Gluten-related disorders Flashcards

1
Q

diet therapy for Wheat allergy?

A

Diet Therapy
 Avoidance of wheat only; barley,rye and oats OK

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2
Q

Reasons for rising prevalence celiac dz?

A

 changes in infant feeding practices
 rise in use of artificial feeds
 shortened duration of breastfeeding
 gluten best introduced whilst breastfeeding
 early introduction of gluten
 before 4 months of age – 500% increased risk!
 before 12 months of age
 increased frequency of C-section births
 alterations in GIT microflora
 Hygiene hypothesis/ Disappearing microbiota hypothesis
 changes in gluten content of wheat varieties
 current varieties of wheat have higher gluten content
 changes in growing techniques/fertilisers applied
 the more nitrogen applied the greater the gluten content
 changes in food preparation techniques
 slow sourdough vs quick yeast breads

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3
Q

Gold standard test for celiac?

A

Small Bowel Biopsy (Alaedini and Green, 2005)
◦ considered the gold-standard

graded by Marsh criteria

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4
Q

CD- Diagnosis
 For serology or biopsy tests to be
accurate:

A

ensure continued daily gluten consumption for
at least 6 weeks prior to testing
 minimum of 4 slices of wheat bread daily (adults)
 minimum 2 slices/day in children
◦ some suggest 2 weeks as adequate in
symptomatic patients

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5
Q

Other indicators of “hidden” coeliac
disease

A

◦ Raised liver enzymes – AST and ALT
(unexplained)
◦ Iron deficiency (unexplained)
◦ Delayed puberty
◦ Infertility

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6
Q

CD - Consequences?

A

Nutritional deficiencies (Presutti et al, 2007)(Tran et al, 2011)(Pietzak,
2012)(Rude and Olerich, 1996)
◦ Protein
◦ Zinc
◦ Iron
◦ Calcium
◦ Magnesium
◦ Folic acid
◦ Selenium
◦ Vitamin B6
◦ Vitamin B12
◦ Vitamin E
◦ Vitamin K
◦ Vitamin D

Disaccharidase deficiency (brush border
enzymes)
◦ moderate-to-severe intestinal lesions (Prasad et al, 2008)
 marked reductions in lactase and sucrase levels
◦ in intact villi - at time of Dx (Mones et al, 2011)
 Lactase – 22% of controls
 Sucrase – 46% of controls
 Maltase – 38% of controls
◦ in remission (O’Grady et al, 1984)
 brush border enzyme levels remain low

Altered xenobiotic metabolism (Lang et al, 1996)
◦ patients with active CD have significantly
reduced intestinal cytochrome P450 3A
(CYP3A) functioning
 reduced metabolism of many pharmaceutical drugs
and other xenobiotics  increased serum levels of
these agents

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7
Q

Coeliac Disease
 Long-term Sequelae?

A

◦ Increased risk of: (Derikx and Bisseling, 2012)(Presutti et al, 2007)
 Osteoporosis
 Small bowel carcinoma
 Oropharyngeal and oesophageal cancers
 Non-Hodgkin’s lymphoma

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8
Q

Coeliac Disease
 Conditions associated with:

A

◦ Graves disease (Ch’ng et al, 2005)
◦ IgA deficiency (Chow et al, 2012)
◦ Epilepsy (Jackson et al, 2012)
◦ Osteomalacia (Sahebari et al, 2011)
◦ Type 1 diabetes (Camarca et al, 2012)
◦ Schizophrenia (Chen et al, 2012)
◦ Juvenile chronic arthritis (Lepore et al, 1996)
◦ Restless legs syndrome (Weinstock et al, 2010)
◦ Hypothyroidism (Collins et al, 2012)
 3-fold higher incidence (Sategna-Guidetti et al, 2001)
◦ Down syndrome (Presutti et al, 2007)
◦ Meniere’s disease (Di Berardino and Cesarani, 2012)
◦ Endometriosis (Stephansson et al, 2011)
◦ Ataxia (Jackson et al, 2012)
◦ Recurrent migraines (Presutti et al, 2007)
◦ Recurrent miscarriage (Soni and Badawy, 2010)
◦ Female infertility (Soni and Badawy, 2010)
◦ Autoimmune disorders (Niewinski, 2008)
 occur 3-10x more frequently in CD patients!!!
◦ Fructose intolerance?

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9
Q

Coeliac Disease – GIT Ecosystem
 GIT Microflora in CD

A

◦ Higher populations of Gram-negative bacteria
◦ Greater diversity of Eubacteria
◦ Increased Bacteroides counts
◦ Less total anaerobes
◦ Less lactobacilli
◦ Less bifidobacteria
◦ Less enterococci
◦ higher faecal SCFA concentrations
 ↑ amount of acetic acid - due to malabsorption of sugars likely

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10
Q

Coeliac Disease
 Nonresponsive CD (NRCD) - why?

A

10-20% of patients Dx with CD will have persistent or
recurring S&S despite following a GFD (Scanlon and Murray,
2012)(Dewar et al, 2012)
 contamination with gluten is most common cause of
lack of response (~30-45% of NRCD)
 refractory CD may be present in ~10% of these
 consider other diagnoses:
 SIBO
 Fructose and/or lactose intolerance
 IBS
 Microscopic colitis
 Crohn’s disease
 Pancreatic insufficiency
 faecal elastase
 Giardiasis

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11
Q

Gluten Sensitivity
◦ S&S?

A

S&S
 GI – abdominal pain, diarrhoea, nausea, vomiting,
bloating, excess flatulence
 systemic – behavioural changes, bone or joint pain,
muscle cramps, leg numbness, weight loss, chronic
fatigue, headaches, “foggy mind”, eczema and/or rash

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12
Q

CD–Treatment
 Nutritional supplementation?

A

Assess vitamin and mineral status and supplement if appropriate
 Fe studies
 FBC/CBC
 B12
 plasma homocysteine
 surrogate marker for B12 and folate status
 BMD (in older patients)
 serum 25-hydroxyvitamin D
 optimal is > 125nmol/L (>50ng/mL)
◦ Supplement other at risk nutrients
 Zinc
 Selenium
 Calcium
 Magnesium
 Vitamin B6
 Vitamin E
 Vitamin K

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13
Q

example of treatment script for celiac dz

A

3 month trial of strict GFD
◦ high potency multivitamin & mineral
◦ vitamin D (5000 IU/day)
◦ To help heal the gut:
 lactulose – starting with 1 tsp daily
 glutamine powder – 2 heaped tsp daily (~10 g/day)
 Turmeric extract (Meriva) – 1 cap bid
 Saccharomyces cerevisiae var boulardii Biocodex
 250mg bid

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