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Gluten intolerance and skin diseases |
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European Journal of Dermatology. Volume 16, Number 1, 4-11, January-February 2006, Review article |
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Author(s) : Philippe Humbert, Fabien Pelletier, Brigitte Dreno, Eve Puzenat, François Aubin , Department of Dermatology, University of Franche-Comté, CHU Saint Jacques, 25030 Besançon, France, Department of Dermatology, Hôtel Dieu, 1 place Alexis Ricordeau, 44093 Nantes Cedex 1, France. | ||||||||||||||||||||||||||||||||||||
Summary : Gluten sensitivity with or without coeliac disease (CD) symptoms and intestinal pathology has been suggested as a potentially treatable cause of various diseases. CD is a chronic disease which improves on withdrawal of wheat gliadins and barley, rye and oat prolamins from the diet. There have been numerous reports linking CD with several skin conditions. A body of evidence shows that dermatitis herpetiformis is actually a cutaneous manifestation of CD. Autoimmune diseases, allergic diseases, psoriasis and miscellaneous diseases have also been described with gluten intolerance. Dermatologists should be familiar with the appraisal of gluten sensitive enteropathy and should be able to search for an underlying gluten intolerance (GI). Serological screening by means of antigliadin, antiendomysial and transglutaminase antibodies should be performed. HLA typing is often useful in association with serologic tests. Intestinal biopsy is usually needed to establish the diagnosis of CD or GI. Thus, gluten intolerance gives rise to a variety of dermatological manifestations which may benefit from a gluten-free diet. | ||||||||||||||||||||||||||||||||||||
Keywords : coeliac disease, dermatitis herpetiformis, gluten free-diet, gluten intolerance | ||||||||||||||||||||||||||||||||||||
ARTICLE
Auteur(s) : Philippe Humbert1, Fabien Pelletier1, Brigitte Dreno2, Eve Puzenat1, François Aubin1 1Department of Dermatology, University of
Franche-Comté, CHU Saint Jacques, 25030 Besançon, France accepté le 15 Juillet 2005 Gluten sensitivity with or without classical coeliac disease (CD) symptoms and intestinal pathology has been suggested as a potentially treatable cause of various diseases. CD is a chronic disease, characterized by small bowel villous atrophy which impairs nutrient absorption and improves on withdrawal of wheat gliadins and barley, rye and oat prolamins from the diet [1]. The alcohol-soluble prolamin fraction of gluten (gliadin in wheat, secalin in rye, avenin in oats, and hordein in barley) is one of the offending substances. CD has a wide variety of clinical manifestations, including failure to thrive, chronic diarrhea, abdominal pain and distension, muscle wasting, irritability. An increasing number of patients should be diagnosed with subclinical forms characterized by minor, transient or apparently unrelated dermatological symptoms [1]. Maki et al. [2] estimate that the prevalence of coeliac disease among Finnish schoolchildren is at least one case in 99 children.Over the last few years there have been numerous reports linking CD with several skin conditions. Thus, gluten intolerance (GI) or CD gives rise to a variety of dermatological manifestations which may benefit from the gluten-free diet (GFD) given for GI or CD (table 1).To establish the diagnosis of CD, an intestinal biopsy is usually needed. Indeed anti-gliadine antibodies are not considered as a good marker for CD. Thus anti-endomysial and anti-transglutaminase antibodies are more specific and more sensitive markers for CD.Many diseases are found with a higher frequency in patients with CD, but also in dermatitis herpetiformis (DH). Some autoimmune diseases linked with HLA DQ2 or DQ8 phenotype (e.g., diabetes mellitus, thyroid disease), are particularly associated with CD. Moreover HLA typing is often useful in association with serologic tests to diagnose CD.Due to the high prevalence of gluten intolerance in the population, it is thus probable that combination of CD with other frequent diseases may be fortuitous. The strength of evident association between gluten intolerance and the main skin diseases is related in table 1.Gluten intolerance and autoimmunityDermatitis herpetiformis( Table 1 )Since the first observation by Marks et al. [3] the relation between CD and dermatitis herpetiformis (DH) has been well established. Nowadays a body of evidence shows that DH is actually a cutaneous manifestation of CD and may affect approximately twenty-five per cent of patients with CD [4]. Twenty percent of patients with DH have clinical symptoms of CD. However, in 80% of cases of DH, intestinal investigation shows endoscopic and histologic changes consistent with CD [5]. From a statistical point of view, the main conditions associated with DH are autoimmune thyroid disease, diabetes mellitus, lupus erythematosus, Sjögren’s syndrome, sarcoidosis, vasculitis, rheumatoid arthritis, vitiligo and alopecia areata [6, 7]. Considered as an autoimmune condition, DH can be associated with more than one other autoimmune condition, leading to the concept of Multiple Autoimmune Syndromes [8]. Nevertheless, in these cases, the role of GI seems to be negligible. There is an increased incidence of lymphoma in patients with DH as there is in patients with CD. It has been shown that a gluten-free diet protects against the development of lymphoma both in CD and DH [9]. Besides, DH is associated in most cases with particular HLA phenotypes, i.e. A1, B8 and/or DR3 [6]. These haplotypes confer a genetic predisposition for autoimmunity. Two recent studies have raised the predominant presence of the alleles DQB2 and DQ8 in both CD and DH [10, 11]. It has now been claimed that transglutaminase (TGT) is the autoantigen in CD and antibodies to TGT are present in the circulation. The mechanism of how it induces the enteropathy has still to be elucidated. In addition transglutaminase antibodies play a role in the production of the skin lesions of patients with DH [6]. Furthermore a long term recent follow-up study of CD and DH showed that first-degree relatives are frequently affected in CD and DH [12].Table 1 Strength of evidence for association between gluten intolerance and main skin diseases
