Keg-letters 1419.1420

physical exercise. The exact pathogenesis of the especially if no signs of (recent) infection are present. It association of UV with malignancy is unclear. It is is considered good clinical practice nowadays to start thought that tumour-associated immune complexes early treatment with anti-rheumatic drugs, including may give rise to complement fixation in the vessel wall corticosteroids or tumour necrosis factor- (TNF-)- and subsequent development of an inflammatory blocking agents. To prevent a life-threatening outcome, process [6]. In exercise-induced UV it has been shown however, some rare infections have to be excluded. We that mast cells are the first to be involved, with the describe a patient who presented with recent-onset activation and subsequent release of proinflammatory mediators, which precede the influx of eosinophils with their release of granule proteins and the influx of A 35-yr-old male was referred to our hospital neutrophils with their release of proteolytic enzymes because of progressive arthralgia over the last 4 [8]. We hypothesize that deposits of immune complexes months despite the use of non-steroidal anti-inflamma- and complement fixation in the vessel wall sometimes tory drugs. His medical history was unremarkable. The need an additional event in order to elicit the initial complaints started after returning from a journey to influx of neutrophils, which are the final effector cells Surinam, South America. He denied having any responsible for the vascular damage.
complaints during or after his travel. At admission, The patient gave informed consent to the investiga- polyarthritis of the shoulders, wrists, hand joints, tions that led to the diagnosis reported here, and knees, ankles and feet was observed. Further physical written permission was given for this case to be Laboratory investigations revealed an erythrocyte sedimentation rate of 80 mm/h, C-reactive protein The authors have declared no conflicts of interest.
level of 121 mg/l and a leucocyte count of 5.8 Â 109/lwith 20% eosinophilia. Routine urine examination F. DI STEFANO, S. SIRIRUTTANAPRUK, M. DI GIOACCHINO was normal. Rheumatoid factor, antinuclear anti-bodies and HLA-B27 were absent. Serological tests for human immunodeficiency virus, human parvovirus University ‘G. D’Annunzio’, Via dei Vestini, 66100 B19 and Borrelia burgdorferi were negative. X-rays of the chest, hands, feet and sacroiliac joints were normal. Only after repeated examination was the Correspondence to: F. Di Stefano, Internal Medicine, Presidio Ospedaliero ‘G. Bernabeo’, C. da S. Liberata, concentrated fresh stool. No micro-organisms or 66026 Ortona (Chieti), Italy. E-mail: distefa.fabio@ larvae could be found in synovial fluid aspirated The patient was treated with albendazole 400 mg once daily for 7 days. Because of persistent eosino- 2. Strickland D, Ware R. Urticarial vasculitis: an autoimmune disorder philia, a second course was given for another 10 days.
following therapy for Hodgkin’s disease. Med Pediatr Oncol Repeated direct stool examination remained free of Strongyloides larvae. In the following months the 3. Highet A. Urticarial vasculitis and IgA myeloma. Br J Dermatol polyarthritis slowly disappeared and laboratory values normalized. More than 1 yr later the patient is still free 4. Lewis JE. Urticarial vasculitis occurring in association with visceral malignancy. Acta Dermatol Venereol 1990;70:345–7.
5. Sprossmann A, Muller RP. Urticarial vasculitis syndrome in metastatic malignant testicular teratoma. Hautarzt 1994;45:871–4.
6. Garcia-Porrua C, Gonzalez-Gay MA. Cutaneous vasculitis as a paraneoplastic syndrome in adults. Arthritis Rheum 1998;41:1133–5.
7. Wilson D, McCluggage WG, Wright GD. Urticarial vasculitis: a paraneoplastic presentation of B-cell non Hodgkin’s lymphoma.
Rheumatology 2002;41:476–7.
8. Kano Y, Orihara M, Shiohara T. Cellular and molecular dynamics in Rheumatology 2003;42:1419–1420doi:10.1093/rheumatology/keg348 Early-onset polyarthritis as presenting feature ofintestinal infection with Strongyloides stercoralis SIR, In a patient with symmetrical polyarthritis the FIG. 1. Rhabditiform larvae of Strongyloides stercoralis in diagnosis of rheumatoid arthritis (RA) is advocated, Ridley concentrate of faeces (100Â).
Rheumatology Vol. 42 No. 11 ß British Society for Rheumatology 2003; all rights reserved Strongyloides stercoralis is a nematode with a Secondly, there is a risk of lethal disseminated infection in patients harbouring Strongyloides in circumstances (sub)tropical regions. It is estimated that, worldwide, associated with suppression of the host’s immune system.
over 100 million people are infected with this parasite If immunosuppressive treatment is considered, a high [1]. The most common type of reproduction is the suspicion of Strongyloides infection and repeated host–soil–host cycle. Fully grown female worms lay examination of faeces is necessary in patients who their eggs in the mucus of the intestinal tract, where the originate from or have travelled in (sub)tropic areas or in eggs hatch and liberate rhabditiform larvae. These larvae leave the body with the faeces and develop intoinfective filariform larvae that can penetrate the skin of The authors have declared no conflicts of interest.
the host and enter the bloodstream. The larvae reach the digestive tract after migration through the lungs.
