CLINICAL MANIFESTATIONS OF CELIAC DISEASE IN CHILDREN

Celiac disease, also known as gluten-sensitive enteropathy is an immune-mediated inflammatory disease of the small intestine caused by sensitivity to dietary gluten and related proteins in genetically predisposed individuals. It differs from food allergies (including wheat allergy), which are mediated by immunoglobulin E (IgE) or immunoglobulin G (IgG). The disorder occurs in 0.5 to 1 percent of the general population. The disorder is commonly referred to as "celiac sprue" or "gluten-sensitive enteropathy" in the United States. It was first described by Samuel Gee in 1887 in a report entitled "On the coeliac affection," although a similar description of a chronic malabsorptive disorder by Aretaeus from Cappadocia (now Turkey) was recorded as far back as the second century AD

The grains that contain the triggering proteins are wheat, barley, and rye. Previously, oats were thought to be harmful but this appears to be from contamination with wheat flour, and most people with celiac disease can tolerate pure oats once they have commenced a gluten-free diet. The small intestinal mucosa improves morphologically when treated with a gluten-free diet and relapses when gluten is reintroduced. The appropriate treatment is a gluten-free diet for life, which results in complete resolution of symptoms for most individuals.

The six key elements in the management of patients with celiac disease can be summarized with the following mnemonic,

●Consultation with a skilled dietician

●Education about the disease

●Lifelong adherence to a gluten-free diet

LATENT TUBERCULOSIS INFECTION- Treatment and Diagnosis

Treatment of individuals with active tuberculosis (TB) is the first priority for TB control; an important second priority is identification and treatment of individuals with latent TB infection (LTBI). LTBI is a clinical diagnosis that is established by demonstrating prior tuberculosis infection and excluding active tuberculosis disease. Available tests to demonstrate prior tuberculosis infection include the Tuberculin Skin Test (TST) and interferon-gamma release assays (IGRAs). These measure immune sensitization (type IV or delayed-type hypersensitivity) to mycobacterial protein antigens that might occur following exposure to mycobacteria.

In most individuals, Mycobacterium tuberculosis infection is contained initially by host defences, and the infection remains in a prolonged, suppressed state termed "latency". However, latent infection has the potential to develop into active infection (termed "active disease") at any time. Identification and treatment of LTBI greatly reduces the likelihood of reactivation and so has potential to protect the health of the individuals as well as the public by reducing the number of potential sources of infection.

 

Following LTBI treatment, the durability of protection against reactivation is variable and depends upon regional prevalence of TB and risk for re-exposure. LTBI treatment may confer lifelong protection against disease; among Alaskan Eskimos, for example, the protective effect of isoniazid prophylaxis has been shown to persist for more than 19 years. Treatment of LTBI should be initiated only once active TB has been excluded. Identification and treatment of individuals with latent tuberculosis infection (LTBI) is an important priority for tuberculosis control.