Introduction
Eating disorders (EDs) are characterized by a persistent disturbance of eating that impairs health or psychosocial functioning. Three main ED categories have been classified by the American Psychiatric Association’s
Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (
DSM-5) [
1]: anorexia nervosa (AN), bulimia nervosa (BN), and eating disorders not otherwise specified (EDNOS). In a recent nationally representative US survey, the estimated lifetime prevalence of AN and BN was 0.6 % and 1.0 % respectively and it was consistently 1.75 to 3 times higher among women as men [
2]. EDs are associated with the highest rates of morbidity and even mortality of any mental disorders especially among adolescents. Failure to recognize their early signs can compromise a patient’s recovery and long-term prognosis.
A large number of individuals seeking or receiving medical treatment for gastrointestinal (GI) symptoms in GI out-patient clinics could mask a concurrent often undiagnosed ED [
3,
4]. However, the early recognition of an ED is sometimes very difficult.
It has been recently demonstrated that patients with ED, when carefully investigated, significantly showed a high prevalence of dyspeptic symptoms fulfilling Rome III criteria for functional dyspepsia (FD). FD is one of the most common functional GI disorders (FGID) [
4]. In particular, patients with FD complain of frequent meal-related symptoms and are diagnosed as having post-prandial distress syndrome (PPDS), which is a subtype of FD. Tooth erosion has been reported as an oral manifestation that might help in the early detection of EDs [
5]. Hence, gastroenterologists should be encouraged to routinely screen for EDs in patients who present with FD/PPDS and deny having an ED.
In this report we describe three cases with undiagnosed ED that came under our observation in a GI out-patient clinic, in which a more comprehensive approach paved the way for reaching a final diagnosis and, eventually, successful treatment.
Discussion
Gastroenterologists are health care providers who may come into contact with patients with an undiagnosed ED early on. In fact, it is a common occurrence that patients, before presenting to health care services with an ED, seek treatment for GI symptoms [
4], such as dyspeptic symptoms that induce high utilization of health care and have a negative impact on quality of life [
6]. Dyspeptic symptoms are very common with a prevalence of approximately 20 to 25 % in Western countries; the prevalence is slightly higher in women [
7].
Currently, internationally accepted clinical criteria (Rome III criteria) are extensively used to diagnose FGIDs [
6]. The Rome III Criteria were developed by a committee that recommended the pragmatic description of FD to be the presence of symptoms such as epigastric pain, epigastric burning, post-prandial fullness and early satiation in the absence of any organic, systemic, or metabolic disease that is likely to explain the symptoms. Furthermore, Rome III criteria help to distinguish whether patients report symptom aggravation after ingestion of a meal, the so-called PPDS characterized by postprandial fullness and early satiation, or meal-unrelated dyspeptic symptoms, the so-called epigastric pain syndrome (EPS), characterized by epigastric pain and epigastric burning [
6]. A distinction between meal-related and meal-unrelated symptoms has been demonstrated as clinically relevant for disclosing differences across EDs [
4]. In our case report, the presence of dental erosions together with the presence of dyspeptic symptoms fulfilling the diagnosis of FD on the basis of Rome III criteria led to the diagnosis of ED. It is well known, however, that patients with an ED commonly refuse to admit having a problem [
8,
9]. For example, our first patient denied any vomiting during the assessment at the dental clinic and only the presence of typical erosion raised the suspicion of an ED.
Dental erosion is commonly described as a progressive loss of hard dental tissue that is unrelated to bacterial activity. Erosion needs to be differentiated from attrition, normal physiological wear of teeth, and abrasion which is the pathologic wear of teeth caused by an involuntary action that is teeth grinding [
5,
10].