IgA linear dermatosisLinear IgA dermatosis is a rare bullous disorder first described by Jablonska and Chorzelski in 1979 [13]. Linear IgA dermatosis is often associated with malignancy, in particular lymphoma. And the occurrence of lymphoma as a complication of CD is well recognized. Nevertheless, the association of IgA linear dermatosis in a patient with lymphoma and subsequent CD should probably be linked more to the malignant condition [14].A recent case report demonstrated that linear bullous dermatosis can respond to gluten restriction if an underlying gluten-sensitive enteropathy is present [15]. Benign chronic bullous dematosis of childhood is a distinct clinical entity among the bullous diseases of childhood. It shares with IgA linear dermatosis some immunopathological features. In an eleven-year old patient, the bullous condition was associated with CD [16] and responded well to GFD. Bullous pemphigoidSome authors showed antigliadin antibodies in the serum of patients with bullous pemphigoid [17] and in chronic benign mucous membrane pemphigoid [18] as well, suggesting similar particularities with DH. If there is no evidence that these patients have gluten-sensitive enteropathy, either clinically or histologically, it is assumed that their mucosa may be permeable to proteins such as gliadin.Alopecia areataPatients with alopecia areata were recently found to be at high risk of gluten-sensitive enteropathy [17]. The prevalence of gluten-induced enteropathy in patients with alopecia is from 1:89 [19] to 1:116 [20], and is significantly higher than that of CD in the general population (1:305) [21]. Thus, only two out of 232 patients with alopecia areata were positive for IgA antibodies, and had a severe partial or subtotal villous atrophy [20]. Nevertheless, in only one of the two cases of this study was the withdrawal of gluten from the diet followed by a partial regrowth of scalp, which was affected by alopecia universalis. Benefits from a GFD also occurred in some other cases [19, 20, 22]. However, in one case, alopecia areata developed after the beginning of such a diet [23], and in five alopecic patients with CD, both conditions seemed to have an independent course, GFD being successful for the CD but not for alopecia areata [24]. In two other reports of three cases [25], low serum zinc levels were detected, but zinc supplementation did not improve the scalp condition, whereas GFD led to regrowth of hair respectively within the year in two cases, and after 2 years in the other one.Recently Storm described a young girl with Down’s syndrome, alopecia areata and documented CD, who displayed a normal growth of hair after a gluten-free regimen [26]. Thus, it is noteworthy that gluten sensitive enteropathy needs to be searched for in alopecia areata, even if the frequency of the association is rare. Indeed, GFD could be beneficial in some patients. VitiligoThe possible relation between vitiligo and GI remains a debated question [27]. In a study, none of the 198 patients with vitiligo who were screened for IgA antibodies, was positive [20], and the authors concluded that the sporadic associated cases must be considered coincidental.Lupus erythematosusA few previous reports of protein-losing enteropathy leading to malabsorption have been described associated with systemic lupus erythematosus (SLE) [28]. In a series of twenty-one SLE patients, the prevalence of malabsorption was approximately ten per cent but the pathogenesis is not yet clear and needs further investigation [29]. Also, gluten enteropathy has been described in a case of sub-acute cutaneous lupus erythematosus [30]. Twelve months after a successful GFD on gastro-intestinal symptoms, the patient developed erythematous annular and gyrate lesions on the face, neck and forearms. The relation between both conditions might be due to the presence of HLA DR3 which has a high incidence in subcutaneous lupus erythematosus and in gluten sensitive enteropathy. However, GFD was unsuccessful in preventing lupus erythematosus. Moreover, a recent American study examined the prevalence of CD autoantibodies in SLE patients [31]. Twenty-four of one hundred and three patients tested positive for antigliadin antibody, whereas none of the twenty-four antigliadin positive patients was found to have endoscopic or histological evidence of CD. Antiendomysial antibodies were also negative in these patients. In fact, false positive antigliadin antibodies with SLE are common. There does not seem to be an association between CD and SLE, although previous cases in the medical literature have described the diagnosis of CD in patients with known SLE and the diagnosis of SLE in patients with CD [32-35].SclerodermaSystemic sclerosis may be associated with other different autoimmune diseases [36].Among these conditions, CD may be one of the different causes of malabsorption in scleroderma patients [37]. Polymyositis and dermatomyositisA wide range of neuromuscular diseases may be the presenting feature of CD [38]. Polymyositis may be associated with CD in some patients [39-42]. In some cases, treatment with GFD resolved clinical and laboratory abnormalities [41, 42].Juvenile dermatomyositis, as well as dermatomyositis in adult patients, may exhibit malabsorption syndrome. Especially when patients present with unusual and unexplained gastrointestinal features, an evaluation for CD should be considered, and