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.
|