fluctuations can be life-threatening and cause unnecessary complications.

Q: What are complications in diabetes?

A: Complications of diabetes include any/all of the following:

  • Peripheral neuropathy that causes burning, numbness, or tingling in the extremities.
  • Skin infections and ulcers that do not heal and can lead to amputation of toes, feet or legs.
  • Damage to retina that can progress to blindness.
  • Cataracts and glaucoma that impair vision and can cause blindness.
  • Increased susceptibility to serious infections of the genitourinary tract, lung and upper respiratory tract that can become systemic and life-threatening.
  • Kidney disease that can lead to kidney failure.
  • Heart disease that can lead to heart failure.
  • Vascular disease that can lead to stroke.
  • Impaired motility in digestive tract that can lead to dyspepsia and constipation.
  • Pregnancy complications.
  • Shortened life expectancy.

The main causes of brittleness include malabsorption, certain drugs (alcohol, antipsychotics), defective insulin absorption or degradation, defect of hyperglycemic hormones especially glucocorticoid and glucagon, and above all delayed gastric emptying as a result of autonomic neuropathy.1

What Is Diabetic Instability In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Vantyghem MC, Press M. Management strategies for brittle diabetes. Ann Endocrinol (Paris). 2006 Sep;67(4):287-96. []

Intraepithelial Lymphocytosis In Normal Small Bowel Samples 

esophageal small cell carcinomaWhat Is Esophageal Small Cell Cancer (Carcinoma)?

E sophageal small cell carcinoma is a rare and aggressive malignancy arising in the esophagus with a poor prognosis.

Q: Where does the cancer occur in the esophagus?

A: Esophageal cancer can occur anywhere in the esophagus.

The esophagus is a muscular tube that transports swallowed substances to the stomach. It begins at the cricoid cartilage (Adam’s apple) as a continuation of the pharynx and ends at the lower esophageal sphincter (LES).

The LES is a circular muscle surrounding the junction of the esophagus and stomach. The LES opens to allow swallowed food and liquids to enter the stomach and closes to prevent their travelling back into the esophagus.

Dysphagia (difficulty swallowing) occurs when the inside diameter of the esophagus constricts to less than 14 millimeters. First there is difficulty swallowing solid food then liquids and saliva due to progressive growth of the cancer.

What Is Esophageal Small Cell Carcinoma In Celiac Disease and/or Gluten Sensitivity?

Cancer Predisposition In Children 

Mesenteric Lymph Node Cavitation. Courtesy
Mesenteric Lymph Node Cavitation.  Courtesy McBride OM, Skipworth RJ, Leitch D, Yalamarthi S.

What Is Mesenteric Lymph Node Cavitation And Hyposplenism?

M esenteric lymph node cavitation and hyposplenism combination is a rare lymphatic entity. It is characterized by involution (degeneration) of a mesenteric lymph node (abdominal) and absence of functional spleen tissue.

Q: What is happening to the lymph nodes?

A: Lymph nodes are enlarged with central, partly cystic degeneration. When cut open either at surgery or autopsy, milky fluid exudes from the cut surface.

In regards to absent spleen function, the body is highly susceptible to bacterial invasion such as pneumonia because tissues of the spleen, called the pulp, produce specialized white blood cells that protect the body against bacterial invasion and trap foreign antigens.

What Is Mesenteric Lymph Node Cavitation And Hyposplenism In Celiac Disease and/or Gluten Sensitivity?

Infertility in Females

Lost patch of hair at base of scalp due to alopecia areata. Courtesy Wikimedia,
Lost patch of hair at base of scalp due to alopecia areata. Courtesy Wikimedia,

What Is Alopecia Areata?

A lopecia areata is an autoimmune attack on hair follicles characterized by sudden hair loss involving scalp or beard, although any hairy area may be affected.

Areas of hair loss have a patchy pattern with sharply defined edges.

Q: Can all hair be affected?

A: All body hair may be lost, which is called alopecia universalis although this is uncommon.

In alopecia areata, white blood cells of the immune system attack the rapidly growing cells in the hair follicles. The affected hair follicles become small and drastically slow down hair production. Fortunately, the stem cells that continuously supply the follicle with new cells do not seem to be targeted. So the follicle always has the potential to regrow hair but regrowth is unpredictable.1

What Is Alopecia Areata In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. http://www.niams.nih.gov/Health_Info/Alopecia_Areata []

Miscarriage (Spontaneous Abortion)

Pitting edema. Right photo shows that indent remains from pressing. Courtesy wikimedia.
Pitting edema. Right photo shows that indent remains from pressing. Courtesy wikimedia.

What Is Edema?

E dema is an abnormal swollen condition of the skin characterized by excess extracellular fluid volume, meaning there is an increase of the fluid that normally surrounds cells. Edema may be hardly noticeable or it can become extensive.

Edema can have various appearances and can develop from various causes.

Q: What are the appearances and causes of edema?

