What Is Fecal Occult Blood In Children?

T he presence of fecal occult blood in children is caused by minimal bleeding of less than a tablespoon a day in the gastrointestinal tract which leads to iron deficiency.

Bleeding is abnormal and needs to be corrected by locating the source.

Q: What does occult blood mean?

A: Occult means the small amount of blood in the stool cannot be seen by the eye when inspecting it. Therefore, suspect bleeding is found through a simple test performed on stool because stool would carry the blood away from the site of bleeding.

A fecal occult blood test is inexpensive and can be done at home or in the doctor’s office.  Most types involve smearing a stool sample onto a test card that either contains a chemical that turn blue if blood is present or else requires applying the chemical to the sample.

What Is Fecal Occult Blood In Children in Celiac Disease?

What Is Dermatitis Herpetiformis In Childhood?

D ermatitis herpetiformis in childhood is an inflammatory skin manifestation of celiac disease in which immunoglobulin A (IgA) autoantibodies target components of the skin, leading to blister formation caused by ingestion of gluten in the diet.  

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 back of 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

Most conditions in the spectrum of autoimmune blistering disorders are uncommonly seen in the pediatric population, even the most common ones, such as dermatitis herpetiformis.² The true incidence  is unknown. 

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

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. Lara-Corrales I1, Pope E. Autoimmune blistering diseases in children. Semin Cutan Med Surg. 2010 Jun;29(2):85-91. doi: 10.1016/j.sder.2010.03.005. [↩]

What Is Chronic Bullous Dermatosis Of Childhood?

C hronic bullous dermatosis of childhood, also termed linear IgA dermatosis, is the most common acquired autoimmune blistering disorder of childhood and is characterized by itchy, urticated papules and plaques as well as polycyclic lesions (merged circles) with blisters at the edge, located on normal looking skin around the mouth and perineum in young children. In children over 7 years, other parts of the body may rather be affected.

Q: What tissue is targeted in chronic bullous dermatosis of childhood?

A: In chronic bullous dermatosis of childhood, there is an autoimmune attack on structural proteins, usually proteolytic fragments of collagen XVII, which renders the dermal-epidermal junction prone to blistering.

The dermal-epidermal junction is where the surface skin layer, or epidermis, meets the lower layer, or dermis. Diagnosis is confirmed by characteristic histology and direct immunofluorescence showing linear IgA (immunoglobulin A antibody) staining of the basement membrane zone.¹

The incidence of chronic bullous disease of childhood is rare. Age of onset is typically before 5 years of age and is seen in all ethnic groups.

What Is Chronic Bullous Dermatosis Of Childhood In Celiac Disease and/or Gluten Sensitivity?

Sources:

1. Mintz EM, Morel KD.Clinical features, diagnosis, and pathogenesis of chronic bullous disease of childhood. Dermatol Clin. 2011 Jul;29(3):459-62, ix. doi: 10.1016/j.det.2011.03.022. [↩]

What Is Delayed Puberty In Girls?

D elayed puberty in girls is a concerning condition characterized by decreased functional activity of the ovaries resulting in late onset of ovulation and secondary sex characteristics.

Q: When should puberty in girls begin?

A: Puberty in girls is a stage of reproductive development that occurs at the average age of 12.1 years (between the ages of 9 and 15 years) and ends in sexual maturity.

Secondary sex characteristics are breast development and appearance of pubic hair that is followed by underarm hair and white vaginal secretion. The first menstrual period (menarche) follows this sequence.

What Is Delayed Puberty in Girls In Celiac Disease and/or Gluten Sensitivity?

What Is Epilepsy?

E pilepsy is a dysfunctional disorder of the brain characterized by recurring seizures also called convulsions.

Q: What happens in a seizure?

A: During a seizure  abnormal electrical discharges occur within the brain. Not all seizures have the same intensity or involvement.

Seizures can be generalized, partial  or unclassified.

• Generalized siezures affect both sides of the brain and the individual usually loses consciousness.
• Partial affect one part of the brain and the individual usually is awake.

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

What Is Juvenile Type 1 Diabetes Mellitus?

