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Psoriatic Arthritis

J. M. H. Mall and V. Wright

T HE idea of psoriatic arthritis as a specific disease entity, as opposed to the


coincidental occurrence of two common diseases, is relatively recent. The
evidence which has led to its general acceptance originates from many sources.
Foremost among these are clinical, serologic and radiologic studies, but epi-
demiologic surveys have also materially enhanced our knowledge of the disease.
The following account will be concerned with these fields of investigation and
their place in securing the present status of psoriatic arthritis as disease sui
generis.

HISTORICAL BACKGROUND

The French should be given credit for initiating and developing the concept
of psoriatic arthritis. Jean Louis Alibert’ is usually regarded as the first to have
recorded the association between psoriasis and arthritis. However, because of
the confusion between psoriasis and leprosy at this time, it is difficult to attach
much significance to this early observation.
The term psoriasis arthritique was originally coined by Pierre Bazin in 1860.*
However, acknowledgment should be given to Bourdi110n,3 who was the first to
examine the disease in detail. These observations were reported in his doctoral
thesis entitled “Psoriasis et Arthropathies” in 1888.
For the next 30 yr interest in the disease lapsed, but was eventually revived
by a number of individual case reports.4m6 Despite some opposition to the idea
of psoriatic arthritis at this stage,7m9 in recent years this has been largely over-
come by several large well-conducted surveys’0m’3 that have provided a firm
basis for regarding the disease as a specific nosologic entity.

TERMINOLOGY

Much inconsistency still exists over the terminology of psoriatic arthritis. The
most popular terms in the English language are psoriatic arthritis and psoriatic
arthropathy. The former is recommended by the American Rheumatism As-
sociation, I4 and it is the term most generally used in American and British text-
books of rheumatology. Nomenclature prevalent among reports from Europe
include: rhumatisme psoriasique, arthropatia psoriatica, psoriasis arthropath-
ica, psoriasis arthritica, arthritis psoriatica, and psoriatischen Arthropathie.

From the Shefleld Centrefor the Investigation and Treatment of Rheumatic Diseases, Nether Edge
Hospital. Shefield, England, and the Rheumatism Research C’nit, Universit?, Department qf‘ Medicine,
Leeds, England.
J. M. H. Mall, B.Sc., D.M., M.R.C.P.: Consultant Rheumatologist, Shefield Centre for the In-
vesiigation and Treatment 01 Rheumatic Diseases, Nether Edge Hospital. Sheffeld, England:
V. Wright, M.D., F.R.C.P.: Professor OJ Rheumatology, Rheumatism Research Unit. University,
Department oJMedicine, Leeds, England.
=I973 bv Prune & Stratton. Inc.

Seminars m Arthritis and Rheumatism. Vol 3, No 1 55


56 MOLL AND WRIGHT

DEFINITION
There is still no entirely satisfactory definition of psoriatic arthritis. This fact
is emphasized by the wide spectrum of definitions to be found in the literature:
(1) Arthritis confined to the distal interphalangeal (DIP) joints associated with
psoriasis. Is ( 2) Atrophic arthritis associated with psoriasis, having synchronous
remissions and relapses of skin and joint changes.6 (3) Arthritis following long-
standing, uncontrolled psoriasis.5 (4) Severely destructive arthritis associated
with psoriasis.i6 (5) Coincidental psoriasis and rheumatoid arthritis.” (6) Atypi-
cal arthritis accompanying atypical psoriasis. ia (7) Psoriasis associated with
erosive polyarthritis and usually a negative serologic test for rheumatoid
factor.19
There is little doubt that most of these definitions are too specific. Invariably
they highlight individual characteristics of psoriatic arthritis and fail to allow
for the wide range of presentation that typifies the disease.
At present we use a slight modification of the last definition listed above. The
specification of injammatory rather than erosive arthritis ensures the inclusion
of many early or mild cases that show no radiological abnormality. We now
prefer the more general term arthritis to pofyarthritis, since this allows the in-
clusion of spinal arthritis (sacro-iliitis or spondylitis) as well as peripheral
arthritis. A further objection to the term polyarthritis is that some cases of
psoriatic arthritis are monarthritic. The term usually describing a negative
serologic test for rheumatoid factor especially applies to occasional patients
in whom otherwise classical clinical and radiologic features of psoriatic arthri-
tis are associated with a positive test for rheumatoid factor. We feel that such
patients probably have true psoriatic arthritis and that the positive serology is
no more than an expression of a phenomenon that has been observed in 5% of
normal individuals.”
EVIDENCE FOR THE CONCEPT OF PSORIATIC ARTHRITIS

Epidemiologic Evidence
Epidemiologic evidence for psoriatic arthritis has been reviewed in consider-
able detail by Baker. *’ In his considerable personal contribution to the subject*’
he divided this type of evidence into three categories: (1) The prevalence of
psoriasis in patients with rheumatoid arthritis. (2) The prevalence of psoriasis
in the general population. (3) The prevalence of arthritis in psoriatic patients.
These studies have shown that psoriasis is more prevalent among patients
with arthritis, and, conversely, arthritis is found more frequently in psoriatic
subjects. However, much of these data are difficult to evaluate. In many of the
surveys it is difficult to determine whether the “arthritis” was inflammatory,
and, if it was inflammatory, whether the arthritis was seronegative or seroposi-
tive. Nevertheless, it is clear that, epidemiologically, a definite association
exists between psoriasis and inflammatory arthritis. Vilanova and Piiioll” ob-
served psoriatic arthritis in 2.5% of 214 patients with psoriasis, and Lane and
Crawfordz3 found an even higher prevalence of “arthritis” in psoriatic subjects
(32% of 23 1 patients). Probably the most reliable estimate is that of Leczinskyz4
who reported inflammatory polyarthritis in 6.8% of his series of 543 psoriatic
patients. A similar figure has been recently reported by Hellgren.25 He observed
PSORIATIC ARTHRITIS 57

Table 1. Characteristics of Seropositive (>l ;320) and Seronegative Inflammatory


Polyarthritis (Mongan and Atwaterz6)

SWOpOSltlYe Seronegative
Feature Affected Total Affected Total P

Subcutaneous nodules 95 216 7 144 ,001


Necrotizmg vasculitis 13 216 0 144 .Ol

Drffuse pulmonary fibrosis 18 216 1 144 .Ol


Peptrc ulceration 42 216 12 144 .Ol
Elevated gamma globulrns 35 133 14 86 .05
Psonasrs 6 216 18 144 ,001

Juvenile onset (< 16 yrl 3 216 45 144 ,001

Ulcerative calms 0 216 15 144 001


Ankylosmg spondyhtis 2 216 25 144 ,001

Sacro-iliitis 1 216 26 144 ,001

Uveitis 3 216 18 144 .Ol


Urethrrtis 3 216 9 144 .05
Aortic or mitral insufficiency 1 216 6 144 .05
Elevated alpha-2 globulins 42 133 43 86 .Ol

“rheumatoid arthritis” in 5.4% of 534 patients with psoriasis, but did not
specify the serology of these patients.
Finally, mention should be made of a recent report by Mongan and
Atwate? in which they compared the clinical, radiologic, and biochemical at-
tributes of patients with seropositive and seronegative rheumatoid arthritis.
Their findings are summarized in Table 1. Of particular interest is the fact that
psoriasis was considerably more frequent (p < .OOl) in the seronegative group
than in the seropositive group.

