However, in addition to this, various studies have reported a consistent comorbidity between AS and Tourette syndrome in the range of 8–20%, with one figure as high as 80% for tics of some kind or another,  for which several explanations have been put forward, including common genetic factors and dopamine, glutamate, or serotonin abnormalities.According to the Adult Asperger Assessment (AAA) diagnostic test, a lack of interest in fiction and a positive preference towards non-fiction is common among adults with AS. Speech and language
Although individuals with Asperger syndrome acquire language skills without significant general delay and their speech typically lacks significant abnormalities, language acquisition and use is often atypical. Abnormalities include verbosity; abrupt transitions; literal interpretations and miscomprehension of nuance; use of metaphor meaningful only to the speaker; auditory perception deficits; unusually pedantic, formal, or idiosyncratic speech; and oddities in loudness, pitch, intonation, prosody, and rhythm. Echolalia has also been observed in individuals with AS.Three aspects of communication patterns are of clinical interest: poor prosody, tangential and circumstantial speech, and marked verbosity. Although inflection and intonation may be less rigid or monotonic than in classic autism, people with AS often have a limited range of intonation: speech may be unusually fast, jerky, or loud. Speech may convey a sense of incoherence; the conversational style often includes monologues about topics that bore the listener, fails to provide context for comments, or fails to suppress internal thoughts. Individuals with AS may fail to detect whether the listener is interested or engaged in the conversation.
Additional features including villous atrophy and crypt hyperplasia are the other findings in other Marsh stages of coeliac disease.Antibodies associated with coeliac disease were reported in around 11% of cases. These IgA endomysial antibodies and anti-transglutaminase antibodies are very sensitive and specific for coeliac disease implying that this proportion of duodenal lymphocytosis cases has definite coeliac disease. Around 33% of cases have the HLA-DQ2 allele, which is found in over 90% of people with coeliac disease. Absence of HLA-DQ2 (and the rarer HLA-DQ8) makes coeliac disease most unlikely. As antibody-negative coeliac disease is recognised, HLA status, persistence or progression of the duodenal IEL numbers following a gluten challenge, followed by symptomatic improvement on a gluten-free diet, has been used to be more certain about the diagnosis, which was made in 22% of one series of over 200 adult cases. Helicobacter infection is a common finding at endoscopy and although duodenal IEL counts were found to be slightly higher with this infection, this was not considered to be a meaningful cause in children. Other infections, including Cryptosporidiosis and Giardiasis can also be associated with an increase in IELs. Management
The management is that of any identified associated disorder such as a gluten free diet for cases with coeliac disease or treatment of associated infections. Prognosis
When duodenal lymphocytosis is associated with other features of coeliac disease, in particular positive antibodies, or HLA-DQ2/8 and a family history, treatment with a gluten-free diet produces an improvement in IEL numbers.