J uvenile diabetes is type I diabetes mellitus that begins in childhood or before the age of 25 years. It is an inherited inflammatory autoimmune disease of the pancreas in which anti-islet autoantibodies destroy the islet cells of the pancreas that secrete insulin hormone, resulting in a lack of insulin.

Loss of insulin production results in failure to metabolize glucose. Glucose is a simple sugar that is a required source of energy for the body, especially the brain and muscles.

Juvenile diabetes is characterized by sustained fasting blood glucose levels above 126 mg/dL (hyperglycemia) with subsequent loss of glucose from the body by removal through the urine (glucosuria) as the body attempts to lower blood glucose, and cell starvation that follows.

That is, while glucose accumulates in blood, the body cannot access it. Without insulin treatment, this disorder quickly produces coma and ultimately results in death. In fact, it is 5th leading cause of death in the United States.

Q: How does insulin work?

A: Insulin moves glucose from the bloodstream into body cells where it is used or reformulated for high energy storage. For example, muscles can use glucose for immediate work or store it in the form of glygogen for later work, depending on need. Healthy insulin production keeps an 8 hour fasting blood glucose level to less than 100 mg/dL. Upon eating carbohydrate food, glucose is digested and absorbed from the small intestine into the bloodstream which then raises blood glucose levels. The elevated level is controlled by prompt action of insulin to lower it to below 140 mg/dL  within 2 hours of eating.

Insulin does not work alone. The islets of Langerhans manage glucose in the body. The islets are specialized formations located on the outer surface of the pancreas. The islets are composed of two different types of cells known as alpha and beta cells. These cells make the competing hormones that keep blood glucose within a healthy range.

Alpha cells secrete glucagon to raise blood glucose levels by triggering the body to release stored energy in the form of glycogen. In the opposite, beta cells secrete insulin to lower blood glucose by opening body cells so that glucose in blood can enter. Without insulin, glucose cannot enter cells but remains in the bloodstream where it accumulates.

Insulin is also needed to move magnesium into cells from the bloodstream. On the other side, magnesium is needed to produce insulin. Insulin has other functions such as building muscle and helping regulate cholesterol which directly impacts the sex hormones, estrogen, progesterone, and testosterone.

Onset of symptoms usually occurs over a period of days or weeks, although beta cell destruction can begin years earlier. The SEARCH for Diabetes in Youth multicenter study, funded by the Centers for Disease Control and Prevention (CDC) and the National Institutes of Health (NIH), has determined that based on data from 2002 to 2003, a total of 15,000 youth in the United States were newly diagnosed with type 1 diabetes each year. Non-Hispanic white youth had the highest rate of new cases of type 1 diabetes according to NIH.

Type 1A diabetes mellitus has become one of the most intensively studied autoimmune disorders. It is now possible to predict its development, beginning with HLA-encoded genetic susceptibility, followed by the development of a series of anti-islet autoantibodies.¹

What Is Juvenile Diabetes In Celiac Disease and/or Gluten Sensitivity?

Sources:

1. Liu E, Eisenbarth GS. Type 1A diabetes mellitus-associated autoimmunity. Endocrinology and Metabolism Clinics of North America. Jun 2002;31(2):391-410, vii-viii. [↩]

What Is Juvenile Idiopathic Arthritis?

J uvenile idiopathic arthritis (JIA) is a rheumatic disorder characterized by chronic, inflammatory disease of large and small synovial joints and other organs in children under age 16 years. Growth and development may be impaired in these children.¹

Q: Which joints are affected in juvenile idiopathic arthritis?

A: In juvenile idiopathic arthritis the joints that are affected are variable and so are the manifestations.

According to the International League of Associations for Rheumatology (ILAR) classification system, there are seven different subtypes of  juvenile idiopathic arthritis. 

The main treatment to reduce inflammation and relieve pain is with non-steroidal inflammatories such as Ibuprofen.

What Is Juvenile Idiopathic Arthritis In Celiac Disease and/or Gluten Sensitivity?

Sources:

1. Stagi S, Giani T, Simonini G, Falcini F. Thyroid function, autoimmune thyroiditis and coeliac disease in juvenile idiopathic arthritis. Rheumatology. Apr 2005;44(4):517-20. [↩]

What Is Glycogenic Acanthosis?