Clinical Evidence
In recent years, several clinical studies of psoriatic arthritis have appeared
from Englandi9**’ and from other parts of Europe.‘0~i’~28-30 Although there are
slight differences between the results of these surveys, the overall clinical picture
of psoriatic arthritis emerging from this work is consistent enough to allow a
characteristic series of features to be delineated.
The sex ratio in psoriatic arthritis varies between series’0~‘3~27*3’~34
but, taking

Table 2. Sex Ratio in Psoriatic Arthritis (Various Authors)

Number of
Author subrects Male Female

Bourdillon (1888. cited by Werssenbach. 1938) 36 27 9

Nob1 (1928. cited by Weissenbach. 1938) 69 16 53

Langlors (1934. cited by Weissenbach. 1938) 14 9 5

Weissenbach (1 938)31 50 20 30
Coste and Forestier (1 935)32 29 15 14

Vilanova and Piiiol (1951) lo 150 82 68

Sherman (1952) 33 15 9 6

Wright (1959) l3 118 41 77

Reed and Becker (1960)34 30 19 11

Baker et al. (1963)” 53 8 45

Total 564 246 318


Ratio 1:1.04
58 MOLL AND WRIGHT

Table 3. Sex Ratio in Uncomplicated Psoriasis (Various Authors)

Numberof
Author subjects Male Female

Church (1958)= 918 403 515


Lane and Crawford (1 937)23 231 108 123
Ingram (1 954)36 1346 551 795
Total 2495 1062 1433
Ratio 1:1.4

the results of a number of studies, the overall male/female ratio is 1: 1.04 (Table
2). This ratio is virtually the same as that seen in uncomplicated psoriasis23,35T36
(Table 3) and contrasts with the larger female preponderance (1:3) found in
rheumatoid arthritis.37
The age of onset of psoriatic arthritis is similar to that of rheumatoid arthri-
tis.27,38 The classical view that the onset of arthritis and onset of psoriasis are
commonly simultaneous has not been confirmed by recent studies.‘0,‘9*27
Wright I9 has found a much closer temporal relationship between nail and joint
changes than between skin and joint changes.
There have been several reports of an acute gout-like onset in psoriatic
arthritis’s~33~39 including, in some cases, involvement of the big toe. An in-
creased serum uric acid level and a good response to colchicine may further in-
crease the diagnostic confusion in these patients.40 In fact, the only way to make
a firm diagnosis of psoriatic arthritis under these circumstances is to exclude
the presence of negatively birefringent urate crystals in the joint Auid.
Although the big toe may on occasions be the first joint affected, we have
found that the proximal interphalangeal (PIP) and DIP joints of the fingers are
the most frequent initial sites for psoriatic arthritis.
The classical picture of psoriatic arthritis having a predilection for the DIP
joints ‘5,33.4’should be revised. It is clear from more extensive clinical surveys’2,‘3
that a variety of presentations ranging from single “sausage” digits3 to arthri-
tis mutilans42 may be observed. Although there is often no clear division be-
tween one type of presentation and another, five broad clinical groups may be
recognized: (1) Patients with classical psoriatic arthritis in which the DIP joints
are predominantly involved. This is relatively uncommon and in our experience
occurs in less than 5% of cases (Fig. 1). (2) Patients with arthritis mutilans often

Fig. 1. Psoriatic arthritis:


Involvement of DIP joints. Note
also the transverse ridging of the
nails.
PSORIATIC ARTHRITIS 59

Fig. 2. Psoriatic arthritis:


Oligo-articular pattern. Note
asymmetrical involvement of
only a few joints.

complicated by digital telescoping or the doigt en lorgnette deformity result-


ing from severe osteolysis. These patients often have sacro-iliitis. The frequency
of this pattern of involvement is approximately the same as in the classical DIP
pattern-about So/,. (3) Patients with a symmetrical pattern of arthritis indis-
tinguishable, apart from the negative serology, from rheumatoid arthritis. This
category constitutes about 15% of all patterns of psoriatic arthritis. (4) Pa-
tients with single or few finger or toe joints involved. This pattern of arthritis,
which usually affects scattered DIP, PIP, and metatarsal phalangeal (MP) joints,
is asymmetrical and in our experience is by far the commonest pattern of psori-
atic arthritis, accounting for over 70’& of all cases (Fig. 2). Patients with sausage
digits due to IP involvement of one finger and flexor tendon sheath effusion
may be included in this category (Fig. 3). This asymmetrical oligo- (or mono-)
articular presentation should therefore be regarded as one of the most frequent
and characteristic features of psoriatic arthritis. This fact has already been
acknowledged by French writers,29 but has so far received little attention in
British and American reports. (5) Patients in whom the predominant feature is

Fig. 3. Psoriatic arthritis:


“Sausage” finger. Nc)te involve-
ment of DIP, PIP, and MCP joint
of right middle finger.
60 MOLL AND WRIGHT

Fig. 4. Psoriatic spondylitis: (A)Sacro-iliitis with bilateral sclerosis and virtual obliteration of the
sacro-iliac joints. (B) Same patient as in (A), but a later stage of sacro-iliitis; the sclerosis has al-
most disappeared and the ankylosis of both sacro-iliac joints is now complete.

ankylosing spondylitis (Figs. 4A, B). The peripheral joints may or may not be
involved in these cases who represent about 5% of all types of psoriatic arthritis.
The association between psoriasis and ankylosing spondylitis has been
termed “psoriatic spondylitis” by some authors. Recent studies have shown
that as many as 20% of patients with peripheral psoriatic arthritis also have
sacro-iliitis.43-45 In a few patients the sacro-iliitis is not associated with the
typical clinico-radiologic picture of classical ankylosing spondylitis, but this is
usually present.
There is still no general agreement on definition of psoriatic spondylitis.
Furthermore, there is no universal acceptance that it represents a disease in its
own right rather than the coincidental occurrence of two diseases, psoriasis and
ankylosing spondylitis. That psoriatic spondylitis is, in fact, a specific entity
has been demonstrated epidemiologically by one of us recently in a family study
of psoriatic arthritis.46 On the basis of this work it would seem reasonable to
regard psoriatic spondylitis simply as an alternative presentation of psoriatic
arthritis.
We agree with Reed4 that the spondylitis associated with psoriasis clinically
resembles that seen in idiopathic ankylosing spondylitis. However, JajiC47 has
found a remarkable lack of back pain and stiffness in his patients and also a
poor correlation between clinical and radiological findings. Distinctive radio-
logic features have also been reported in psoriatic spondylitis. Most notable
among these is paravertebral ossification.48 However, we have not been able to
confirm this feature in a radiologic study of over 200 patients with psoriatic
arthritis and conclude that its rarity almost precludes its acceptance as a char-
acteristic feature of psoriatic spondylitis. More recently, destruction of adjacent
intervertebral surfaces resulting in solid fusion of vertebrae associated with
disc calcification has been described in psoriatic spondylitis by Langeland and
Roaas.49 The authors sugges t that this is specific for psoriatic spondylitis and
PSORIATIC ARTHRITIS

Fig. 5. Psoriatic arthritis: Nail pitting.

that the feature is not found in patients with coincidental psoriasis and
ankylosing spondylitis.
In contrast to earlier reports, there is little evidence to suggest any distinctive
pattern of dermal psoriasis in psoriatic arthritis compared with uncomplicated
psoriasis. All patterns of psoriasis, from small patches of psoriasis vulgaris to
widespread exfoliative psoriasis, may be observed in association with the ar-
thritis. A point that has been insufficiently stressed is the frequency with which