A: Here are the appearances of edema:

  • Pitting edema. It is called pitting edema if when the skin is pressed with a finger, the indent remains. This edema results from fluid leaking out of the bloodstream into the surrounding tissues. Pitting edema can be a feature of many disorders including heart disease, kidney disease, vascular disease, cancer, and malnutrition.
  • Myxedema is a firm swelling or thickening of subcutaneous skin that does not pit, as seen in thyroid disease.

Here are causes of edema:

  • Local edema as a response to trauma or infection.
  • Lower extremity edema from poor circulation and malnutrition.
  • Edema in the lungs from right sided heart disease.
  • Abdominal edema from liver disease, intestinal disease.
  • Body wide edema from heart disease, kidney disease, thyroid disease.

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

Mesenteric Lymph Node Cavitation And Hyposplenism

GERD Gluten Celiac Disease
Arrows Show Abnormal Movement of Gastric Acid in Gastroesophageal Reflux Disease.

What Is Gastroesophageal Reflux Disease (GERD)?

G ERD is an upper digestive disorder that is characterized by a decrease in lower esophageal sphincter pressure (LES,) which allows the abnormal reflux or backflow of stomach contents into the esophagus. It is also called erosive esophagitis or reflux esophagitis and is the most common disorder of the esophagus.

The esophagus is a muscular tube that transports swallowed substances to the stomach. It begins at the cricoid cartilage (Adam’s apple) as a continuation of the pharynx and ends at the lower esophageal sphincter (LES).

The lower esophageal sphincter is located at the junction of the esophagus and the stomach. It functions like a circular band to tighten after food is ingested in order to prevent its going back up the esophagus.

Q: How does reflux damage the esophagus?

A: Damage to the lining of the esophagus is induced by the caustic, chemical action of acid and pepsin in gastric juice and, in severe cases, also bile salts, that back upwards from the stomach through an impaired LES. Gastric acid combined with pepsin or bile salts seems to be more harmful to the esophageal epithelial layers than gastric acid alone.1

Pepsin is normally produced by the stomach to dissolve protein in swallowed food. Unfortunately, when the esophagus is inflamed, pepsin will act on it to break down the protein in its sore wall. These sores are called erosions.

Importantly, refluxate to the esophagus in patients with acid suppression therapy is different from those in patients without. Higher levels of secondary bile acids are detected in patients with acid suppression therapy. Even if acid suppression is successful, weakly acidic reflux with bile acids can damage the esophagus.1

Damage starts at the luminal surface (inside where food passes through) of the squamous epithelium (tough surface cells) and progresses through the underlying layers into the submucosa.

One of the primary functions of the esophageal epithelium is to protect the underlying tissue from mechanical and chemical damage by acting as a barrier. The epithelial layers of the distal esophagus need to withstand reflux from the stomach and its contents. When the epithelium fails to protect the underlying tissue from this damage, it leads to erosions, esophagitis, and may lead to Barrett’s esophagus.1

Barrett’s esophagus and esophageal small cell cancer are severe complications of GERD that can be fatal.

GERD can result from too much, or more commonly, too little stomach acid.

What Is Gastroesophageal Reflux Disease (GERD) In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Chen X, Oshima T, Tomita T, Fukui H, Watari J, Matsumoto T, Miwa H. Acidic bile salts modulate the squamous epithelial barrier function by modulating tight junction proteins. Am J Physiol Gastrointest Liver Physiol. 2011 Aug;301(2):G203-9. doi: 10.1152/ajpgi.00096.2011. Epub 2011 May 26. [] [] []

Lymphoma, Enteropathy-Associated T-Cell (EATL) 

A real photomicrograph of carcinoma of the esophagus. Panorama of 6 photos of a slide at 40x through the microscope. Some areas may appear blurry due to shallow DOF.
A real photomicrograph of carcinoma of the esophagus. Panorama of 6 photos of a slide at 40x through the microscope. Some areas may appear blurry due to shallow DOF.

What Is Cancer Of The Esophagus?

C ancer of the esophagus is a malignancy arising in the stratified squamous cell lining of any part of the esophagus and having a poor prognosis.

This tumor first invades the deeper layers of the esophagus which includes the layer beneath the mucosa (submucosa) and muscle before it may invade structures close to it including the aorta and trachea. Later, it may spread to organs further away such as the liver, lungs and bones.

Q: What is the stratified squamous cell lining of the esophagus?

A: Stratified squamous cells are flat epithelial cells that are composed of several layers, called the epithelium. This type of epithelium forms the surface mucosa that lines the inside of the esophagus.

The esophagus itself is a muscular tube that transports swallowed substances to the stomach. It begins at the cricoid cartilage (Adam’s apple) as a continuation of the pharynx in the throat and ends at the lower esophageal sphincter (LES).

The LES is a circular muscle surrounding the junction of the esophagus and stomach. The LES opens to allow swallowed food and liquids to enter the stomach and closes to prevent their travelling back into the esophagus.

Who is Affected in the General Population?

Esophageal cancer is the fifth leading cause of death in men from cancer worldwide.1

What Is Cancer Of The Esophagus In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Feldman M, Friedman LS, Brandt LJ. Sleisenger & Fordtran’s Gastrointestinal and Liver Disease. ed 9. Philadelphia: Saunders; 2010. pp. 745–767. []