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Paper text:
using multiple terminology in defining atypical celiac disease ( cd ) has confused many of the clinicians to recognise atypical forms of this common disorder .
cd is not considered an uncommon disorder any longer and is not a disease of essentially european origin ( 1 ) .
nevertheless , recognising the existence of atypical forms known under the old terminologies like latent , silent and potential cd has introduced a new insight on clinical behaviour of this condition . that way the age of presentation of the disease has changed dramatically (
1 , 2 ) and the factors responsible for this change are mainly attributed to advances in diagnostic tools in recognising atypical and subclinical forms of the disease .
population screening with serological tests , have shown a cd screening prevalence of the order of 1% in the western hemisphere ( 3 ) .
european and asian studies involving healthy blood donors found a prevalence rate of 1 in 166 - 330 ( 4 , 5 ) subclinical cd . according to the previous studies , screening based on antibodies
only would underestimate the prevalence of cd due to false - negative results caused by the low sensitivity of tests ( 610 ) .
however , some studies suggest that the overestimation of cd frequency could also result from antibody based screening programmes due to a high rate of false positives ( 11 ) .
terminologies like latent , silent and potential celiac disease can be confusing for clinicians and patients .
silent cd is not absolutely silent after all ; patients show signs of cd with no significant symptoms .
t - cell - mediated autoimmune processes are initiated by gluten exposure , leading to both intestinal and atypical extraintestinal manifestations .
more and more diseases are proven to be associated with cd . in these conditions , screening is strongly recommended .
malabsorption can be silent like a mild anaemia ( better defined under subclinical ) , or there is usually only moderate malabsorption , if any at all .
since gluten sensitivity is no longer limited to overt villous atrophy , and given the results of many studies ( 1315 ) , we believe the answer is yes .
subclinical or so called silent cd cases are being detected in increasing numbers because of raised awareness of the disease .
presentations with atypical symptoms are the dominant form of disease manifestation and these comprise the sole and main part of the celiac iceberg ( 16 ) . whether they have positive serology with negative biopsy or increased  t cells receptors with symptoms compatible with cd they could be classified as atypical cd .
we are moving towards a lower threshold in implementing a gluten free diet ( gfd ) .
villous atrophy is not mandatory any longer to qualify a patient for gfd . in fact
a large number of patients present with non - celiac gluten sensitivity with completely normal biopsy and negative serology .
there is a need to re - define the terminologies according to the modified treatment strategy in gluten related disorders .
the main strategy for treatment should target symptomatic typical or atypical patients , and not asymptomatic cases .
we propose a simplified classification by dividing and replacing previous terminology to typical , atypical and subclinical instead of silent / latent and potential .
celiac and non - celiac gluten sensitivity * suclinical : previously known as silent and atypical as known under latent and potential cd
the disorder is now considered the result of a complex interaction between genetic and environmental factors such as gluten that classified from subclinical to severe malabsorption .
in contrast to gluten sensitivity celiac disease development has a strong genetic component with a sibling relative risk ( lambda ( s ) ) of 30 .
recent studies using the human genome screening technique in families with multiple siblings suffering from cd have suggested the presence of at least 4 different chromosomes in the predisposition to suffer from cd ( 17 ) .
one susceptibility locus is the mhc ( major histocompatibility complex ) region , with a particular association with the hla - dq alleles dqa1 * 0501 and dqb1 * 0201 .
however , shared - haplotype studies suggest that genes within the mhc complex contribute no more than 40% to the sibling familial risk of disease .
early studies showed that gliadin elicits an inflammatory t - cell reaction when added to intestinal biopsy specimens of celiac patients in vitro and a link to the genetic predisposition was provided by the isolation of gliadin - specific hla - dq2-restricted t - cell clones from cd mucosa ( 18 , 19 ) .
however , the prevalence of hla - dq2 is high in the normal population ( 25 - 45% ) , suggesting the involvement of additional , and probably non - hla - linked genes in cd pathogenesis .
the pathologic spectrum of the mucosal abnormalities seen on small intestinal biopsies , range from microscopic enteritis ( marsh 0-ii ) to macroscopic forms ( marsh iiia - c ) ( 20 ) .
not every gluten - sensitised individual inevitably develops cd and not every celiac patient develops the destructive lesions such as marsh iii .
celiac disease is not exclusively due to antibody production either . a large proportion of the patients present with microscopic enteritis ( marsh i - ii ) whose diagnoses
these 6 distinct and sequential phases of the cd are microscopic enteritis ( me ) marsh ( 0-ii ) .
some patients could still have subtle abnormalities at this stage like increased  t cell receptors or alteration of enterocytes and microvillis .