Fig. 6. Psoriatic arthritis: Transverse ridging cIf


the nails.
62 MOLL AND WRIGHT

Fig. 7. Psoriatic arthritis: Separation


of the nail plate (onycholysis).

patients are unaware that they have psoriasis and also the frequency with
which minimal psoriasis in “hidden” areas (scalp, natal cleft, perineum, and
umbilicus) remains undetected by the clinician, Often, the only manifestation
of the rash is a tiny patch either in one of the hidden areas or in one of the
classical sites (back of the elbow or front of the knee). In these cases the pres-
ence of nail involvement or a family history of psoriasis helps to clinch the
diagnosis. The difficulties in diagnosing minimal psoriasis have been examined
by Baker, who has outlined a number of criteria to facilitate diagnosis in bor-
derline cases.22
WrightI and Baker, Golding, and ThompsonSo have observed that nail in-
volvement occurs in over 80% of patients with psoriatic arthritis in contrast to
30% in patients with uncomplicated psoriasis. Furthermore, a topographical
relationship between involvement of distal joints and adjacent nails has also
been observed.5’ The type of nail psoriasis differs in no way from that seen in
uncomplicated psoriasis, and all varieties including pitting (Fig. 5), transverse
ridging (Fig. 6), onycholysis (Fig. 7), keratosis, yellowish discoloration, and
even total destruction of the nail (Fig. 8) may be observed. Zaias,52 in an ex-
cellent clinico-pathologic study, has summarized the clinical signs of nail
psoriasis and the site of origin of these lesions (Table 4). Figure 9 shows the
anatomical features relevant to this study. In addition to clinical involvement,
the psoriatic nails may also become calcified.53 This appears as a radioopaque
rim delineating the exposed part of the nail.
None of the nail abnormalities observed in psoriasis is specific for this
disease. Even pitting, which is usually regarded as highly characteristic, may be
encountered in other conditions such as dermatitis, alopecia areata, and oc-
casionally in normal subjects. 54The most important conditions to be considered
in the differential diagnosis of psoriatic nail dystrophy (all patterns) include:
fungal and bacterial infections, trauma, lichen planus, and dermatitis. Of these,
the most common diagnostic problem is nail infection-particularly infection
by Trichophyton rubrum and T. mentagrophytes. Zaiass2 has drawn attention to
the fact that a number of microorganisms can be isolated from psoriatic nails
(Table 5), but these are usually commensals. In particular, dermatophytes like
T. rubrum do not usually infect psoriatic nails: this has been ascribed to the
presence of a glycoprotein dermatophyte inhibitor.55
Several clinical features have been reported in association with psoriatic ar-
thritis. However, in view of the small numbers involved in these reports, it is
PSORIATIC ARTHRITIS 63

Fig. 8. Psoriatic arthritis: Advanced nail disease. The


nail has become thickened, roughened and partially destroyed.

Table 4. Clinical Signs of Nail Psoriasis and Origin of Lesions (Zaiass2)

ClInIcal Lesml Orlgln of Lesion

Nail plate
Ptts Psoriasis of proximal matnx
Transverse depressions (Beau’s lines) Psonasrs of proxtmal and mtd matnx
Crumblmg nail plate Psoriasis of entire matrcx
Leukonychia with rough surface Psonasis of proximal matrix
Leukonychia wtth smooth surface Psonasis of mrd matrix
Nail bed
Splmter hemorrhages Dermal ridge hemorrhage m nail bed
Large red patches Psoriasis of natl bed
Horny mass Longstanding psonasis of nail bed
Hyponychium
Subungual keratosrs Psonasts of hyponychwm
Yellow-green discoloration of subungual debns Secondary colonization by Yeasts and
Onycholysls pseudomonas
Atr under separated nail plate

nailfold
Ptoximal

Nal plate

HYPonychwm

Matrix

Fig. 9. Diagrammatic representa-


tion of nail structure (after Zaias” ).
64 MOLL AND WRIGHT

Table 5. Microorganisms Isolated From Subungual Debris in


40 Psoriatic Nails of 15 Patients (Zaias6*)

Microorganism Number

Dermatophytes 0
Saprophytes 12
Arthroderma quadrifidum 2
Cephalosporium roseogriseum 1

Curvolaria lunata 3
C. geniculata 1
Didymobotryum cookei 1

Helminthosporium satinum 1
Hormodendrum nigrescens 1
Penicillium citrinum 1
Torula allii 1
Yeasts 22
Candida albicans 3
Candida parapsilosis 12
Rhodotorula mucilagenosa 4
Rhodotorula rubra 1
Trichosporon beigelii 2
Bacteria 20

Grampositive micrococcus 12
Pseudomonas aeruginosa 2
Gram negative rods; other 2

impossible to evaluate fully the significance of these relationships. The as-


sociated features include high fever,” rarity of adenopathy,33 infrequent muscle
wasting,56 infrequent tendon sheath effusions,” sclerodactyly,” ocular inflam-
mation,” gastrointestinal amyloidosis,57 and aortic incompetence.” Although
not yet reported in psoriatic arthritis, extensive psoriasis may be associated with
steatorrhea.59 Perhaps the most convincing negative relationship is the absence
of rheumatoid nodules in patients with psoriatic arthritis.”
We have recently drawn attention to a number of clinical and familial asso-
ciations between psoriatic arthritis and other seronegative arthritides (Reiter’s
disease, the intestinal arthropathies, idiopathic ankylosing spondylitis, and
Behcet’s
s syndrome).46,60 The chief common denominators between these closely
interrelated diseases, which we have named seronegative spondarthritides,
include seronegative polyarthritis, sacro-iliitis or spondylitis, familial aggrega-
tion, and evidence of clinical “overlap.” The latter is best illustrated by a num-
ber of patients, reported previously, in whom features of psoriatic arthritis and
Reiter’s disease coexisted.6’ In these patients, it was impossible to make a di-
agnosis other than “psoriatic arthritis with features of Reiter’s disease” or
“Reiter’s disease with features of psoriatic arthritis.”

Radiological Evidence
Several radiologic studies of psoriatic arthritis have been reported
recently,43+” and the subject has been critically reviewed by Baker.”
The following are probably the most convincing radiographic features of
psoriatic arthritis: (1) Erosion of terminal phalangeal tufts (acre-osteolysis).
(2) Whittling of phalanges, metacarpals, and metatarsals (Figs. 10 and 12).
PSORIATIC ARTHRITIS 65

Fig. 10. Psoriatic arthritis: “Whittling”


of second to fifth metatarsals and MTP
ankylosis of the hallux.