could lead to its early management [43-46]. Sclero-atrophic lichenProbably due to its low frequency, only one report of sclero-atrophic lichen has been described associated with CD [47].Cutaneous vasculitisWhen associated with cryoglobulinemia, it is not surprising to observe cutaneous vasculitis in the course of CD [48]. In other cases [49-51], cutaneous vasculitis occurred in the presence of severe, poorly controlled bowel disease. The increased intestinal permeability of CD [52] (intestinal hyper-permeability does not mean increased absorption, both mechanisms being different) could induce the production of immune complexes which are the pathophysiological factors involved in leucocytoclastic vasculitis. Thus, these patients are likely to improve on a GFD [51].Erythema elevatum diutinumErythema elevatum diutinum should be regarded as a rare variant of cutaneous leucocytoclastic vasculitis. Dapsone is known to be effective in some cases. A few cases have been described in association with CD [53, 54]. In these cases GFD was successful in improving cutaneous symptoms. The erythema elevatum diutinum skin lesions could be the result of immune complex deposition composed of IgA, which could merely constitute a marker of the disease.Gluten intolerance and allergic diseasesUrticariaDifferent immuno-allergical manifestations, such as asthma, eczema, hayfever and urticaria could be improved by a GFD, when they are associated with CD [55, 56]. Moreover, histological alterations of the small bowel mucosa consistent with the diagnosis of CD were found in some patients with urticaria [57]. These experiences suggest that CD should at least be considered when studying patients with chronic urticaria, even in the case of hereditary angioneurotic, which can be associated with CD [58].Atopic dermatitisCereal allergy or intolerance can be one of the underlying causes of atopic dermatitis in some patients. Despite the role of cereal products in the beginning or the course of the disease in some patients with atopic dermatitis, the coexistence of CD seems to be rare [59], with a prevalence of 1%, which is nevertheless higher than that in the general population [60]. Atopic dermatitis can be one of the underlying symptoms of the so-called subclinical CD (the characteristic symptoms of CD being absent), especially in children [61]. Since food allergy seems to play an important role in atopic dermatitis, occult enteropathy should thus be suspected in patients with atopic dermatitis [57]. Skin prick tests and radioallergosorbent tests allow the detection of wheat-allergic atopic dermatitis patients, suggesting in such cases an IgE-dependent allergic mechanism [62]. On the contrary, the presence of IgA and IgG antibodies to different cereal antigens displays little diagnostic significance in atopic dermatitis [63].Prurigo nodularisPrurigo nodularis is sometimes considered as an itching condition related to psychological disorders, or due to different mechanisms [64]. Since the description by Wells in 1962 of six patients with eczematous skin manifestation associated with steatorrhea [65], one of them having been cleared after a GFD [66], the underlying role of GI was suggested again. Howell [67] described a female aged 53 years who was shown to have gluten enteropathy associated with a so-called exsudative nummular prurigo. Appropriate treatment of her gut and skin led to substantial improvement. McKenzie et al. [66] reported two female patients with suspected GI in whom a GFD did not clear nodularis prurigo, but increased the sense of well-being. The underlying intestinal disturbance in patients with prurigo nodularis seems to be unquestionable when considering some published cases with malabsorption. Gluten might be one of the related factors responsible for malabsorption. Two other cases give clues to this pathological link between both skin and gut conditions [68, 69] since both patients significantly improved under GFD. In one case, prurigo nodularis preceded by 15 years the onset of CD, and both conditions showed a similar and concomitant course [70]. The combination of CD, DH and prurigo nodular has just been reported in a 40-year-old woman [71]. The response to gluten withdrawal of both skin diseases suggests the possibility that prurigo nodular also should alert to CD.Gluten intolerance and deficienciesThe following skin conditions may be due to deficiency symptoms related to malabsorption. Hemorrhagic diathesis [72], iron deficiency, and scurvy have a clinical dermatological expression, and should be explored to detect subclinical CD.Scurvy is usually due to alcoholism, a limited diet and poor socio-economic conditions. It has been described related to Whipple disease [73], Crohn’s disease [74] and CD [75]. When not diagnosed, CD induces long term malabsorption of different nutriments. Among them, ascorbic acid deficiency occurs very early on. Indeed, only a three-month deficiency period is necessary to completely deplete the vitamin C stocks of the body. Gluten intolerance and psoriasis and related conditionsPsoriasisIn 1971, Shuster and Marks described a psoriatic enteropathy in a small group of patients with severe psoriasis and gastro-intestinal changes similar to CD [76], In 1976, Bazex et al. [77] examined 16 patients with severe psoriasis. In 11 patients, they showed a clear atrophy of the intestinal mucosa. All four patients with psoriatic rheumatism presented with malabsorption. It was not possible to precisely evaluate the benefit of GFD in this series, nevertheless the conviction of the authors was that patients got better and that psoriasis improved. In one case, they observed the relapse of psoriasis three days after the withdrawal of the GFD. For many years, Michaëlsson et al. have been taking into consideration the role of gluten in the determinism of psoriasis [78-84]. Their first