i ) recruitment of t - lymphocytes > 25/100 enterocytes ( intestinal - intraepithelial lymphocyte or iel ; marsh i ) , ii ) lymphocyte infiltration and crypt hyperplasia ( marsh ii ) , iii ) macroscopic enteritis ( marsh iiia - c ) partial villous atrophy ( marsh iiia ) , iv ) subtotal villous atrophy ( marsh iiib ) and v ) total atrophy ( marsh iiib ) and total villous atrophy ( marsh iiic ) ( 6 , 8) .
this sequential cascade suggests that a t - cell response to gliadin precedes , and very likely produces , the complete pattern of cd .
the statistical comparison between antibody - positive and antibody - negative cases shows that the appearance of antibodies was seen predominantly in cases with serious mucosal damage in which iels was highly increased .
however , it is hard to rule out the contribution of antibodies in genesis of an autoimmune condition like cd .
the screening value of autoantibodies has been too optimistically overestimated , especially those on tissue transglutaminase antibodies ( ttga ) ( 24 , 25 ) . however , comparing the ttga to ema and aga , the sensitivity of ttga does not offer any advantages over ema for screening of the populations at high risk of cd ( 2628 ) .
it is time to re - evaluate our perception of intestinal pathology ( 29 ) in such terms , rather than by continued use of subjective degrees of villous atrophy ( va ) , since absence of va is not evidence of absence of cd .
such terminology obscures the recognition of fundamental changes occurring within small bowel mucosa . in simple words , increased density of iel 's and crypt hyperplasia form an essential phase in the disease pathogenesis sequence of progression .
as cd with milder enteropathy is the most common form , histology can not be considered as the gold standard any longer .
gluten sensitivity ( gs ) is characterised by negative antibodies and normal histology ; it is defined as a non - allergic and non - autoimmune condition in which the consumption of gluten can lead to symptoms similar to those seen in cd . until recently the terms gs and cd were used synonymously in literature ( 33 ) and it is not clear yet whether patients affected by gs will have some subtle intestinal and mucosal changes consistent with microscopic enteritis .
some gs patients would tolerate even more than 5 g gluten / day and still remain symptom free with negative serology ( 34 , 35 ) .
gs patients are gluten intolerant and gluten consumption does not lead to small intestinal damage , so it is not accompanied by the concurrence of ttg autoantibodies or autoimmune disease . in the study by kaukinen et al . out of 94 adults with gi symptoms ,
63% were affected by gluten foods and neither classified as cd nor as allergic ( 36 ) . on the other hand around 50% of the gs patients
were dq2/dq8 positive , which is similar to that of the general population , while celiac patients carry more than 95% in most regions of the word .
however , while the prevalence of cd is roughly 1% within the general population , gs is thought to affect 6 to 10% of the general population ( 37 ) . in some cases gs can present with normal or milder enteropathy seen as increased intestinal permeability , ibs , abdominal discomfort , pancreatic disorders , pain or diarrhoea ; or it may present with a variety of extraintestinal symptoms including lymphoma , attention deficit disorder and neuropathy , autism and schizophrenia , infertility , ibd , muscular disturbances as well as osteopenia and osteoprosis ( 3842 ) . according to current literature , a gfd is recommended to gluten sensitive cases with / without enteropathy .
this policy includes a range of symptomatic gluten sensitive cases with atypical presentation including those with small bowel microscopic changes ( marsh 0-ii ) who are antibody negative or show characteristic features of other conditions .
this is because these common systemic disorders have multifactorial etiology with a multitude of symptoms and complications inside and outside the small bowel .
we still do n't know how seriously subclinical cd will be affected by the long term complications if they are not treated with gfd . a marked increase in the prevalence of cd , especially the subclinical cd forms and non - celiac gluten sensitivity , seem to become a major health problem ( 4346 ) .
the clinician may often face the variability of histological and clinical aspects of cd ( 46 ) with uncertainty , as they might not quite fit into the diagnostic models in the current guidelines .
accumulated evidence supports that decreasing the treatment threshold for cases with atypical cd and those with gluten sensitivity , as the life quality of these cases will improve with gfd and the long - term health benefit of this strategy , would perhaps be also cost effective .
atypical presentation is the most common form of celiac disease ( cd ) . 
 although the terminologies like latent , silent and potential have expressed different aspects of clinical and pathological behaviour of cd , they also have contributed in some extent to confusion between clinicians and patients due to the multiple definitions and uncertainty around them . in the light of new advances and the discovery of entities such as non - celiac gluten sensitivity , using subclinical instead of silent and atypical instead of potential / latent 
 may simplify the understanding behind the clinical behaviour of atypical cd . the evidence behind a lower threshold for starting a gluten free diet ( gfd ) in non - celiac gluten sensitive patients would strongly support applying a gfd treatment strategy in any forms of cd 
 .