Fig. 11. Psoriatic arthritis: lnterphalangeal and MTP “cupping” of proximal ends of the left
third and fourth proximal phalanges.
66 MOLL AND WRIGHT

(3) Cupping of the proximal ends of phalanges, metacarpals, and metatarsals


(Figs. 11 and 12). When the distal ends of these bones are whittled, the appear-
ance at the IP and MP joints has been aptly termed the “pencil-in-cup” deform-
ity. (4) Ankylosis of phalanges, metacarpals, and metatarsals (Figs. 10 and 11).
(5) Lack of symmetry (Fig. 13). (6) Severe destruction of isolated small joints
(Fig. 13). (7) Predilection for DIP and PIP joints with relative sparing of meta-
carpo-phalangeal (MCP) and metatarso-phalangeal (MTP) joints (Fig. 14).
(8) Sacro-iliitis or ankylosing spondylitis (Fig. 4).
It should be emphasized, however, that most of these characteristic features
are relatively uncommon, with the exception of asymmetry and destruction of
isolated small joints. The latter is not always gross, and in the early phase of the
disease may be manifest radiologically only by juxta-articular soft tissue swell-
ing and minimal joint erosion.
The changes of sacro-iliitis or spondylitis associated with psoriatic arthritis
are usually identical to those observed in idiopathic ankylosing spondylitis
(Fig. 4).
It is possible to summarize the radiological characteristics of psoriatic ar-
thritis in terms of a tendency to affect fewer and smaller peripheral joints com-
pared with rheumatoid arthritis. Moreover, the involvement of these joints is
often more severe, particularly with regard to osteolysis and ankylosis, than
would be expected in rheumatoid arthritis.

Laboratory Findings and Pathology


The most distinctive and generally accepted feature among the laboratory
investigations in psoriatic arthritis is a persistently negative test for rheuma-
toid factor.
Hyperuricemia may be found in lo%-20% of patients.” Eisen and Seeg-
miller65 have shown that hyperuricemia reflects increased purine metabolism in
the skin, and serial biopsies of affected and clinically normal skin in psoriatics
have shown increased DNA synthesis. 66 However, it should be emphasized that
minimal psoriasis is not usually accompanied by an elevated serum uric acid
level; therefore, unless the rash is extensive, hyperuricemia in a patient thought
to have psoriatic arthritis usually indicates gout.
Other miscellaneous and often conflicting biochemical findings include:
,,normal erythrocyte phosphoglucose-isomerase activity6’; absence of anti-
nuclear factor68*69; elevated gamma and alpha-2-globulins”; decreased IgM
levels in mild psoriatic arthritis and elevated levels in severe psoriatic arthritis”;
elevated IgA levels in two-thirds of patients with psoriatic arthritis and one-
third of patients with psoriasis’*; elevated IgA and IgM globulins in 30”/,
of patients with psoriasis and 300/, with psoriatic arthritis, contrasted with
80% in rheumatoid arthritis.‘* The last observation is at variance with the work
of Heiskell et al.” who found a consistent elevation of beta globulins in
psoriatic arthritis, but not in rheumatoid arthritis. Zachariae and Zachariae74
have been unable to find any specific immunologic pattern in psoriatic arthritis,
and Baker et a1.27have found no consistent correlation between clinical activity
or severity and the degree of protein disturbance.
Other nonspecific laboratory findings include anemia, elevated ESR, and
transient leukocytosis.*’
Fig. 12. Psoriatic arthritis:
Gross phalangeal ostaolysis. Cup
deformity at proximal end of fifth
middle phalanx and whittling at
the distal end of this bone.

Fig. 13. Psoriatic arthritis: Typical asymmetrical involvement of relatively few joints. Note
that joints which are involved are severely affected.
68 MOLL AND WRIGHl

Fig. 14. Psoriatic arthritis: Erosion of most DIP joints and some PIP joints. The MCPs are rel-
atively spared.

There has been little convincing evidence, either from studies of synovial
fluid70,75 or from portmortem specimens, to suggest any histologic difference
between psoriatic arthritis and rheumatoid arthritis.15 However, Sherman33
and Coste and Solnica 76 have commented on the excessive fibrous reaction
found in joint tissues of patients with psoriatic arthritis.
Several capillaroscopic differences between psoriatic and rheumatoid arthritis
have been observed by a New York group. 77 Using a binocular microscope,
both rheologic and morphologic differences were noted in the nailfold capil-
laries. The findings of this valuable study are summarized in Tables 6 and 7.
The most characteristic features in psoriatic arthritis were tight terminal con-

Table 6. Incidence of Rheologic Changes Observed in Patients With


Rheumatoid and Psoriatic Arthritis (Redisch et al.“)

Psoriatic
Arthritis Arthritvs
RheologlcFeature %(N = 31) %(N = 9)

Increased plasma skimming (separation of cells from plasma) 71 0


Sluggish flow 58 100
Dusky color of blood column 52 100
Increased cellular aggregation with delayed dispersion of cell
aggregates 39 67
Extravasation 13 67
Stasis of erythrocytes 13 67
PSORIATIC ARTHRITIS 69

Table 7. incidence of Morphologic Changes Observed in Patients With

Rheumatoid and Psoriatic Arthritis (Redisch et al.“)

Rheumatoid Psorlatlc
Arthntas Arthrlfis
Morphologic feature %iN = 311 %lN = 9)

Meandering with tight terminal CO~VO~U~IO~S 0 100


Meandenng with loose convolutions 0 0
Increased tortuosity (transitional and efferent limbs) 48 67
Dlsproportlonate widening of efferent limb 6 0
Widencng of all three limbs (afferent, transitional and efferent) 42 44

Aptcal widening 16 0
Venular plexus widening and engorgement 42 11

Focal narrowing and widening of efferent limb and venules 10 0


Elongatkon of loops 42 0
Dlmmlshed number of loops associated with enlargement
of loops 0 0
Paucity of visible capillanes 71 0
Disarrangement of capillary polarity 13 0

volutions of the nailfold capillaries (Fig. 15). These changes have been observed
in psoriatic and normal skin of patients with uncomplicated psoriasis and
psoriatic arthritis, but not at all in patients with rheumatoid arthritis. Rheo-
logically, increased plasma skimming was the most obvious difference between
psoriatic and rheumatoid arthritis (Table 6).

DIAGNOSTIC PROBLEMS

Problems in the diagnosis of psoriatic arthritis may conveniently be divided


into the separate diagnostic difficulties posed by individual features of the
disease (psoriasis, polyarthritis, and spondylitis).
Psoriasis of the skin and scalp may be so minimal as to escape the attention
of both patient and clinician. Particularly elusive are small lesions at the inter-
natal cleft, perineum, umbilicus, submammary area, axilla, and groin. Scalp
lesions may also be confined to a small plaque, often in the occipital region.
As this may be the only manifestation of psoriasis, the scalp should always be
examined meticulously in any patient with an arthritis of psoriatic pattern but
without obvious psoriasis of skin or nails. Scalp psoriasis must be differ-
entiated from seborrhoea capitis. The latter is characterized by poor demarca-
tion between involved and normal scalp and also the fact that seborrhoeic
lesions are not usually palpable. Other seborrhoeic features, such as scaly in-
volvement of the eyebrows and otitis externa, may further simplify diagnosis.
Psoriatic nail involvement may be the only manifestation of psoriasis, and in

Fig. 15. (A) Normal hairpin-


shaped nailfold capillary. (6) “Mean-
dering” of nailfold capillary in psori-
atic arthritis. Note tight terminal
convolutions.
70 MOLL AND WRIGHT

Fig. 16. Reiter’s disease: Keratoderma blen-


orrhagica. Note similarity to pustular psoriasis.