When infection is limited to the digestive tract, treatment with an anthelmintic agent usually clears 1Rheumatology and 2Internal Medicine, VU Medical Centre, Amsterdam and 3Rheumatology, Jan van Breemen The so-called autoinfective cycle is an alternative within the intestinal tract into infective filariform Correspondence to: A. E. Voskuyl, Department of larvae, which may penetrate immediately into the gut Rheumatology, 4A-42, VU University Medical Centre, wall or peri-anal skin and enter the bloodstream. In normal circumstances this autoinfection does not seem to be a problem. The infection can persist for years oreven decades with hardly any symptoms. This balance 1. Mahmoud AAF. Strongyloides. Clin Infect Dis 1996;23:949–53.
can be disturbed when the host becomes immuno- 2. Brocq O, Breuil V, Agopian V et al. Reactive arthritis induced by compromised by either disease (haematological malig- Strongyloides stercoralis. Rev Rhum Engl Ed 1996;63:217–9.
nancies, malnutrition or AIDS) or treatment with 3. Bocanegra TS, Espinosa LR, Bridgeford LR, Vasey FB, Germain corticosteroids or cytostatic agents. An overwhelming BF. Reactive arthritis due to parasitic infection. Ann Intern Med1981;94:207–9.
systemic parasitic load can result because of the 4. Doury P. Parasitic rheumatism. Arthritis Rheum 1981;24:638–9.
5. Doury P, Pattin S, Durosoir JC, Voinesson A, Dienot B, Duret JC.
circumstances [1, 2]. A serious medical condition Anguillulose et manifestations articulaires. A propos d’une observa- tion. Ann Me´d Interne 1974;125:743–7.
Strongyloidiasis may develop rapidly, and is character- 6. Amor B, Benhamou CL, Dougados M, Grant A. Arthrites a` e´osinophiles et revues ge´ne´rale de la signification de l’e´osinphilie ized by pneumonitis, respiratory failure, cerebral articulaire. Rev Rhum Mal Osteoartic 1983;50:659–64.
infiltration and a high mortality rate.
7. Akoglu T, Turner I, Erken E, Gurcay A, Ozer FL, Ozcan K.
Arthritis is a rare feature of a parasitic infection Parasitic arthritis induced by Strongyloides stercoralis. Ann Rheum including Strongyloides [3, 4]. We found nine earlier rheumatism presenting as oligoarthritis. A case report. Trop Geogr Strongyloides infection [2, 3, 5–10]. In six of these nine 9. Forzy G, Dhondt JL, Leloire O, Shayeb J, Vincent G. Reactive patients, aspiration of synovial fluid was performed, arthritis and Strongyloides. J Am Med Assoc 1988;259:2546–7.
and no larvae were seen. All nine patients recovered 10. Patey O, Bouhali R, Breuil J, Chapuis L, Courillon-Mallet A, Lafaix C. Arthritis associated with Strongyloides stercoralis. Scand J Infect fully after anthelmintic treatment only, as did our patient. The mechanism of the development of arthritisis unknown. Although Strongyloides larvae have oncebeen observed in a synovial biopsy specimen, suggestingan infectious type of arthritis [7], most authors consider this to be a reactive arthritis [2–10].
The distribution of the symmetrical polyarthritis in Musculoskeletal examination for medical students this patient was highly suggestive of RA. In view of theearly diagnosis and aggressive treatment of RA today,this patient could have been exposed to immunosup- We would like to compliment Drs Kay and Walker [1] pressive treatment with high-dose corticosteroids or a for their excellent summary of current musculoskeletal TNF--blocking agent, potentially resulting in disse- teaching practice and future approaches for improve- minated Strongyloides. Repeated examination of stool ment and research. We agree that the lack of specimens resulted in the diagnosis of reactive arthritis unanimity over the curriculum confuses not only associated with Strongyloides, and treatment with medical students but also their teachers, who are not anthelmintic drugs was therefore the appropriate entirely sure of what the students need to know. While therapy rather then immunosuppressive therapy.
there is some degree of agreement among rheumatol- Two lessons can be learned from this case. First, ogists across the country with regard to a core infection with S. stercoralis can present as (poly)arthritis.
curriculum, this has not yet been formally defined Rheumatology Vol. 42 No. 11 ß British Society for Rheumatology 2003; all rights reserved

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