Auergrumbach, Piet

Kerl, Helmut

Soyer, H. Peter

Wolf, Peter

University of Queensland eSpace

out that invasion and metastasis in typical Bowen's disease is
not common, and the absence of a fully documented case with
metastatic disease cannot be used to eliminate the possibility
that malignant transformation may rarely occur.
Another possible factor in the development of these lesions
could be human papilloma virus. Recently, human papilloma
virus has been found in some seborrheic kératoses with histo¬
logie changes consistent with a viral effect.8 Human papilloma
virus has been associated with various tumors and is felt to be
a cofactor in the development of at least some malignancies.9
The most striking feature of the lesion we report is that it is
a mucin-positive adenocarcinoma arising in the center of a
lesion clinically and histologically seborrheic keratosis. In this
case, there are three possible explanations for the occurrence
of adenocarcinoma in seborrheic keratosis. These include me¬
tastasis from a distant primary tumor to the seborrheic kera¬
tosis, incidental origin of an adnexal carcinoma at the site of
the seborrheic keratosis, and origin of an adenocarcinoma
from the seborrheic keratosis. Since no other primary tumor
was found, and since there was no evidence of any other
cutaneous or malignant tumor after 10 years, the adenocarci¬
noma was probably not a metastasis. While incidental origin
at the site of a seborrheic keratosis cannot be absolutely
disproven, an epidermal origin of seborrheic keratosis is sup¬
ported by direct dermal invasion of the tumor from the epider¬
mis rather than from an adnexal structure, the central loca¬
tion of the adenocarcinoma, and the clinical history. As with
some cases of extramammary Paget's disease, in which rau-
cin-producing epithelial cells are present within the epidermis
with no primary tumor and with no evidence of adnexal
involvement, only theories exist to explain this phenomenon.
These theories could include malignant transformation of a
pluripotential germinative cell within the epidermis or trans¬
formation of a cell from the distal portion of an adnexal
structure located within the epidermis. Cells from these
structures would be at least partially committed toward ad¬
nexal differentiation.
LTC Kathleen J. Smith, MC, USA
Department ofDermatology
Walter Reed Army Medical Center
Washington, DC 20307
CDR Henry G. Skelton III, MC, USA
COL George P. Lupton, MC, USA
Department ofDermatopathology
Armed Forces Institute ofPathology
Washington, DC 20306
NolaJ. Palomino, MD
Department ofPathology
Miami Valley Hospital
Dayton, OH 45409
1. Baer RL, Garcia RL, Partsalidou V, Ackermann AB. Papillated squa-
mous cell carcinoma in situ arising in a seborrheic keratosis. J Am Acad
Dermatol. 1981;5:561-565.
2. Goette DK. Basal cell carcinoma arising in seborrheic keratosis. JDerma-
tol Surg Oncol. 1985;1:1014-1016.
3. Christeler A, Delacretaz J. Verrues s\l=e'\borrh\l=e'\iqueset transformation
maligne. Dermtologica. 1966;133:33-39.
4. Kwittken J. Squamous cell carcinoma arising in seborrheic keratosis. Mt
Sinai JMed. 1981;48:61-62.
5. Bloch PH. Transformation of seborrheic keratosis in Bowen's disease. J
Cutan Pathol. 1978;5:361-367.
6. Monteagudo JC, Jorda E, Terencio C, Llombort-Bosch A. Squamous cell
carcinoma in situ (Bowen's disease) arising in seborrheic keratosis: three
lesions in two patients. J Cutan Pathol. 1989;16:348-352.
7. Clemmensen OJ, Sjolin KE. Malignancy in seborrheic keratoses. Acta
Derm Venereol (Stockh). 1986;66:158-161.
8. Zhao Y, Lin Y, Luo R, et al. Human papillomavirus (HPV) infection in
seborrheic keratosis. Am J Dermatopathol.1989;11:209-212.
9. Arends MJ, Wyllie AH, Bird CC. Papillomaviruses and human cancer.
Hum Pathol. 1990;21:686-698.
Widespread Cutaneous Necrosis in a Patient
With Rheumatoid Arthritis Associated With
Anticardiolipin Antibodies
To the Editor. \p=m-\Antiphospholipid antibodies, detected by the
presence of lupus anticoagulant and/or abnormally high levels
of anticardiolipin antibodies, have been shown to be associ-
ated with an increased risk of arterial or venous thrombosis.
The association between antiphospholipid antibodies and
thrombotic events was first noted in patients with systemic
lupus erythematosus but were later also observed in a variety
of other disorders and as an isolated finding. The existence of
