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Coexisting gout, erythrodermic psoriasis and psoriatic arthritis


European Journal of Dermatology. Volume 19, Number 2, 184-5, March-April 2009, Correspondence

DOI : 10.1684/ejd.2008.0607


Author(s) : Mei Liu, Jiu-Hong Li, Bo Li, Chun-Di He, Ting Xiao, Hong-Duo Chen , Department of Dermatology, No. 1 Hospital of China Medical University, 155 North Nanjing Street, Shenyang 110001, China.

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ARTICLE

Auteur(s) : Mei Liu1, Jiu-Hong Li1, Bo Li, Chun-Di He, Ting Xiao, Hong-Duo Chen

Department of Dermatology, No. 1 Hospital of China Medical University, 155 North Nanjing Street, Shenyang 110001, China

We report the first case of the coexistence of gout, erythrodermic psoriasis and psoriatic arthritis (PsA).

A 59-year-old Chinese man presented with a 30-year history of psoriasis vulgaris, a 13-year history of polyarthralgia and a 5-year history of a painful mass on the right foot. He did not take any diuretics or other drugs interfering with uric acid metabolism. He had no addiction to alcohol. His family history was negative for gout or psoriasis. He took ibuprofen for arthralgia intermittently. Two months before admission, he began to take compound Chinese traditional medicine (including Eupolyphaga Seu Steleophaga, Olibanum, Myrrh, Pyritum, Flos Carthami, Rhizoma Drynariae, Radix et Rhizoma Rhei, Borax and Radix Angelicae Sinensis) for arthralgia for two weeks. Twenty days before admission, his psoriatic lesions exacerbated and fused into diffuse erythematous patches. Physical examination disclosed generalized scaly erythema, deformities of the distal interphalangeal (DIP) joints and proximal interphalangeal (PIP) joints of the ring and little fingers of his right hand (figure 1A), swelling of bilateral ankle joints and a 3.5 × 3.3 cm mass on his right foot with tenderness. Digital radiography showed characteristic findings of PsA and gout (figures 1B-D). Ultrasonography showed multiple calculi in his left kidney, right ureter and urinary bladder. Histopathology from the mass revealed tophaceous monosodium urate (MSU) crystals (figures 1E and F). Laboratory tests revealed erythrocyte sedimentation rate 55 mm/h (0-15 mm/h), C-reactive protein 2 mg/dL (0-0.8 mg/dL), serum uric acid 845 umol/L (143-416 umol/L), creatinine 361 umol/L (53-133 umol/L), urea nitrogen 12.92 mmol/L (3.2-7.1 mmol/L), and 24-hour urine protein 0.399 g (0.028-0.141 g). Rheumatoid factor and HLA-B27 were negative. Diagnoses of gout, erythrodermic psoriasis and PsA were made.

The patient was advised to follow a low purine diet. Intravenous compound ammonium glycyrrhetate 120 mg, oral sodium bicarbonate 3 g and loratadine 10 mg daily were administered. On Day 7 of admission, two ulcers were found in the mass of gout, draining with white, chalky substances (figure 1G). On Day 9, he suffered from septicemia, confirmed by leukocytosis and repeated blood cultures, showing growth of methicillin resistant staphylococcus aureus. Intravenous immunoglobulin 400 mg/kg and linezolid 1.2 g daily were administered for 5 and 10 days respectively. Then he was discharged.

The etiology for the coexistence of the conditions may be speculative. Hyperuricemia is a frequent finding in patients with psoriasis (especially PsA), some of whom may develop gout [1-3]. Several mechanisms may contribute to the development of hyperuricemia in psoriasis: increased purine production from the rapid epidermal cell turnover, genetic predisposition, hyperalimentation, and disorder of purine metabolism [1, 4, 5]. Goldman found MSU crystals in psoriatic plaques and speculated that MSU crystals may be responsible for the cell proliferation of psoriasis [5]. With the development of gout in the patient, the purine metabolism disorder aggravated, which could increase MSU crystals in the skin. We speculated that increased MSU crystals in the skin of the patient might play some roles in the pathogenesis of erythrodermic psoriasis. The development of erythrodermic psoriasis in this patient may also have been triggered by either ibuprofen or Chinese herbs, or both. Moreover, De Bari et al. proposed that pre-existing joint damage by PsA could predispose to crystal deposition [6]. This may also explain the association of these conditions in this patient.

Acknowledgements

This work was supported by the Program for Innovative Research Team in University (IRT0760) from the Ministry of Education of China. Conflict of interest: none.

References

1 Eisen AZ, Seegmiller JE. Uric acid metabolism in psoriasis. J Clin Invest 1961; 40: 1486-94.

2 Steinberg AG, Becker Jr. SW, Fitzpatrick TB, Kierland RR. A genetic and statistical study of psoriasis. Am J Hum Genet 1951; 3: 267-81.

3 Baumann RR, Jillson OF. Hyperuricemia and psoriasis. J Invest Dermatol 1961; 36: 105-7.

4 Brenner W, Gschnait F. Serum uric acid levels in untreated and PUVA-treated patients with psoriasis. Dermatologica 1978; 157: 91-5.

5 Goldman M. Uric acid in the etiology of psoriasis. Am J Dermatopathol 1981; 3: 397-404.

6 De Bari C, Lapadula G, Cantatore FP. Coexisting psoriatic arthritis, gout, and chondrocalcinosis. Scand J Rheumatol 1998; 27: 306-9.

1 Mei LIU and Jiu-Hong LI contributed equally to this work.


 

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