these cases it is important to exclude other causes of nail dystrophy. If fungal


infection is suspected, cuttings of the nail should be examined microscopically.
Mention has already been made of the considerable difficulty in diagnosing
certain cases of psoriatic arthritis from Reiter’s disease.6’ Particularly confusing
are the close similarities between nail involvement in these two conditions and
also the difficulty in distinguishing keratoderma blenorrhagica (Fig. 16) from
pustular psoriasis of the palms and soles.
Other causes of asymmetrical DIP and PIP arthritis in a patient with
psoriasis may be mistaken for true psoriatic arthritis. Recently, erosive78-8’ and
ankylosing” forms of osteoarthrosis have been described, and, because of their
predilection for scattered DIP and PIP joints, it may be impossible to dis-
tinguish these forms of arthritis from psoriatic arthritis. Osteoarthrosis may
also cause diagnostic confusion when associated with Heberden’s nodes: early
active nodes may be red and swollen in the same way as in psoriatic arthritis
of the DIP joints (Fig. 17). In osteoarthrosis, often it is only later that the
single globular swelling of the DIP joint settles to reveal the hard double node
so typical of the disease. Advanced osteoarthrosis of the DIP joint may be sim-
ilar radiologically to psoriatic arthritis. This is due to gross irregularity of the
joint margin and subchondral cysts, which, even to an experienced eye, may
be mistaken for erosions.
We have observed several psoriatic patients who have presented with post-
traumatic pain and swelling of the knee. These patients were usually diagnosed
as having a mechanical derangement until arthrotomy revealed synovial pro-
liferation and not a torn meniscus. The susceptibility of patients with psoriatic
arthritis to trauma has already been mentioned, and we suggest that any
“traumatic” arthritis in a patient with psoriasis failing to settle in the usual
way should be considered to be monarticular psoriatic arthritis until proved
otherwise.
PSORIATIC ARTHRITIS 71

Fig. 17. Psoriatic arthritis: Globular


swelling due to DIP joint involvement.

Occasionally, patients with the classical clinico-radiologic picture of psoriatic


arthritis are found to be seropositive. We now regard most of these patients
as having true psoriatic arthritis associated coincidentally with a positive test
for rheumatoid factor on the basis that positive serology is present in 5’:;, of the
general population.”

ETIOLOGY AND PATHOGENESIS

Etiology: Genetic and Familial Aspects


In view of the convincing evidence for genetic factors in the etiology of un-
complicated psoriasis83m85 and the close relationship between psoriasis and
arthritis, the possibility of heredity as a factor in the etiology of psoriatic
arthritis itself has been examined in recent years. Evidence in favor of this con-
cept is now substantial and stems from both individual pedigree studies5’,86m”8
and family surveys.46*89m92M011,~~ in a controlled study of over 100 families of
patients with psoriasis and arthritis, found arthritis to be aggregated in first-
degree relatives of psoriatic arthritis probands almost 50 times more often than
has been reported in the general population.90,93 A significant difference was
also found between the prevalence of the disease in first-degree relatives and
the prevalence in spouse controls, thus suggesting genetic rather than environ-
mental factors as the cause of the familial aggregation. No definite Mendelian
pattern of inheritance was encountered in Mall’s pedigrees or the pedigrees re-
ported by other workers, and it was concluded that inheritance is likely to be
multifactorial.
72 MOLL AND WRIGHl

Pathogenesis
It seems likely that environmental factors as well as genetic factors are re-
sponsible for the development of psoriatic arthritis.46p94 It is possible that en-
vironmental factors trigger arthritis in genetically predisposed individuals, but
the nature of these triggering mechanisms is not yet known. However, several
theoretical possibilities have been suggested. Buckley and Raleigh95 proposed
that trauma might act as an arthritis-triggering factor, operating as a “deep
Koebner effect.” These workers supported their concept by reporting a psori-
atic patient who developed acre-osteolysis after a blow on the finger. A similar
phenomenon has been observed in a psoriatic subject in whom generalised acro-
osteolysis followed needle puncture of one nail.96 Furthermore, Polish work-
ers9’ have observed trauma-related osteolysis of the MTP joints in patients with
psoriatic spondylitis. Williams and Scott98 have reported a further example in
which trauma appeared to influence the onset of arthritis in a patient with
psoriasis. We have also observed trauma-induced chronic arthritis in previously
normal joints of patients with psoriatic arthritis and also in patients with
psoriasis uncomplicated by arthritis. An enzyme defect resulting in a joint
deficiency of hyaluronic acid, thus rendering the tissues more liable to damage
from minor trauma, has been suggested by Cotton and Mier.99
Another theory invokes a neurotrophic effect similar to that observed in
diabetes and leprosy,‘@ and to support this there has been a recent demonstra-
tion of abnormal nervous structures in psoriatic skin.“’
A further concept is based on the finding of abnormal capillaries in the af-
fected and unaffected skin of patients with psoriasis,“’ and the supposition that
a capillary defect may contribute to the synovial abnormality in psoriatic sub-
jects who develop arthritis.lo3
Staphylococcal alpha antitoxin levels are raised in a quarter of patients with
psoriatic arthritis, and particularly in those with DIP involvement. It has been
suggested that blood-borne infection may be encouraged by stagnation of blood
in dilated distal phalangeal capillaries. ‘04 However, this would not explain the
development of arthritis in the majority of patients with psoriatic arthritis in
whom there is no DIP involvement.
An abnormally high fecal flora of atypical Clostridium perfringens has been
found in a large proportion of patients with psoriatic arthritis.lo5 However,
similar findings are also present in patients with rheumatoid arthritis and
systemic lupus erythematosus. It is likely, therefore, that these organisms re-
flect a nonspecific reaction to severe disease rather than a feature specific to
psoriatic arthritis.53
The possibility that an abnormality in delayed hypersensitivity may be im-
plicated in psoriasis has been recently investigated but with negative results.‘06

TREATMENT

Conservative Measures
Generally, the treatment of the skin disease, the peripheral arthritis, and the
spondylitis of psoriatic arthritis patients follows the normal lines employed for
treatment of the uncomplicated disorders. However, antimalarial drugs are
contraindicated as they may provoke exfoliative reactions.“’ Gold, however, is
PSORIATIC ARTHRITIS 73

not contraindicated, as it has been shown that no more skin reactions are
experienced in psoriasis than have been found to occur in rheumatoid ar-
thritis.43 The arthritis does not normally subside with treatment of the
psoriasis, although some dramatic examples of this phenomenon have
been described with indomethacin,lo8 cyclophosphamide,“’ and methotrexate
(amethopterin).“‘*“’ However, a more recent report,‘12 although confirming
the beneficial effect of methotrexate on the psoriatic rash, has not demon-
strated a similar effect on the arthritis of psoriatic patients. In view of the toxic-
ity of methotrexate and its capricious therapeutic effect it would seem reason-
able to reserve the drug only for cases of psoriatic arthritis which have
remained refractory to treatment by simpler and less harmful agents.
Viglioglia et al. 113have tried allopurinol in patients with psoriasis. This treat-
ment is based on the hyperuricemia which often accompanies the disease. These
authors found a diminution of dermal scaling and erythema, and also an im-
provement in the nail dystrophy and joint symptoms of patients treated with
this drug. Another approach has been tried by Walz and Berkoff,1’4 who have
tried the effect of antipsoriatic agents on inflammatory joint disease. Using a
dithranol preparation, they observed an antirheumatic effect in rats suffering
from adjuvant-induced arthritis.