reports involved six patients with moderate to severe psoriasis, and one with severe palmo-plantar pustulosis, with durations of 6-37 years, and total or almost total clearance of the lesions on a GFD with no other treatment [78]. Their conclusion was that the response to a GFD was impressive. These results prompted them to question whether GI might be more common in patients with psoriasis than in healthy subjects [79]. Three hundred and two patients were compared with blood donors. Sixteen per cent of the patients had IgA antigliadin antibodies values above the 90th percentile of the reference subjects. There was a more pronounced tendency in male than in female patients, and in the male group a trend to a correlation between IgA antigliadin antibodies and the age of the patient was demonstrated. The authors noticed that raised serum levels of antibodies to gliadin were more common in patients with psoriasis requiring systemic therapy.The question remains as to whether the enteropathy is secondary or not to the skin disease. Different data, including increased intestinal permeability [85] suggest an intestinal involvement in psoriatic patients. Moreover, 42% of psoriasis patients with moderately elevated levels of serum IgA and/or IgG antibodies to gliadin had an increased number of mononuclear cells in the duodenal epithelium [80]. Independently of the presence of IgA antigliadin antibodies, psoriasis patients may have a pronounced increase of EG2+ eosinophils and tryptase + mast cells in their duodenal stroma [81, 82]. Furthermore, the effect of a GFD in the 33 previously reported patients was evaluated [84]. After a 3-month GFD period followed by all these patients, thirty of them, who were suspected to have GI, showed a highly significant decrease in mean PASI (psoriasis area and severity index). In addition, six of the antigliadin antibody-negative patients did not improve. The positive effects were observed not only in patients with an increased number of lymphocytes in the duodenal epithelium but also in some patients with seemingly normal epithelium. All these findings raise questions about how they could be explained [86]. Nevertheless, Reunala et al. did not observe any increased incidence of psoriasis among patients with CD or DH [7]. It has been suggested that determining the levels of tissue transglutaminase antibodies in psoriasis patients improves the sensitivity and the specificity of the research of gluten sensitive enteropathy [87, 88]. However, the absence of randomized studies concerning the beneficial effect of a GFD in psoriasis still suggests a placebo effect of this therapy. In addition, due probably to its frequency, CD has been associated with psoriatic arthritis [88]. Lindqvist et al. [89] showed that patients with psoriatic arthritis had an increased prevalence of raised serum IgA antibodies to gliadin and of coeliac disease (4.4%). Patients with raised IgA antibodies to gliadin seemed to have more pronounced inflammation than those with low IgA antibodies to gliadin concentration. Palmoplantar pustulosisAmong the conditions known to be associated with palmoplantar pustulosis, Eriksson et al. [83] noticed a high prevalence of antigliadin antibodies in ten of 39 patients examined. Two of them were known to have gluten hypersensitivity.Pityriasis rubra pilarisPityriasis rubra pilaris (PRP) is a disease of unknown etiology. The association of PRP with CD in one case [90] may bring a clue to its cause. If malabsorption may be present in some patients with PRP, causing decreased concentrations of serum carotene and vitamin A, the origin of the enteropathy remains unknown. In the present case, the enteropathy preceded the PRP by more than thirty years. The authors came to the conclusion of a coincidental finding, even if hyperkeratosis became minimal after vitamin A therapy followed by a GFD.ErythrodermaPruritic eczema of a seborrheic or psoriasiform pattern has been reported as a cutaneous manifestation of CD. A minority of adults can be affected, but also children, where the condition can be of particular severity [91].Gluten intolerance and miscellaneousNecrolytic migratory erythemaNecrolytic migratory erythema (NME) is a characteristic skin disease mainly associated with glucagonoma. The skin eruption may occur during the course of other conditions, some of them being characterized by intestinal dysfunction. Deficiencies in zinc, amino acids or essential fatty acids have been taken into consideration. Three cases of NME have been described in patients with gluten sensitive enteropathy [92, 93] in which symptoms completely resolved with adherence to a GFD. In one case NME was associated with an excess production of enteroglucagon by the intestinal mucosa, which could be due to exposure of the distal gut to unabsorbed nutrients because of the associated CD [92].Annular erythemaAnnular erythema might also be considered as a clinical manifestation of DH or from a more general point of view, as the expression of GI. The successful GFD in a 5-year old girl with annular erythema and cutaneous histopathological aspects of DH [94] shows that annular erythema is a plurifactorial condition and that the role of GI must be evoked in some cases.MalignanciesPatients with CD have a higher risk than the general population for the development of malignancies and particularly lymphomas [95-99]. Lymphomas usually involve gut and lymph nodes, but can also have skin locations, as it was presumed in a case of primary T cell CD30-positive anaplastic large-cell lymphoma [100]. A Swedish study followed up 12,000 patients with CD or DH and evaluated cancer incidence [101]. Adults (but not children or adolescents) with CD had an elevated overall risk of cancer that declined with time. Elevated risks were found for malignant lymphoma, small-intestinal, oro-pharyngeal, esophageal, large