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Abstracts of the 22

nd

National Congress of Digestive Diseases / Digestive and Liver Disease 48S2 (2016) e67–e231

e149

reported the hydropic degeneration of basal layer, subepithelial T

cell infiltrate, epithelial hyperplasia, hyperkeratosis, acanthosis,

necrotic keratinocytes. The picture was compatible with the

diagnosis of lichen planus. A second anamnesis revealed the

presence of a long lasting oral lichen planus nearby a mobile dental

bridge. Patient was treated with endoscopic dilatations by the use of

bougies over a Savary guidewire by increasing the diameters until 9

French (fig 3).

Results:

Patient reported an immediate symptoms relief. Dilatation

in lichen planus stenosis is not the first choice due to the risk of

Koebner phenomenon but this patient the comorbidity did not

allowed systemic steroid therapy.

Conclusions:

Lichen planus is an idiopathic disorder with clinical

manifestation in the skin, mucous membranes, genitalia, hair

and nails. Esophageal involvement by lichen planus is rare,, more

commonly found in middle-aged woman, mostly associated with

oral lesions. It can be missed because a long time (years) is necessary

from the disease onset and the development of dysphagia. Even if

esophageal localization of lichen is rare, it must be considered in

the differential diagnosis of dysphagia and esophageal stricture

especially in elderly women, along with peptic disease and

esophageal adenocarcinoma.

Our case demonstrated that clinical, endoscopic and histologic data

may narrow a broad list of differential diagnoses for the esophageal

stricture and in this case allowed the diagnosis of the rare esophageal

lichen planus.

P.05.6

A RARE CASE OF CELIAC DISEASE IN A PATIENT WITH COMMON

VARIABLE IMMUNODEFICIENCY: WHEN VILLOUS ATROPHY IS

NOT ENOUGH

Morreale G.C.*

1

, Sinagra E.

2

, Rizzo A.

3

, Amvriosadis G.

1

,

Montalbano L.M.

1

1

(1) Gastroenterology Unit, Ospedali Riuniti Villa Sofia-Cervello,

Palermo, Palermo, Italy,

2

(2) Fondazione Istituto S. Raffaele G. Giglio,

Gastroenterlogy and Endoscopy Unit, Cefalù, Cefalù, Italy,

3

(3)

Pathology Unit, Ospedali Riuniti Villa Sofia-Cervello, Palermo, Palermo,

Italy

Background and aim:

We present a case of a woman with a

diagnosis of celiac disease (CD) histological documented by villous

atrophy; other test demonstrated the presence of common variable

immunodeficiency (CVID) complicated by Giardia Lamblia infection,

an other cause of villous atrophy. In this case, HLA and histological

response to a glutenfree diet (GFD) confirmed CD and GFD resolved

clinical manifestation and villous atrophy.

Material and methods:

A 40 years old woman presented with

chronic diarrhea, weight loss of about 8 kg in 2 months, and iron

deficiency anemia (Hb:8 g/dl); in 2013 patient receive diagnosis of

CD based on histological characteristics (marked chronic inflam­

mation with intraepithelial lymphocytosis, severe flattening of the

villi “March 3 C”). She started gluten free diet. For persistence of

clinical symptoms despite GFD, an other planned disease revaluation

was performed in 2014. Research of abnormal hemoglobin chains

showed no tassemia and other hemoglobinopathies; laboratory test

showed negative celiac markers (transglutaminase IgA and IgG

antibodies) but very low levels of all classes of immunoglobulin (Ig)

(IgA <6.67 mg / dl, IgG <119 mg / dl, IgM <4.17 mg / dl. Abdomen

ultrasound showed only mild splenomegaly (Dt 13 cm). The

esofagogastroduodenoscopy (EGDS) showed on duodenum mucosa,

nodules of various sizes, up to 5 mm. At Hystological exam: severe

villous atrophy, nodular lymphoid infiltration of the lamina propria,

no evidence of plasma cells, presence of many spheroidal

morphology forms compatible with Giardia lamblia (GI). (Fig 1A,B,C);

CD5 glycoprotein expression positive (as a marker of intraepithelial

T lymphocytes); CD20 negative (B-lymphocytes absent) (Fig. 2A,B,C);

switch on D-Immunoglobulin (IgD) for absence of other classes of

Immunoglobulin in CVID (Fig 3). There was also follicular lymphoid

hyperplasia. CVID complicated by GI infection was diagnosed;

patient started antibiotic therapy with metronidazole; CD was

excluded so it was placed indication to practice free diet. Patient had

an increase of weight but diarrhea and anemia not resolved. A new

research of GI in the stool was negative.

Results:

The patient was referred to our Gastroenterology Unit.

We decided to perform genetic test with evidence of HLA-DQ2

Fig. 1.

(A,B) Hystological view of duodenitis by Giardia Lamblia: many spheroidal

morphology forms CPAS positive stanining (x40 magnification). (C) the trophozoites

of Giardia Lamblia. This parasitic infection is typical of patients with CVID and is

associated with villous atrophy.

Fig. 2.

(A,B,C) CD5 glycoprotein expression positive (as a marker of intraepithelial T

lymphocytes); CD20 glycoprotein are negative(B-lymphocytes absent).

Fig. 3

The switch on D-Immunoglobulin (IgD) for absence of other classes of

Immunoglobulin in CVID.