The major cause of dental erosion is a chemical action associated with habitual vomiting or regurgitation or the eating of acid foods producing progressive wear of the anterior teeth in the maxillary arch. This is caused by the direction of the vomit as well as the position of the tongue during the episodes. The lingual surfaces of the maxillary anterior teeth are disintegrated by the acid during vomiting episodes, including the palatal part of the maxillary posterior teeth. In contrast, the mandibular anterior teeth appear normal since the tongue protects them. Cratering or cupping could be present, and amalgam restorations, if present, appear raised. It has been previously demonstrated that it could be important to differentiate dental erosion caused by habitual vomiting or regurgitation from that caused by eating habits such as Coke-swishing or vegetable and/or fruit-mulling [
10‐
12]. The latter can be easily excluded by taking a careful medical record because patients usually admit to eating these kinds of food and beverages and have the typical appearance of wear abnormalities. In a recent systematic review and meta-analysis, purging practices seem to increase the risk of tooth erosion. Nevertheless, there is a significant lack of scientific evidence to fulfill the basic criteria of causation between tooth erosions and EDs [
5]. Other oral signs such as sialadenosis and oropharyngeal erythema have been previously described more frequently in patients with anorexia and bulimia and could be taken into account to suspect an ED. In our three cases, dental erosion captured our attention; gastroenterologists would concentrate on the presence of sialadenosis [
13] but it is quite difficult to perform this assessment.
Our combined (gastroenterologists and dentists) approach to the patients raised the suspicion of an ED and although communication with patients with an ED is very difficult, our approach helped patients to admit their ED problem and accept the psychiatric help that is the first step to ensuring future optimal treatment success.
The hallmarks of EDs are clinical disturbances in body image and eating behavior resulting in physical and psychological impairment. AN, BN and EDNOS are more common in women and can result in long-term health consequences even in increased mortality. The core presentation of AN is characterized by the inability or refusal to maintain a minimally normal weight, and a profoundly distorted perception of body weight and shape. Amenorrhea commonly occurs in AN. Under the definition of BN are included individuals with comorbid psychopathology who engage in recurrent binge-eating episodes and recurrent inappropriate compensatory behaviors that are intended to rid calories that they voraciously ingested. EDNOS involves milder versions of AN and BN that do not satisfy all the criteria [
1]. Previous studies have suggested that patients with anorexia frequently complain of GI symptoms hinting at a disordered gastric motility, especially when they are in a refeeding phase [
14]. Dyspeptic symptoms such as epigastric fullness and distension were found to be significantly more prevalent and intense than in healthy individuals and may serve as an argument for food refusal [
15]; however, they are often overlooked or misinterpreted. In patients with bulimia the large quantities eaten during a binge not only lead to a feeling of loss of control but also to a sensation of epigastric distension. The latter as well as the often associated epigastric pain are terminated by self-induced vomiting, which allows either continuation or termination of the binge. The mechanisms underlying dyspeptic symptoms in EDs are still unclear, although malnutrition and the resultant metabolic myopathy, along with electrolyte depletion seem to play a crucial role in determining the demonstrated abnormalities in gastric emptying, gastric capacity and blunted endocrine control [
14].
Once established, the psychological and physiological GI disturbances can perpetuate and strengthen each other resulting in an FGID that can persist independently of the ED that originally caused the motor and sensitivity disturbances [
16].
A limitation of this study is the failure to register the presence of sialadenosis [
13].
Conclusions
It is conceivable that a large number of individuals receiving medical treatment for meal-related symptoms in GI out-patient clinics could be better managed by the identification of a concurrent ED. This is an important issue given that the ultimate goal of therapy in patients with a suspected ED is the normalization of gastric motor function with the resumption of normal eating behavior enabling the patient’s social reintegration and restoration to an appearance acceptable to the social environment.
However, these cases highlight the difficulties in reaching a diagnosis of ED and should encourage the routine screening for oral signs of recurrent vomiting in patients fulfilling the Rome III Criteria for PPDS in GI out-patient clinics.
Special attention should be given to detect subclinical cases of EDs to avoid the progression of disease and further comorbidities that expand its clinical impact across different specialties.
Competing interests
The authors declare that they have no competing interests.
Authors’ contributions
PI: patient enrollment, conception and study design, collection and interpretation of data, drafting of the article and final approval of the version to be published. MA: patient enrollment, drafting of the article and final approval of the version to be published. SC: interpretation of data, drafting of the article and final approval of the version to be published. VB: conception and study design, collection and interpretation of data, drafting of the article and final approval of the version to be published.