intestinal, hepatobiliary and pancreatic carcinomas.Pseudopurpuric palmar lesionsPseudopurpuric palmar involvement could be now considered as an unusual clinical manifestation of DH [102], and has been reported associated with IgA linear dermatosis [103]. In the reported cases, the palmar lesions looked like purpuric angiokeratomas, their intermittence allowing to distinguish them from this condition. These lesions respond partially to a GFD or sulfone treatment.Partial lipodystrophyIn a patient with serum IgA and C3 complement deficiencies and CD, partial lipodystrophy was described [104]. Partial lipodystrophy is characterized by a noticeable global reduction of adipose tissue above the waist and a normal or hypertrophic appearance of the buttocks and lower limbs. This condition is coupled with C3 hypocomplementemia due to accelerated C3 complement factor degradation because of the presence of a serum complex, the so-called C3 nephritic factor, stabilizing the C3 convertase enzyme. Partial lipodystrophy has been reported in combination with different autoimmune conditions. The underlying immunological abnormalities in the course of this condition could induce the development of autoimmunity.Generalized acquired cutis laxaA possible immunological abnormality has been postulated by some authors to explain the destruction of elastic tissue in the course of acquired cutis laxa (ACL). Glutenin which is one of the main components of gluten, presents a secondary structure and several amino acid sequences similar to elastin [105]. The association of progressive ACL and patterns of CD in a patient [106] and the moderate improvement of the papular eruption with dapsone and GFD support the hypothesis of a link between GI and the condition. The possible role of some antibiotics, especially penicillin, is of a particular interest in patients with gluten sensitive enteropathy who developed generalized ACL [107].Cutaneous amyloidosisLichen amyloidosis is one of the clinical patterns of primary cutaneous amyloidosis. It may succeed to an itching condition such as chronic eczema, the deposition of amyloid being considered as secondary to lichenification. Thus, since eczema may be a cutaneous manifestation of gluten sensitive enteropathy, the report of a case where lichen amyloidosis followed chronic eczema associated with CD is not surprising [108]. Amyloid deposits were not responding to a GFD whereas eczema significantly improved.Oral mucosaApart from the intestine and the skin, coeliac sprue can also involve oral mucosa. Recurrent oral ulceration is the most frequent presenting symptom. Mouth ulcers are one of the most common complaints of the population. Recurrent oral aphthae may be the unique manifestation of GI, and may lead to the diagnosis of CD [109]. About 4% of patients with recurrent aphthae are supposed to have CD [110]. In such cases aphthae can result from iron, folate or vitamin B12 deficiency induced by CD. The oral cavity of patients suspected of having CD needs to be examined, since no less than 66% of the patients have oral mucosal lesions or dental enamel defects [111].Even if CD has been excluded in some patients with recurrent aphthous stomatitis, a GFD shows a beneficial therapeutic effect in 25% of them [112]. Furthermore, the association with oral mucosal lichen planus should be considered, since one patient suffered from both conditions in a series of 39 patients with oral mucosal lichen planus. Moreover, about one third of these patients had IgA anti-gliadin autoantibodies [113]. In 1990, Jaremko et al. [114] identified a new disease involving the oral mucosa which was named chronic ulcerative stomatitis. Unusual anti-nuclear antibodies (stratified epithelium-specific antibodies) SES-ANA have been described in the course of chronic ulcerative stomatitis. Chorzelski et al. [115] have published a cohort which comprised 15 cases of chronic ulcerative stomatitis with typical clinical features and immunological findings. Among these cases, one woman had high titers of IgA EmA detected in the serum, and a duodenal biopsy disclosed flat mucosa and inflammatory infiltrates in the lamina propria. The diagnosis of latent coeliac disease was confirmed. A gluten free diet was able to clear the mucosal and skin lesions, with occasional slight cutaneous relapses. The relationship between chronic ulcerative diseases and CD is not known, however both cutaneous and mucosal lesions responded to the gluten free diet. IchthyosisMenni et al. [116] described a patient with coeliac disease revealed by the sudden appearance of a keratinization disorder. The woman presented with lamellar scaling lasting for some months. Anti-endomysial antibodies were positive, and a duodenal biopsy showed total atrophy of the villi. A gluten-free diet corrected the biological markers of malabsorption. Six months later, milder lamellar scaling was still detectable and serum values were normal except for sideraemia.Acquired ichthyosis with bowel disorders such as Crohn’s disease and coeliac disease has also been already reported [117]. NailsTransverse leukonychia in severe hypocalcemia caused by hypoparathyroidism and coeliac disease has been reported [118]. Transverse leukonychia disappeared after calcium supplementation. Persistant lower calcium levels were probably due to the concomitant presence of coeliac disease.ConclusionGI or CD should be kept in mind when investigating certain cutaneous conditions, and especially diseases with immunological or allergic pathophysiological mechanisms [119]. Dermatologists should be familiar with the appraisal of gluten sensitive enteropathy, and should be able to search for an underlying GI. GI or CD is a frequent disorder: coincidental observations can be observed with other common diseases. Moreover, high titers of anti-gliadine antibodies are not synonymous with GI. To establish whether some cutaneous conditions, especially immunologically mediated skin diseases, could be related to gluten-sensitive enteropathy, a serological screening by means of antigliadin, antiendomysial and transglutaminase antibodies, which are considered to be the most reliable serological markers of CD [120, 121] in large series of consecutive patients with these conditions should be performed. HLA typing can be a good tool to reveal links between skin diseases and GI. The diagnosis is confirmed by intestinal biopsy. Such an analysis could lead to establish the prevalence of CD among these patients.References1 Corazza GR, Gtasbarrini G. Coeliac disease in adults. Clin Gastroenterol 1995; 9: 329-50.2 Maki M, Mustalahti K, Kokkonen J, et al. Prevalence of celiac disease among children in Finland. N Engl J Med 2003; 348: 2517-24. 