a separate entity, the anticardiolipin or antiphospholipid syn-
drome, was suggested in several studies.1 Cutaneous symp-
toms linked to the antiphospholipid syndrome include throm-
bophlebitis, leg ulcers, livedo reticularis, livedo vasculitis,
unfading acral microlivedo, peripheral gangrene, hemor-
rhage (ecchymosis and hematoma), and necrotizing purpu-
ra. 1,2 We observed widespread cutaneous necrosis3 as a rare
manifestation of the antiphospholipid syndrome in a patient
with rheumatoid arthritis.
Report of a Case.\p=m-\A 73-year-old woman with long-standing de-
forming arthritis, fulfilling the criteria of the American College of
Rheumatism, Atlanta, Ga (formerly the Arthritis and Rheumatism
Association), for "classic" rheumatoid arthritis, was admitted to our
department in July 1988 because ofpainful widespread skin lesions of
4 days' duration. On clinical examination, several sharply demar¬
cated, hemorrhagic patches with a bizarre configuration were ob¬
served on her arms (Fig 1), breasts, and legs.
A skin biopsy specimen of a hemorrhagic area on the left thigh (Fig
2) revealed thrombi within capillaries, venules, and small- and medi¬
um-sized vessels throughout the dermis and subcutaneous fat with¬
out any evidence of fibrin in the vessel walls. No nuclear "dust" was
present. In addition, a sparse, perivascular mixed-cell infiltrate and
extravasation oferythrocytes was observed.
Results or findings from laboratory studies were as follows: eryth-
rocyte sedimentation rate, 108 mm/h; erythrocytes, 3.97x10 L;
hemoglobin, 87 g/L; leukocytes, 6.9 x 109/L, with 0.69 neutrophils,
0.1 band forms, 0.1 eosinophils, and 0.29 lymphocytes; platelets,
336 x 109/L; serum electrolyte, serum urea nitrogen level, serum
glucose level, and urinalysis, normal; liver function test results,
Fig 1.—Widespread cutaneous necrosis. Sharply demarcated, hem¬
orrhagic patches with bizarre configuration on the left arm.
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normal, except for the alkaline phosphatase level (216 U/L) and the
cholinesterase level (3395 U/L); direct Coomb's test, VDRL, and the
test for cryoglobulins, negative; immunoelectrophoresis, increase of
polyclonal immunoglobulins; latex rheumatoid factor, 3390 U/mL;
and latex C-reactive protein, 32 mg/L (both positive); antinuclear
antibodies, 1:1280 (speckled type, positive titer); antibodies against
double-stranded DNA, Sjögren syndrome associated antigens A and
B, SM-SCL-70, and nuclear ribonucleoprotein, not detectable; par¬
tial thromboplastin time, Russell's viper venom test, and prothrom-
bin time, normal; lupus anticoagulant, none detected; tests for clot¬
ting factors, fibrinogen, 4.8 g/L; factor II, 0.82; factor V, 0.74; factor
X, 0.74; factor III, 0.66; protein C, 0.75; enzyme-linked immunosor-
bent assay for anticardiolipin antibodies, IgG, 27.7 U/mL (normal,
<12.0 U/mL); and IgM, 3.5 U/mL (normal, <6 U/mL) (Elias, Frei¬
burg, Germany).
Initial therapy was prednisolone (50 mg/d). Within 7 weeks, skin
lesions healed with moderate scarring. Six months later, anticardioli¬
pin antibodies were still present but the level was clearly reduced(IgG, 15.7 U/mL).
Comment.—Widespread cutaneous necrosis, which is
characterized by painful purpuric and necrotic areas with
underlying dermal thrombosis, was first reported by Dodd et
al3 in 1985 in a patient with lupus anticoagulant. Subsequent¬
ly, further cases with identical clinical and histologie features,
but different serological profile of antiphospholipid antibod¬
ies, were described in systemic lupus erythematosus and in
patients with no demonstrable underlying disease (Table).u
Cutaneous phenomena, including purpura resulting from
disseminated intravascular coagulation, coumarin necrosis,
coumarin-induced skin lesions in protein C deficiency, hepa-
rin necrosis, and purpura cryoglobulinemia, may present as
widespread cutaneous necrosis, and all of these conditions
should be considered in the clinical differential diagnosis. The
significance of anticardiolipin antibodies in the development
of skin lesions in our patient is suspected because of the lack of
other possible causes and because the titer of these antibodies
decreased after therapy. The histologie findings of thrombo¬
sis in dermal and subcutaneous vessels without any evidence