Surgical Implications
It has been said”’ that patients with psoriatic arthritis are particularly
prone to infection after prosthetic surgery. This assumption was based on two
infected PIP Swanson prostheses in one patient. Although this was not specified
in the particular patient reported, it was customary in this unit to treat psoriatic
arthritis patients with cytotoxic and immunosuppressive drugs; it is possible,
therefore, that infection may have been related to therapy rather than disease.
We have not been able to confirm a higher prevalence of wound infection in
patients with psoriatic arthritis compared with rheumatoid arthritis. Occasion-
ally, however, psoriatic plaques form at the site of the wound, but these do not
appear to delay healing, nor do they appear to increase the risk of infection.
Although this has not yet been formally tested, it is interesting to speculate
whether or not the more exuberant fibrotic reaction in psoriatic arthritis com-
pared with rheumatoid arthritis might interfere with restoration of joint mo-
bility after surgery. Judging this subjectively from the progress of our own
patients, this does not seem to be the case.
In our view, the indications for prosthetic surgery apply as much to psoriatic
arthritis as they do to rheumatoid arthritis, but in some patients the extra
problems associated with ankylosing spondylitis will have to be considered.
However, with regard to this complication, we have recently observed excellent
results in two previously bedridden patients with psoriatic spondylitis who,
after bilateral Charnley total hip replacement, were restored to useful inde-
pendence and mobility.

PROGNOSIS

In almost 50% of the deaths in the series of Reed and Wright,56 the cause was
attributed to corticosteroid therapy. Apart from the rare arthritis mutilans,
74 MOLL AND WRIGHT

psoriatic arthritis tends to cause less pain and less disability than rheumatoid
arthritis.5’ This is consistent with the clinical observation that psoriatic arthritis
is often oligoarticular and tends to affect small rather than large peripheral
joints. Moreover, Vilanova and Piiiol’” have found that if the arthritis remains
confined to small joints over a long period, the ultimate progress is favorable.

SUM MARY

(1) Epidemiologic, clinical, radiologic and serologic evidence suggests that


psoriatic arthritis is a specific entity and not the coincidental occurrence of two
common diseases, psoriasis and rheumatoid arthritis.
(2) Psoriatic arthritis may be defined as psoriasis associated with inflam-
matory arthritis (peripheral arthritis and/or spondylitis) and usually a negative
serologic test for rheumatoid factor.
(3) Epidemiologic evidence for psoriatic arthritis is based on the finding of a
significantly higher prevalence of psoriasis in arthritic populations and, con-
versely, a significantly higher prevalence of arthritis in psoriatic populations
compared with controls.
(4) Clinical characteristics of the disease include: almost equal distribution
between males and females; peripheral arthritis involving few small joints in
asymmetrical fashion; involvement of DIP joints; sausage digits; arthritis
mutilans; ankylosing spondylitis; gout-like onset; higher incidence of nail in-
volvement than occurs in uncomplicated psoriasis. The rash may present with
arthritis, or, equally, may precede or succeed joint involvement.
(5) Radiologic characteristics of the disease include: erosion of terminal
phalangeal tufts (acre-osteolysis); whittling of phalanges, metacarpals, and
metatarsals; cupping of proximal ends of phalanges, metacarpals, and metatar-
sals; ankylosis of IP and MP joints; lack of symmetry; severe destruction of
isolated small joints: predilection for DIP and PIP joints with relative sparing
of MP joints; sacro-iliitis or ankylosing spondylitis.
(6) Laboratory characteristics are: negative serologic tests for rheumatoid
factor; hyperuricemia; various changes of doubtful specificity in blood proteins
and enzymes.
(7) Morbid anatomical findings include excessive fibrous tissue in affected
joints and abnormal nailfold capillaries in both normal and psoriatic skin.
(8) Family studies have shown that psoriatic arthritis is probably determined
genetically in a multifactorial manner. Environmental factors such as trauma
may be important in triggering arthritis in the genetically predisposed.
(9) Familial and clinical interrelationships exist between psoriatic arthritis
and other seronegative arthritides, particularly Reiter’s disease, idiopathic
ankylosing spondylitis, and the intestinal arthritides.
(10) Treatment of psoriatic arthritis is the same as the routine treatment of
the individual components of the disease (psoriasis, peripheral arthritis, and
spondylitis). However, antimalarials should be avoided as they exacerbate the
rash. Folate antagonists (e.g., methotrexate) may be tried in severe cases not
responding to traditional and less potentially harmful treatment.
(11) With regard to pain and disability, the prognosis in psoriatic arthritis
is better than in rheumatoid arthritis.
PSORIATIC ARTHRITIS 75

REFERENCES
1. Ahbert JL: P&is Theorique et Pratique arthritis. Tram Assoc Am Physicians 53:303,
sur les Maladies de la Peau. Paris, Caille et 1938
Ravier, 1818, p. 21 19. Wright V: Psoriasis and arthritis. Ann
2. Bazin P: Lecons Theoriques et Cliniques Rheum Dis 15:348, 1956
sur les Affections Cutanees de Nature Arthri- 20. Wailer M, Toone EC: Normal indivtd-
tique et Dartreux. Paris, Delahaye, 1860, pp uals with positive tests for rheumatoid factor.
154~~161 Arthritis Rheum I1:50, 1968
3. Bourdillon C: Psoriasis et Arthropathies. 21. Baker H: Epidemiological aspects of
These, Paris. 1888 psoriasis and arthritis. Br J Derm 78:249, 1966
4. Strom S: A case of arthropatia psoriatica. 22. Baker H: The relationship between
Acta Radio1 (Sth) 1:21, 1921 psoriasis, psoriatic arthritis and rheumatoid
5. Hench PS: Arthropathia psoriatica: pre- arthritis. An epidemioiogical, clinical and
sentation of a case, Proc Staff Meet Mayo Clin serological study. MD thesis, University of
2:80. 1927 Leeds, 1965
6. Jeghers H, Robinson LJ: Arthropathia 23. Lane CC, Crawford EM: Psoriasis a
psoriatica: report of a case and discussion of statisticai study of 231 cases. Arch Dermatol
the pathogenesis, diagnosis and treatment. Syph 35:1051, 1937
JAMA 108:949, 1937 24. Leczinsky CC: The incidence of arthrop-
7. Brocq L: Quelques reflexions sur l’etio- athy in a ten-year series of psoriasis cases.
logic du psoriasis a propos de rtcentes publi- Acta Dermatol vener (Sth) 28:483, 1948
cations Americans. Ann Dermatol Syph I: 156, 25. Hellgren L: Association between rheuma-
1910 toid arthritis and psoriasis in total populations.
8. Margolis HM: Arthritis and Allied Dis- Acta Rheum Stand I5:3 16, 1969
orders. New York, Hoeber, 194 I, p 125 26. Mongan ES, Atwater EC: A comparison
9. Romanus T: Psoriasis from a prognostic of patients with seropositive and seronegative
and hereditary point of view. Acta Dermatol rheumatoid arthritis. Med Clin N. Am 52:533,
vener (Sth) 26: (Suppl) 12:6, 1945 1968
10. Vilanova X, Pifiol J: Psoriasis arthro- 27. Baker H, Golding DN, Thompson M:
pathica. Rheumatism 7: 197, I95 I Psoriasis and arthritis. Ann Intern Med 58:909,
I I. Coste F, Francon J, Touraine R, Loyau I963
G: Polyarthritis psoriasique. Revue Rhum 28. Tesarek B: Some differential problems of
Mal Osteo-artic 25:75, 1958 psoriatic arthritis. Vnitr Lek 12:486, 1966
12. Wright V: Rheumatism and psoriasis: a 29. Serre H, Simon L, Sany J: Le rhuma-
re-evaluation. Am J Med 27:454, 1959 tisme psoriasique. J Med Montpellier 4:3, 1969
13. Wright V: Psoriatic arthritis: a compara- 30. Theiss B: Zur Differentialdiagnose der
tive study of rheumatoid arthritis and arthritis Gelenkerkrankungen bei Psoriatikern. Dtsch
associated with psoriasis. Arch Dermatol 80:27, Med Wochenschr 96:300, 1971
I959 31. Weissenbach RJ: Le psoriasis arthro-
14. Blumberg BS, Bunim JJ, Calkins E, pathique. Archs dermato-syph. Clin Hop
Pirani CL, Zvaifler NJ: ARA nomenclature and S-Louis lO:l3, 1938
classification of arthritis and rheumatism (tenta- 32. Coste F, Forestier J: Remarques sur le
tive). Arthritis Rheum 7:93, 1964 rhumatisme psoriasique. Rev Rhum Mal Osteo-
15. Bauer W, Bennett GA, Zelier JW: artic 2:554, 1935
Pathology of joint lesions in patients with 33. Sherman M: Psoriatic arthritis: observa-
psoriasis and arthritis. Tram Assoc Am Physi- tions on the clinical, roentgenographic and
cians 56:349, 1941 pathological changes. J Bone Joint Surg 34A:
16. Fawcitt J: Bone and joint changes as- 831, 1952
sociated with psoriasis. Br J Radio1 23:440, 34. Reed WB, Becker SW: Psoriasts and
1950 arthritis. Arch Dermatol 81:577, 1960
17. Pillsbury DM, Shelley WB, Kligman 35. Church R: The prospect of psoriasis.
AM: Dermatology. Philadelphia, Saunders, Br J Dermatol 70: 139, 1958
1956, pp 728-829 36. Ingram JT: The significance and manage-
18. Dawson MH, Tyson TL: Psoriasis ment of psoriasis, Br Med J 2:823, 1954
arthropathica with observations on certain 37. Duthie JJR: Rheumatoid arthritis. in
features common to psoriasis and rheumatoid Copeman WSC (ed): Textbook of the Rheu-
76 MOLL AND WRIGHT