3 Marks J, Shuster S, Watson AJ. Small-bowell changes in dermatitis herpetiformis. Lancet 1966; 2: 1280-4. 4 Collin P, Reunala T. Recognition and management of the cutaneous manifestations of celiac disease: a guide for dermatologists. Am J Clin Dermatol 2003; 4: 13-20. 5 Gregory B, Ho VC. Cutaneous manifestations of gastrointestinal disorders. Part II. J Am Acad Dermatol 1992; 26: 371-83. 6 Fry L. Dermatitis herpetiformis: problems, progress and prospects. Eur J Dermatol 2002; 12: 523-31. 7 Reunala T, Collin P. Diseases associated with dermatitis herpetiformis. Br J Dermatol 1997; 136: 315-8. 8 Humbert P, Dupond JL, Vuitton D, Agache P. Dermatological autoimmune diseases and the multiple autoimmune syndromes. Acta Derm Venereol (suppl) 1989(148): 1-8. 9 Lewis HM, Renaula TL, Garioch JJ, et al. Protective effect of glutenfree diet against development of lymphoma in dermatitis herpetiformis. Br J Dermatol 1996; 133: 363-7. 10 Spurkland A, Ingvarsson O, Falk ES, et al. Dermatitis herpetiformis and coaliac disease and both primarily associated with HLA-DQ [alpha 1*0501, beta 1*02] or the HLA-DQ [alpha 1*03, beta 1*0302] heterodimers. Tissue Antigens 1997; 49: 29-34. 11 Balas A, Vicario L, Zambrano A, et al. Absolute linkage of coeliac disease and dermatitis herpetiformis to HLA-DQ. Tissue Antigens 1997; 50: 52-6. 12 Hervonen K, Hakanen M, Kaukinen K, et al. First-degree relatives are frequently affected in coeliac disease and dermatitis herpetiformis. Scand J Gastroenterol 2002; 37: 51-5. 13 Jablonska S, Chorzelski T. Dermatose à IgA linéaire. Ann Dermatol Venereol 1979; 106: 651-5. 14 Kapur A, Isaacs PET, Kelsey PR. Linear IgA dermatosis, celiac disease, and extraintestinal B cell lymphoma. Gut 1995; 37: 731-3. 15 Egan CA, Smith EP, Taylor TB, et al. Linear IgA bullous dermatosis responsive to a gluten-free diet. Am J Gastroenterol 2001; 96: 1927-9. 16 Brandrup F, Schmidt H. Benign chronic bullous dermatosis of childhood associated with coeliac disease. Clin Exp Dermatol 1981; 6: 569-70. 17 Kieffer M, Barnetson R. StC. What is the role of gliadin in bullous pemphigoid? Lancet 1981; 2: 806. 18 Leonard JN, Fry L, Wright P, et al. Gliadin in bullous pemphigoid. Lancet 1981; 2: 1111-2. 19 Corazza GR, Andreani ML, Venturo N, et al. Coeliac disease and alopecia areata: report of a new association. Gastroenterology 1995; 109: 1333-7. 20 Volta U, Bardazzi F, Zauli D, et al. Serological screening for coeliac disease in vitiligo and alopecia areata. Br J Dermatol 1997; 136: 801-2. 21 Catassi C, Ratsch IM, Fabiani E, et al. Coeliac disease in the year 2000: exploring the iceberg. Lancet 1994; 343: 200-3. 22 Barbato M, Viola F, Grillo R, et al. Alopecia and coeliac disease: report of two patients showing response to GFD. Clin Exp Dermatol 1998; 23: 236-7. 23 Bondavalli P, Quadri G, Parodi A, Rebora A. Failure of gluten-free diet in coeliac disease associated alopecia areata. Acta Derm Venereol (Stockh) 1998; 78: 319. 24 Bardella MT, Marino R, Barbareschi M, et al. Alopecia areata and coeliac disease: no effect of a gluten-free diet on hair growth. Dermatology 2000; 200: 108-10. 25 Naveh Y, Rosenthal E, Ben-Arieh Y, Etzioni A. Coeliac disease-associated alopecia in childhood. J Pediatr 1999; 134: 362-4. 26 Storm W. Celiac disease and alopecia areata in a child with Down’s syndrome. J Intellect Disabil Res 2000; 44: 621-3. 27 Catassi C, Fabiani E, Ratsch IM, et al. The coeliac iceberg in italy: a multicentre antigliadin antibodies screening for coeliac disease in school-age subjects. Acta Paediatr 1996; 85(suppl. 412): 29-35. 28 Wood ML, Foulds IS, French MA. Protein losing enteropathy due to systemic lupus erythematosus. Gut 1984; 25: 1013-5. 29 Madder R, Adawi M, Schonfeld S. Malabsorption in systemic lupus erythematosus. Clin Exp Rheumatol 1997; 15: 659-61. 30 Roberts DL. Sub-acute cutaneous lupus erythematosus and gluten sensitive enteropathy. Br J Dermatol 1998; 118: 731-2. 31 Rensch MJ, Szyjkowski R, Shaffer RT, et al. The prevalence of celiac disease antibodies in patients with systemic lupus erythematosus. Am J Gastroenterol 2001; 96: 1113-5. 32 Varkel Y, Braester A, Suprun H, et al. Silmutaneous occurrence of systemic lupus erythematosus and coeliac disease-like features. Postgrad Med J 1989; 65: 766. 33 Komatireddy GR, Marshall JB, Aquel R, et al. Association of systemic lupus erythematosus, and gluten enteropathy. South Med J 1995; 88: 673-6. 34 Rustgi AK, Peppercorn MA. Gluten-sensitive enteropathy, and systemic lupus eryrthematosus. Arch Intern Med 1988; 148: 1583-4. 35 Mukamel M, Rosenbach Y, Zagavi I, et al. Celiac disease and systemic lupus erythematosus. Isr J Med Sci 1994; 30: 656-8. 36 Sheehan NJ, Stanton-King K. Polyautoimmunity in a young woman. Br J Rheumatol 1993; 32: 254-6. 37 Marguerie C, Kaye S, Vyse T, et al. Malabsorption caused by celiac disease in patients who have scleroderma. Br J Rheumatol 1995; 34: 858-61. 38 Hadjivassiliou M, Chattopadhyay AK, Davies-Jones GA, et al. Neuromuscular disorder as a presenting feature of celiac disease. J Neurol Neurosurg Psychiatry 1997; 63: 770-5. 