Glycogenic acanthosis is a benign thickening of the esophageal squamous epithelium (surface cell lining)  characterized by the presence of numerous, uniformly grey-white plaques made up of large squamous cells filled with glycogen.

The wax-like plaques in glycogenic acanthosis are usually 2-10 mm in diameter and may be confluent round elevations involving the entire esophageal surface.¹

On x-ray  views of the well-distended esophagus, the plaques appear as a finely nodular or cobblestone mucosal pattern.

The findings are not associated with mucosal ulcerations, luminal narrowing, or mobility disturbance, although some patients may have coexistent hiatal hernia and gastroesophageal reflux.²

What Is Glycogenic Acanthosis In Celiac Disease and/or Gluten Sensitivity?

Sources:

1. Suoglu OD, Emiroglu HH, Sokucu S, Cantez S, Cevikbas U, Saner G. Celiac disease and glycogenic acanthosis: a new association? Acta Paediatrica. Apr 2004;93(4):568-70. [↩]
2. Ghahremani GG, Rushovich AM. Glycogenic acanthosis of the esophagus: radiographic and pathologic features. Gastrointest Radiol. 1984;9(2):93-8. [↩]

What Is Stroke In Childhood?

S troke in childhood is a medical emergency during which blood flow to an area of the brain is stopped, causing infarction or death of the area of cells in the brain fed by the blocked artery. Stroke is characterized by loss of muscle and brain function according to the location of the lost cells.

The brain is a highly active metabolic and complex organ of our body that performs important functions, therefore, any disruption in its normal functioning can have devastating effects on whole body.

After stroke, an immune response is initiated that leads to production of proinflammatory cytokines (chemicals) and gathering of various inflammatory cells like neutrophils, T-cells, macrophage, and monocytes to the affected area that exacerbate or worsen the ischemic (oxygen starved) injury.¹

Arterial ischemic stroke is an important cause of acquired brain injury in children.² This stroke results from loss of adequate blood flow through an artery that supplies the affected area of the brain with oxygen and nutrients.

A recent study found the majority of  children (85%) had focal features (most commonly one sided weakness or paralysis) at presentation to their medical practitioner. Seizures were more common in younger children a year old or younger and headache was more common in children 5 years or older.³

Who is at Risk in the General Population?

• A British study in 2014 found the crude incidence of childhood arterial ischemic stroke was 1.60 per 100,000 per year.
• The incidence of arterial ischemic stroke was highest in children aged under 1 year (4.14 per 100,000 per year).
• There was no difference in the risk of arterial ischemic stroke between sexes.
• Asian and black children were at higher risk than were white children.³

What Is Stroke in Childhood In Celiac Disease and/or Gluten Sensitivity?

Sources:

1. Andrabi SS, Parvez S, Tabassum H. Melatonin and Ischemic Stroke: Mechanistic Roles and Action. Adv Pharmacol Sci. 2015;2015:384750. doi: 10.1155/2015/384750. Epub 2015 Sep 7. [↩]
2. Mallick AA, Ganesan V, Kirkham FJ, et al. Childhood arterial ischaemic stroke incidence, presenting features, and risk factors: a prospective population-based study. Lancet Neurol. 2014 Jan;13(1):35-43. doi: 10.1016/S1474-4422(13)70290-4. Epub 2013 Dec 2. [↩]
3. Mallick AA, Ganesan V, Kirkham FJ, et al. Childhood arterial ischaemic stroke incidence, presenting features, and risk factors: a prospective population-based study. Lancet Neurol. 2014 Jan;13(1):35-43. doi: 10.1016/S1474-4422(13)70290-4. Epub 2013 Dec 2. [↩] [↩]

What Is Developmental Delay?

D evelopmental delay is failure in infants and young children to meet expected milestones, such as smiling for the first time or taking the first steps, due to an impairment in physical, learning, language, or behavior areas.

These conditions begin during the developmental period, may impact day-to-day functioning, and usually last throughout a person’s lifetime.¹

What Is Developmental Delay In Celiac Disease and/or Gluten Sensitivity?

Sources:

1. Developmental Disabilities: Delivery of Medical Care for Children and Adults. I. Leslie Rubin and Allen C. Crocker. Philadelphia, Pa, Lea & Febiger, 1989. [↩]