matic Diseases, ed 4. Edinburgh, Livingstone, 57. Ferguson A, Downie WW: Gastroin-


1969, p 260 testinal amyloidosis in psoriatic arthritis. Ann
38. Short CL, Bauer W, Reynolds WE: Rheum Dis 27:245, 1968
Rheumatoid Arthritis. Cambridge, Harvard 58. Reed WB, Becker SW, Rohde R, Heis-
Univ Pr, 1957, pp 38-42 kell CL: Psoriasis and arthritis. Clinico-
39. Barber HW: Psoriasis. Br Med J 1:219, pathologic study. Arch Dermatol 83:541, 1961
1950 59. Shuster S, Marks J: Dermatogenic en-
40. Huskisson EC, Balme HW: Pseudo- teropathy. A new cause of steatorrhoea.
podagra: differential diagnosis of gout. Lancet Lancet 1:1367, 1965
21269, 1972 60. Wright V: Seronegative Spondarthritis.
41. Plenk HD: Psoriatic arthritis. Report of a Gilbert Scott Memorial Lecture, Royal Society
case. Am J Roentgen 64:635, 1950 of Medicine, London, 197 I
42. Clarke 0: Arthritis mutilans associated 61. Wright V, Reed WB: The link between
with psoriasis. Lancet 1:249, 1950 Reiter’s syndrome and psoriatic arthritis. Ann
43. Wright V: Psoriatic arthritis: a compara- Rheum Dis 23: 12, 1964
tive study of rheumatoid arthritis and arthritis 62. Avila R, Pugh DG, Slocumb CH, Win-
associated with psoriasis. Ann Rheum Dis 20: kelmann RK: Psoriatic arthritis: a roentgen-
123, 1961 ological study. Radiology 75:691, 1960
44. Reed WB: Psoriatic arthritis. A complete 63. Rozin R, Mikulski J, Schwartz A:
clinical study of 86 patients. Acta Dermatol Radiological signs of psoriatic arthritis. Hare-
Vener (Sth) 41:396, 1961 fuah 79:549, 1970
45. Hill AGS: Sacro-iliiac joint in adult 64. Petres J, Kliimper A, Majert P: Zur
rheumatoid arthritis and psoriatic arthropathy Differentialdiagnose der psoriatischen Arthro-
by Dixon, A St J, Lience E. Ann Rheum Dis pathie auf Grund rbntgenmorphologischer
201247, 1961 Befunde. Hautarzt 21:26, 1970
46. Mall JMH: A Family Study of Psoriatic 65. Eisen AZ, Seegmiller JE: Uric acid
Arthritis, DM thesis, University of Oxford, metabolism in psoriasis. J Clin Invest 40: 1486,
1971 1961
47. JajiC I: Radiological changes in the 66. Hell E, Hodgson C: The uptake of 3H
sacro-iliac joints and spine of patients with thymidine by epidermal cells in normal and
psoriatic arthritis and psoriasis. Ann Rheum psoriatic subjects. Br J Dermatol78:262, 1966
Dis 27:1, 1968 67. Gaedicke H, Kaiser W, Mathies H: Die
48. Bywaters EGL, Dixon A St J: Paraver- Bestimmung der Phosphoglucose-Isomerase-
tebral ossification in psoriatic arthritis. Ann Aktivatlt in den Erythrocyten und ihre Bedeu-
Rheum Dis 24:313, 1965 tung als diagnostisches Kriterium der Arthritis
49. Langeland N, Roaas A: Spondylitis psoriatica. Klin Wochenschr 48:1456, 1970
psoriatica. Acta Orthop Stand 42:391, 1971 68. Sonnichsen N: Immunologische Unter-
50. Baker H, Golding DN, Thompson M: suchungen zur nosologischen Stellung der
The nails in psoriatic arthritis. Br J Dermatol Psoriasis arthropathica. Allergic Asthma 15:
761549, 1964 124, 1969
5 1. Wright V: Psoriatic arthritis, in Copeman 69. Sonnichsen N: Vergleichende immuno-
WSC (ed): Textbook of the Rheumatic Dis- logische Untersuchungen bei Lupus erythema-
eases, ed 4. Edinburgh, Livingstone, 1969, todes primar chronischer Polyarthritis und
pp 632-633 Psoriasis arthropathica. Allergie Asthma 15: 1,
52. Zaias N: Psoriasis of the nail: a clinico- 1969
pathological study. Arch Dermatol 99:567, 1969 70. Robillard J: Le Rhumatisme Psoriasique
53. Boyle JA, Buchanan WW: Clinical (a propos de 53 observations). These, Lyon,
Rheumatology. Oxford, Blackwell, 1971, pp 1968
304-317 7 1. Petres J, Majert P: Immunelektrophorese
54. Samman PD: The formation of nails and bei psoriatischer Arthropathie. Arch Klin Exp
their diseases. Hosp Med 1:237, 1966 Dermatol232:398, 1968
55. Vanbreuseghem R: The early diagnosis 72. Danielsen L: Immune-electrophoretic
of mycetoma. Dermatol Int 6:123, 1967 analysis of serum proteins in psoriasis and
56. Reed WB, Wright V: Psoriatic arthritis. psoriatic arthritis. Acta Rheum Stand 11:112,
in Hill, AGS (ed): Modern Trends in Rheu- 1965
matology. Butterworths, London, 1966, pp 73. Heiskell CL, Reed WB, Weimer HE,
3755383 Becker SW, Carpenter CM: Serum protein
PSORIATIC ARTHRITIS 77