39 Vilppula AH, Aine RA. Polymyositis associated with several immunological disorders. Clin Rheumatol 1984; 3: 533-9. 40 Henriksson KG, Hallert C, Norrby K, Walan A. Polymyositis and adult celiac disease. Acta Neurol Scand 1982; 65: 301-19. 41 Evron E, Abarbanel JM, Branski D, Sthoeger ZM. Polymyositis, arthritis, and proteinuria in a patient with adult celiac disease. J Rheumatol 1996; 23: 782-3. 42 Henriksson KG, Hallert C, Walan A. Gluten-sensitive polymyositis and enteropathy. Lancet 1976; 2: 317; (letter). 43 Marie I, Lecomte F, Hachulla E, et al. An uncommon association: celiac disease and dermatomyositis in adults. Clin Exp Rheumatol 2001; 19: 201-3. 44 Buderus S, Wagner N, Lentze MJ. Concurrence of celiac disease and juvenile dermatomyositis: result of a specific immunogenetic susceptibility? J Pediatr Gastroenterol Nutr 1997; 25: 101-3. 45 IaIannone F, Lapadula G. Dermatomyositis and celiac disease association: a further case. Clin Exp Rheumatol 2001; 19: 757-8. 46 Falcini F, Porfirio B, Lionetti P. Juvenile dermatomyositis and celiac disease. J Rheumatol 1999; 26: 1419-20; (letter). 47 Essoussi AS, Jomaa B, El Fehaiel A. Association of celiac disease with sclero-atrophic lichen in a child with the HLA-B8 group. Tunis Med 1981; 59: 506-7. 48 Doe WF, Evans D, Hobbs J, Booth CC. Coeliac disease, vasculitis and cryoglobulinemia. Gut 1972; 13: 112-23. 49 Holdstock DJ, Oleesky S. Vasculitis in coeliac disease. BMJ 1970; 4: 369. 50 Katz A, Dyck RF, Bear RA. Coeliac disease associated with immune complex glomerulonephritis. Clin Nephrol 1979; 11: 39-44. 51 Meyers S, Dikman S, Spiera H, et al. Cutaneous vasculitis complicating coeliac disease. Gut 1981; 22: 61-4. 52 Menzies IS, Laker MF, Pounder R, et al. Abnormal intestinal permeability to sugars in villous atrophy. Lancet 1979; 2: 1107-9. 53 Rodriguez-Serna M, Fortea JM, Perez A, et al. Erythema elevatum diutinum associated with coeliac disease: response to a gluten-free diet. Pediatr Dermatol 1993; 10: 125-8. 54 Tasanen K, Raudasoja R, Kallioinen M, Ranki A. Erythema elevatum diutinum in association with coeliac disease. Br J Dermatol 1997; 136: 624-7. 55 Green FHY, Carty JE. Celiac disease and autoimmunity. Lancet 1976; 1: 964; (letter). 56 Scala E, Giani M, Pirrotta L, et al. Urticaria and adult celiac disease. Allergy 1999; 54: 1008-9. 57 Gallo C, Vighi G, Schroeder J, et al. Chronic urticaria atopic dermatitis and celiac disease. Am J Gastroenterol 1992; 87: 1684. 58 Farkas H, Visy B, Fekete B, et al. Association of celiac disease and hereditary angioneurotic edema. Am J Gastroenterol 2002; 97: 2682-3. 59 Räsänen L, Lehto M, Turjanmaa K, et al. Allergy to ingested cereals in atopic children. Allergy 1994; 49: 871-6. 60 Zauli D, Grassi A, Granito A, et al. Prevalence of silent coeliac disease in atopics. Dig Liver Dis 2000; 32: 780-1. 61 Mazzetti di Pietralata M, Giorgetti GM, Gregori M, et al. Subclinical coeliac disease. Ital J Gastroenterol 1992; 24: 352-4. 62 Varjonen E, Vainio E, Kalimo K. Antigliadin IgE-indicator of wheat allergy in atopic dermatitis. Allergy 2000; 55: 386-91. 63 Varjonen E, Kalimo K, Savolainen J, Vaino E. IgA and IgG binding components of wheat, rye, barley and oasts recognized by immunoblotting analysis with sera from adult atopic dermatitis patients. Int Arch Allergy Immunol 1996; 111: 55-63. 64 Accioly-Filho JW, Nogueira A, Ramos-e-Silva M. Prurigo nodularis de Hyde: an update. J Eur Acad Dermatol Venereol 2000; 14: 75-82. 65 Wells GC. Skin disorders in relation to malabsorption. BMJ 1962; 4: 937. 66 McKenzie AW, Stubbing DG, Elvy BL. Prurigo nodularis and gluten enteropathy. Br J Dermatol 1976; 95: 89-92. 67 Howell R. Exsudative nummular prurigo with idiopathic malabsorption syndrome. Br J Dermatol 1967; 79: 357-8. 68 Goodwin PG. Nodular prurigo associated with gluten enteropathy. Proc R Soc Med 1977; 70: 140-1. 69 Suarez C, Pereda JM, Martin Moreno L, et al. Prurigo nodularis associated with malabsorption. Dermatologica 1984; 169: 211-4. 70 Francesco Stefanini G, Resta F, Marsigli L, et al. Prurigo nodularis (Hyde’s prurigo) disclosing celiac disease. Hepatogastroenterology 1999; 46: 2281-4. 71 Delfino M, Nino M, Delfino G, et al. Dermatitis herpetiformis and gluten-sensitive enteropathy in a patient with nodular prurigo. J Eur Acad Dermatol Venereol 2002; 16: 88-9. 72 Cabrera Chaves T, Gomollon Garcia F, Simon Marco MA, et al. Hemorrhagic diathesis as initial clinical manifestation of celiac disease. Rev Clin Esp 1996; 196: 28-31. 73 Berger ML, Siegel DM, Lee EL. Scurvy as an initial manifestation of Whipple’s disease. Ann Intern Med 1984; 100: 58-9. 74 Linaker BD. Scurvy and vitamin C deficiency in Crohn’s disease. Postgrad Med J 1979; 55: 26-9. 75 Zultak M, Mollet E, Rotty JM, et al. Scorbut révélant une maladie coeliaque. Presse Med 1986; 15: 1730. 76 Shuster S, Marks J. Psoriasic enteropathy. Arch Dermatol 1971; 103: 676-8. 77 Bazex A, Gaillet L, Bazex J. Régime sans gluten et psoriasis. Ann Dermatol Syphiligr (Paris) 1976; 103: 648-50. 78 Michaëlsson G, Gerdén B. How common is gluten intolerance among patients with psoriasis? Acta Derm Venereol (Stockh) 1991; 71: 90. 79 Michaëlsson G, Gerden B, Ottosson M, et al. Patients with psoriasis often have increased serum levels of IgA antibodies to gliadin. Br J Dermatol 1993; 129: 667-73. 80 Michaëlsson G, Kraaz W, Gerden B, et al. Increased lymphocyte infiltration in duodenal mucosa from patients with psoriasis and serum IgA antibodies to gliadin. Br J Dermatol 1995; 133: 896-904. 81 Michaëlsson G, Kraaz W, Gerdén B, et al. Patients with psoriasis have elevated levels of serum eosinophil cationic protein and increased numbers of EG2 positive eosinophils in the duodenal stroma. Br J Dermatol 1996; 135: 371-8. 82 Michaëlsson G, Kraaz W, Hagforsen E, et al. Psoriasis patients have highly increased numbers of tryptase-positive mast cells in the duodenal stroma. Br J Dermatol 1997; 136: 866-70. 