of leukocytoclastic vasculitis is also characteristic for skin
lesions of the antiphospholipid syndrome.1,2
Antiphospholipid antibodies in rheumatoid arthritis have
been investigated in a number of studies, but estimates of its
prevalence are conflicting and the clinical implications of
these antibodies in rheumatoid arthritis remain controversial
at present.M Our case, however, shows that anticardiolipin
antibodies may be involved at least occasionally in the patho¬
genesis of skin lesions in rheumatoid arthritis.
Fig 2.—Widespread cutaneous necrosis. Thrombi within dermal ves¬
sels (arrows). Extravasated erythrocytes in the papillary dermis. No
signs of vasculitis.
Reports of Widespread Cutaneous Necrosis Associated
With Antiphospholipid Antibodies *
No. of Underlying
Source, y Cases Disease ACA LAC VDRL ds-DNA
Dodd et al,3
1985 1 No ND + ND
-
Frances et al,"
1989 3f SLE - +
O'Neill et al,5
1990 1 No
Present case 1 RA
*ACA indicates anticardiolipin antibodies; LAC, lupus anticoagulant;
ds-DNA double-stranded DNA antibodies; RA, rheumatoid arthritis; ND,
not done; plus sign, condition present; and minus sign, condition absent.
fAII three reported cases revealed the same sérologie profile.
Peter Wolf, MD
H. Peter Soyer, MD
Piet Auer-Grumbach, MD
Helmut Kerl, MD
Department ofDermatology
University ofGraz
Auenbruggerplatz 8
8036 Graz, Austria
1. Sontheimer RD. The anticardiolipin syndrome: a new way to slice an old
pie, or a new pie to slice? Arch Dermatol. 1987;123:590-595.
2. Alegre VA, Gastineau DA, Winkelmann RK. Skin lesions associated with
circulating lupus anticoagulant. Br J Dermatol. 1989;120:419-429.
3. Dodd HJ, Sarkany I, O'Shaughnessy D. Widespread cutaneous necrosis
associated with the lupus anticoagulant. Clin Exp Dermatol. 1985;10:581-586.
4. Frances C, Tribout B, Boisnic S, et al. Cutaneous necrosis associated with
the lupus anticoagulant. Dermatologica. 1989;178:194-201.
5. O'Neill A, Gatenby PA, McGaw B, Painter DM, McKenzie PR. Wide-
spread cutaneous necrosis associated with cardiolipin antibodies. J Am Acad
Dermatol. 1990;22:356-359.
6. Keane A, Woods R, Dowding V, Roden D, Barry C. Anticardiolipin
antibodies in rheumatoid arthritis. Br J Rheumatol. 1987;26:346-350.
7. Love PE, Santoro SA. Antiphospholipid antibodies: anticardiolipin and
the lupus anticoagulant in systemic lupus erythematosus (SLE) and in non-
SLE disorders: prevalence and clinical significance (review). Ann Intern Med.
1990;112:682-698.
Friction Dermatitis of the Thumbs
Caused by Pantyhose
To the Editor. \p=m-\Dermatitisof the volar aspect of the thumb
pads can be a difficult problem in clinical diagnosis. The thick
skin here is rather resistant to many contactants, but friction
may produce irritation.
Report of a Case.\p=m-\A 57-year-old woman was seen because of
persistent fissured dermatitis limited to the volar aspect of the thumb
pads. When asked if some activities had become awkward or difficult
because of the dermatitis, she answered that none had, but then
added, "Except for putting on my pantyhose."
Millions of women carry out this daily maneuver that puts quite a
lot of friction on the volar aspect of the thumb pads. Consider the
following: the garment is gathered up, one leg at a time, thumbs on
the inside. The toes are put in and the user, maintaining lateral
pressure with the thumbs, pulls the garment up into place. It is
during this latter action that the thumb pads run quickly up a long
length of nylon. Repeated daily, this may produce enough of a fric-
tional stimulus to cause skin irritation.
"It was the pantyhose that caused the problem," the patient wrote
in a follow-up letter. "It has only come back (the dermatitis) when I
use a certain type hose and/or don't protect the area from the abrasive
pressure caused by pulling on the hose."
Comment. —Here is yet another example of the value of
careful history taking when faced with a puzzling clinical
problem.
William M. Gould, MD
Department ofDermatology
Stanford University
Stanford, CA 94305
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Widespread Cutaneous Necrosis in a Patient with Rheumatoid-Arthritis Associated with Anticardiolipin Antibodies

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Widespread Cutaneous Necrosis in a Patient with Rheumatoid-Arthritis Associated with Anticardiolipin Antibodies

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