profiles in psoriasis and arthritis. Arch Der- 91. Theiss B, Schnyder UW, Boni A: Intra-
matol 85:708, 1962 familiare tmmunochemische Untersuchungen
74. Zachariae H, Zachariae E: Antinuclear bei Psoriasis-Arthritis und Psoriasis-Spondyl-
factors, the anti-human globulin consumption arthritis. Arch Klin Exp Dermatol 239:70,
test, and Wassermann reaction in psoriatic 1970
arthritis. Acta Rheum Stand 15:62, 1969 92. Vilaghy I, Krebs A: Untersuchungen
75. Delbarre F: interest in the study of in- tiber die Vererblichkeit des Syndroms Psoriasis
traleucocyte “inclusions” in the diagnosis of arthropathica. Dermatologica 140:209, 1970
seronegative polyarthritis. 6th European Con- 93. Lead article: Psoriatic arthritis. Magazine
gress of Rheumatology, Lisbon, 1967, p 65 of the Arthritis and Rheumatism Council, p 5,
76. Coste F, Solnica J: La polyarthrite No. 7, 1967
psoriasique. Revue fr Stud Clin Biol ll:578, 94. Wright V, Mall JMH: Psoriatic arthri-
1966 tis. Bull Rheum Dis 2 1:627, 197 I
77. Redisch W, Messina EJ, Hughes G, 95. Buckley WR, Raleigh RL: Psoriasis
McEwen C: Capillaroscopic observations in with acre-osteolysis. New Eng J Med 261:539,
rheumatic diseases. Ann Rheum Dis 29:244, 1959
1970 96. Miller JL, Soltani K, Tourtellotte CD:
78. Crain DC: lnterphalangeal osteoarthritis Psoriatic acre-osteolysis without arthritis. J
characterised by painful inflammatory episodes Bone Joint Surg 53A:37 I, 197 I
resulting in deformity of the proximal and 97. Biernacki R, Sadowska-Wroblewska M,
distal articulations. JAMA 175: 1049, 1961 Zabokrycki J: Acre-osteolysis in the course of
79. Peter JB, Pearson CM, Marmor L: Ero- ankylosing spondylitis. Reumatologia 6: 163,
sive osteoarthritis of the hands. Arthritis 1968
Rheum 9:365, 1966 98. Williams KA, Scott JT: Influence of
80. Kidd KL, Peter JB: Erosive osteoarthri- trauma on the development of chronic intlam-
tis. Radiology 86:640, 1966 matory polyarthritis. Ann Rheum Dis 26:532,
81. Swezey RL, Alexander SJ: Erosive I967
osteoarthritis and the main en lorgnette defor- 99. Cotton DK, Mier PD: An hypothesis on
mity. Arch Intern Med 128:269, 1971 the aetiology of psoriasis. Br J Dermatol 76:
82. Smukler NM, Edeiken J, Giuliano, VJ: 519, 1964
Ankylosis in osteoarthritis of the finger joints. 100. Brailsford JF: The Radiology of Bones
Radiology 100:525, 1971 and Joints, ed 4. Churchill, London, 1953,
83. Hoede K: Zur Frage Erblichkeit der p 668
Psoriasis. Hautarzt 8:433, 1957 101. Weddell G, Cowan MA, Palmer E,
84. Lomholt G: Psoriasis: Prevalence, Ramaswamy S: Psoriatic skin. Arch Dermatol
Spontaneous Course and Genetics. A Census 91:252, 1965
Study on the Prevalence of Skin Diseases in the 102. Ross JB: The psoriatic capillary: its
Faroe Islands, Copenhagen, Gad, 1963, pp 157- nature and value in the identitication of the
184 unaffected psoriatic patient. Br J Dermatol
76:51 1, 1964
85. Steinberg AC, Becher SW, Fitzpatrick
103. Lawrence JS: in Discussion following:
TB, Kierland RR: A genetic and statistical
Microcirculatory studies of the skin on the in-
study of psoriasis. Am J Hum Genet 3:267, 1951
vestigation of seronegative polyarthritis,
86. Bauer J, Vogl A: Psoriasis und Gelen-
Thompson M, Holti G: 6th European Congress
kleiden. Klin Wschr 10:1700, 1931
of Rheumatology, Lisbon, 1967, pp 29 39
87. Tiedemann G: Symptomatologie und 104. Mustakallio KK, Lassus A: Staphy-
aetiologie der Psoriasis arthropathica. Z lococcal alpha-antitoxin in psoriatic arthrop-
Mensch Vererg Konstit Lehre 30:248, 1951 athy. Br J Dermatol 76:544, 1964
88. Ward JH, Stephens FE: Inheritance of 105. Mansson I, Olhagen, B: Intestinal
psoriasis in a Utah kindred. Arch Dermatol Clostridium perfringens in rheumatoid arthri-
84:589, 1961 tis and other connective tissue disorders. Stud-
89. Baker H, Golding DN, Thompson M: ies of fecal flora, serum antitoxin levels and
Atypical polyarthritis in psoriatic families. skin hypersensitivity. Acta Rheum Stand 12:
Br Med J 2:348, 1963 167, 1966
90. Theiss B, Schnyder UW, Bijni A, Wagen- 106. Landau JW, Gross BG, Newcomer
hauser F: Intrafamiliare Untersuchungen bei VD. Wright ET: Immunologic response of pa-
Psoriasis-Arthritis. Z Rheumaforsch 28:403, tients with psoriasrs. Arch Dermatol 91:607.
I969 1965
70 MOLL AND WRIGHT

107. Cornbleet T: Action of synthetic anti- ate) in connective tissue disease-psoriasis and
malarial drugs on psoriasis. J Invest Dermatol polyarthritis. Ann Rheum Dis 27:64, 1968
26:435, 1956 112. Chaouat Y, Kanovitch B, Faures B,
108. Cappelli, E: Abstract. A case of severe Grupper C, Bourgeois-Spinasse J: Le rhuma-
arthropathic pustulous psoriasis clearing tisme psoriasique. Traitement par le mttho-
up
during lndocid treatment. Excerpta Med 24: trexate. Rev Rhum Mal Osteoartic 38:453, 1971
16, 1970 113. Viglioglia PA, Plante GE, Viglioglia J,
Saraceno EF: Allopurinol in psoriasis. Derma-
109. Maxdyk H, Chwalinska-Sadowska H:
tologica 141:203, 1970
Results of treatment with Endoxan of the
114. Walz DT, Berkoff CE: Arthritis and
psoriatic arthropathy and of rheumatoid ar-
psoriasis: the effects of antipsoriatic agents in
thritis. Reumatologia 6: I I 1, 1968
the adjuvant-induced arthritic rat (35138). Proc
110. O’Brien WM. Scott EJ Van, Black RL, Sot Exp Biol Med 135:760, 1970
Eisen AZ, Bunim JJ: Clinical trial of amethop- 115. Ktimmerle F, Wessinghage D,
terin (Methotrexate) in psoriatic and rheuma- Schweikert CH: Risks of alloplastic replace-
toid arthritis. Arthritis Rheum 5:3 12. 1962 ments in degenerative and inflammatory dis-
I 1 1. Kersley GD: Amethopterin (Methotrex- eases of joints. Acta Orthop Belg 37:541, 197 1

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