83 Eriksson MO, Hagforsen E, Lundin IP, Michaëlsson G. Palmoplantar pustulosis: a clinical and immunohistological study. Br J Dermatol 1998; 138: 390-8. 84 Michaelsson G, Gerden B, Hagforsen E, et al. Psoriasis patients with antibodies to gliadin can be improved by a gluten-free diet. Br J Dermatol 2000; 142: 44-51. 85 Humbert P, Bidet A, Treffel P, et al. Intestinal permeability in patients with psoriasis. J Dermatol Sci 1991; 2: 324-6. 86 Chalmers RJG, Kirby B. Gluten and psoriasis. Br J Dermatol 2000; 142: 5-7. 87 Lock RJ, Pitcher MC, Unsworth DJ. IgA anti-tissue transglutaminase as a diagnostic marker of gluten sensitive enteropathy. J Clin Pathol 1999; 52: 274-7. 88 Cottafava F, Cosso D. Psoriatic arthritis and celiac disease in childhood. A case report. Pediatr Med Chir 1991; 13: 431-3. 89 Lindqvist U, Rudsander A, Bostrom A, et al. IgA antibodies to gliadin and celiac disease in psoriatic arthritis. Rheumatology 2002; 41: 31-7. 90 Randle HW, Winkelmann RK. Pityriasis rubra pilaris and coeliac sprue with malabsorption. Cutis 1980; 25: 626-7. 91 Woolfson H, McQueen A, Stephen M. Erythroderma in a child with coeliac disease. Br J Dermatol 1974; 90: 691-5. 92 Kelly CP, Johnston CF, Nolan N, et al. Necrolytic migratory erythema with elevated plasma enteroglucagon in celiac disease. Gastroenterology 1989; 96: 1350-3. 93 Thorisdottir K, Camisa C, Tomecki KJ, Bergfeld WF. Necrolytic migratory erythema: a report of three cases. J Am Acad Dermatol 1994; 30: 324-9. 94 Maleville J, Mollard S, Tamisier JM, et al. Dermatite herpétiforme chez une fillette de 6 ans. Aspect d’érythème annulaire centrifuge type Colcott-Fox contrôlé par le régime sans gluten. Ann Dermatol Venereol 1979; 106: 707-9. 95 Cooper BT, Holmes GKT, Ferguson R, Cooke WT. Coeliac disease and malignancy. Medicine 1980; 59: 249-61. 96 Nielsen OH, Jacobsen O, Pedersen ER, et al. Non-tropical sprue: malignant diseases and mortality rate. Scand J Gastroenterol 1985; 20: 13-8. 97 Selby WS, Gallagher ND. Malignancy in a 19 year experience of adult celiac disease. Dig Dis Sci 1979; 24: 684-8. 98 Swinson CM, Coles EC, Slavin G, Booth CC. Coeliac disease and malignancy. Lancet 1983; 1: 111-5. 99 Wright DH, Jones DB, Clark H, et al. Is adult-onset celiac disease due to a low-grade lymphoma of intra-epithelial T lymphocytes? Lancet 1991; 2: 1373-4. 100 Mantovani G, Esu S, Astara G, et al. Primary T cell CD30-positive anaplastic large-cell lymphoma associated with adult-onset celiac disease and presenting with skin lesions. Acta Haematol 1995; 94: 48-51. 101 Askling J, Linet M, Gridley G, et al. Cancer incidence in a population-based cohort of individuals hospitalized with celiac disease or dermatitis herpatiformis. Gastroenterology 2002; 123: 1428-35. 102 Moulin G, Barrut D, Franc MP, et al. Localisations palmaires pseudo-purpuriques de la dermatite herpétiforme. Ann Dermatol Venereol 1983; 110: 121-6. 103 Safai B, Rappaport I, Matsuoka L, et al. Childhood dermatitis herpetiformis: review of the new aspects and report of a case. J Am Acad Dermatol 1981; 4: 435-41. 104 O’Mahony D, O’Mahony S, Whelton MJ, McKiernan J. Partial lipodystrophy in celiac disease. Gut 1990; 31: 717-8. 105 McFadden JM, Leonard JN, Powles A, et al. Homology between glutenin and human connective tissue proteins. Br J Dermatol 1990; 123(suppl.37): 61. 106 Garcia-Patos V, Pujol RM, Barnadas MA, et al. Generalized acquired cutis laxa associated with coeliac disease: evidence of immunoglobulin A deposits on the dermal elastic fibres. Br J Dermatol 1996; 135: 130-4. 107 Kerl H, Burg G, Hashimoto K. Fatal penicillin-induced genralized postinflammatory elastolysis (cutis laxa). Am J Dermatopathol 1983; 5: 267-76. 108 Presbury DGC, Griffiths WAD. Coeliac disease with primary cutaneous amyloidosis. Br J Dermatol 1975; 92: 109-12. 109 Biel K, Böhm M, Luger TA, Bonsmann G. Long-standing oral aphthae: a clue to the diagnosis of coeliac disease. Dermatology 2000; 200: 334-40. 110 Ferguson MM, Wray D, Carmichael HA, et al. Coeliac disease associated with recurrent aphthae. Gut 1980; 21: 223-6. 111 Lahteenoja H, Toivanen A, Viander M, et al. Oral mucosa changes in coeliac patients on a gluten-free diet. Eur J Oral Sci 1998; 106: 899-906. 112 Wray D. Gluten-sensitive recurrent aphthous stomatitis. Dig Dis Sci 1981; 26: 737-40. 113 Jokinen J, Peters U, Mäki M, et al. Celiac sprue in patients with chronic oral mucosa symptoms. J Clin Gastroenterol 1998; 26: 23-6. 114 Jaremko WM, Beutner EH, Kumar V, et al. Chronic ulcerative stomatitis associated with a specific immunologic marker. J Am Acad Dermatol 1990; 22: 215-20. 115 Chorzelski TP, Olszewska M, Jarzabek-Chorzelska M. Is chronic ulcerative stomatitis an entity? Clinical and immunological findings in 18 cases. Eur J Dermatol 1998; 8: 261-5. 116 Menni S, Boccardi D, Brusasco A. Ichthyosis revealing coeliac disease. Eur J Dermatol 2000; 10: 398-9. 117 Marks R, Dykes PJ. Growth characteristics of the epidermis in the ichthyotic disorders. In: Marks R, Dykes PJ, eds. The ichthyoses. Proceedings of the 2nd Annual clinically orientated symposium of the European Society for Dermatological Research. London: MTP Press, 1978: 37-42. 118 Foti C, Cassano N, Palmieri VO, et al. Transverse leukonychia in severe hypocalcemia. Eur J Dermatol 2004; 14: 67-8. 119 Scott BB, Losowsky MS. Coeliac disease: a cause of various associated diseases? Lancet 1975; 2: 956-7. 120 Lerner A, Kumar V, Iancu TC. Immunological diagnosis of childhood coeliac disease: comparison between antigliadin, antireticulin and anti-endomysial antibodies. Clin Exp Immunol 1994; 95: 78-82. 121 Volta U, Molinaro N, Fusconi M, et al. IgA anti-endomysial antibody test: a step forward in coeliac disease screening. Dig Dis Sci 1991; 36: 752-6. |
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