Rheumatology 2001; 40: 110
© 2001 British Society for Rheumatology
Letters to the Editor |
Does pantoprazole alleviate mouth dryness in patients with Sjögren's syndrome?
Departments of Internal Medicine I and
1 III, University of Vienna, Austria
SIR, Sjögren's syndrome is an autoimmune condition resulting in impaired function of the salivary and lachrymal glands. The resulting dryness causes severe discomfort and interferes strongly with essential everyday activities such as eating [1]. At the moment, there is no standard treatment for patients with pronounced symptoms [2], apart from the use of saliva substitute, which is sometimes able to alleviate symptoms. A 56-yr-old woman with a 6-yr history of Sjögren's syndrome was referred to our institution because of a diagnosis of Helicobacter pylori (HP)-associated gastric lymphoma of the mucosa-associated lymphoid tissue type. After the bacteria had been eradicated with antibiotics, the patient was put on continuous oral treatment with the proton pump blocker pantoprazol (2x40 mg), but was taking no other medication apart from topical saliva substitute (Sialin Sigma; Sigma-Pharm, Vienna, Austria). Five weeks after the initiation of treatment, the patient reported a pronounced improvement in her mouth dryness, along with return of her ability to eat almost normally. Discontinuation of pantoprazole 7 weeks later, however, led to recurrence of symptoms within 4 days. In view of this, we have treated a total of four patients with primary Sjögren's syndrome (according to the criteria established by Vital et al. [3]) and pronounced mouth dryness with pantoprazole at a dose of 2x40 mg. All patients were informed about the nature of therapy and consented to oral intake of the proton pump inhibitor. All individuals were asked to record both subjective symptoms as well as their weekly intake of saliva substitute for 3 weeks before the start of therapy and for the whole period of pantoprazole application. To evaluate subjective symptoms, a visual analogue scale ranging from 0 (no dryness) to 10 (worst dryness ever experienced) was used. Three patients reported a durable, subjective improvement in their mouth dryness of at least 2 points on the visual analogue scale 2–6 weeks after the start of treatment, and one patient reported no change. In addition, the weekly intake of saliva substitute decreased by 35, 45 and 65%, respectively, compared with the baseline value. In one patient, however, the effect was not maintained after an improvement lasting 2 weeks; the remaining two patients continued pantoprazole intake because of successful alleviation of dryness for 9 and 11 weeks. We cannot offer a definite explanation for our findings at the moment. Whereas a psychological effect might have been involved in the patient who experienced only brief improvement, this is unlikely to have been the case in the patients with prolonged benefit; such an effect cannot be ruled out with certainty as this was an open pilot series. Because the exact mechanism of the potential beneficial effect of pantoprazole is unknown, we cannot exclude the possibility that the increased production of certain prostaglandins that is seen after the intake of pantoprazole, not only in the gastric mucosa [4] but also in the oral cavity, might contribute to the effect, as prostaglandin E1 may be an active agent in the treatment of Sjögren's syndrome [5]. In addition, the influence of proton pump blockers on acidity in the mouth has not been investigated, and the possibility that the upregulation (at least temporary) of muscarinic receptors contributed to our findings cannot be ruled out with certainty, as these receptors have also been implicated in the control of gastric acid production. Therefore, an indirect feedback mechanism triggered by blockade of acid output by proton pump inhibitors might be postulated as affecting the oral mucosa. Nevertheless, we think that our findings warrant further investigation in the absence of effective therapy, as mouth dryness in patients with Sjögren's syndrome profoundly influences their quality of life.
Notes
Correspondence to: M. Raderer, Department of Internal Medicine I, Division of Oncology, University of Vienna, Währinger Gürtel 18–20, A-1090 Vienna, Austria. 
References
- Fox RI, Tornwall J, Michelson P. Current issues in the diagnosis and treatment of Sjögren's syndrome. Curr Opin Rheumatol1999;11:364–71.[Medline]
- Thomas E, Hay EM, Hajeer A, Silman AJ. Sjögren's syndrome: a community based study of prevalence and impact. Br J Rheumatol1998;37:1069–76.
[Abstract/Free Full Text] - Vital C, Bombardieri S, Moutsopoulos HM, Balestrieri G, Bencivelli W, Bernstein RM et al. Preliminary criteria for classification of Sjögren's syndrome. Results of a prospective concerted action supported by the European Community. Arthritis Rheum1993;36:340–7.[ISI][Medline]
- Blandizzi C, Natale G, Gherardi G, Lazzeri G, Marveggio C, Colucci R et al. Gastroprotective effects of pantoprazole against experimental mucosal damage. Fundam Clin Pharmacol2000;14:89–99.[Medline]
- Horrobin DF, Campbell A. Sjögren's syndrome and the sicca syndrome: the role of prostaglandin E1 deficiency. Treatment with essential fatty acids and vitamin C. Med Hypotheses1980;6:225–32.[ISI][Medline]
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