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Vasculitis of the breast. An unusual manifestation of polyarteritis

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An Unusual Manifestation of Polyarteritis
Francis J. Dega and Gene G. Hunder
A 72-year-old woman had a tender breast mass due to arteritis. A diagnosis of polyarteritis rather than cranial or focal arteritis (as suspected
in previously reported similar cases) was indicated by a muscle biopsy,
which showed arteritis, and a temporal artery biopsy, which was normal.
Although vascular lesions in polyarteritis
are usually widespread, clinically evident
lesions in the breast rarely have been reported. A patient with polyarteritis, whose
initial symptoms were due to involvement
of arteries in the breast, is reported.
REPORT OF A CASE
A 72-year-old white housewife was seen on May
5, 1965. She was well until March 1965. when she
noted a firm, tender mass (2 X 3 cm) in the upper
portion of the left breast. Biopsy of the tumor revealed panarteritis with rare giant cells (Figure 1
and 2). Several days after the biopsy, she noted
onset of aching in both calves. In the ensuing
weeks, the aching, described as “burning,” became
worse and spread to include the thighs, hip and
shoulder girdles, arms, forearms, and both breasts.
Pain in the extremities was worse with movement,
and she felt weak. She had di5culty getting out of
bed. Night sweats, severe fatigue, and anorexia deFrom the Mayo Clinic and Mayo Foundation,
Rochester, Minnesota. FRANCIS J DEGA, MD: Resident in Rheumatology, Mayo Graduate School of
Medicine (University of Minnesota), Rochester, Minnesota; GENE G HUNDER. MD, MS (Medicine), FACP:
Consultant, Division of Rheumatology and Internal
Medicine, Mayo Clinic and Mayo Foundation; Associate Professor of Medicine, Mayo Medical School,
Rochester, Minnesota.
Address reprint requests to Dr. G G Hunder.
Division of Rheumatology, Mayo Clinic, 200 First
Street SW, Rochester, MN 55901.
Submitted for publication March 26, 1974; accepted June 17, 1974.
veloped, and she lost 6.8 kg. She had no history of
allergies, joint swelling, erythema, phlebitis, claudication, headaches, or visual impairment.
Examination on May 5, 1965, revealed that she
was chronically ill and could not walk without support because of unsteadiness. Her temperature was
37.2”C and her pulse 100 beats/min, with a regular
rhythm. Blood pressure was 105/70 mm Hg in both
arms (patient sitting). Optic fundi, lungs, and heart
were normal. The liver edge was palpated at the
right costal margin. Moderate motor weakness and
muscle tenderness were noted, especially involving
muscles of the pelvic and shoulder girdles and
calves. All arterial pulses, including the temporal
arteries, were normal. No bruits were audible over
the carotid or subclavian arteries or the orbits.
Several small (0.5 X 1 cm), firm, discrete, nontender
nodules were present in both breasts. The site of
the recent breast biopsy was healing well.
Laboratory tests revealed the following: Hemoglobin 10.5 g/100 ml and leukocytes 9,500/mma,
with 84y0 neutrophils, 4% monocytes, 11% lymphocytes, and 1% eosinophils. T h e ESR was 112 mm
in 1 hour (Westergren). Urinalysis showed a specific
gravity of 1.012, acid pH, grade 1 protein, and grade
3 leukocytes. The fasting blood sugar level was 94
mg/lOO (normal: 65 to 90), the serum albumin was
1.32 g/100 ml, al-globulin 0.69 g/100 ml, ar-globulin
1.18 g/100 ml, p-globulin 0.66 g/100 ml, and 7-globulin 0.80 g/100 ml. The alkaline phosphatase value
was 25.4 U/100 ml (normal up to 14), the serum
glutamic oxalacetic transaminase (SGOT) was 42 U/
liter (normal up to 24). T h e blood creatinine level,
creatinine kinase value, Venereal Disease Research
Laboratories test, prothrombin consumption, LE clot
test, bilirubin level, amylase level, electrocardiogram,
and roentgenograms of the chest, kidneys, and stom-
AlthrIUr and Rheumatism, Vol. 17, No. 6 (November-December 1974)
973
DEGAANDHUNDER
Fig 1. Breast artery showing panarteritis
with disruption of internal elastic lamina
and extensive thickening of subintimal tissues with nearly complete obliteration of
arterial lumen (H&E, X64).
ach were negative or normal. Urine culture grew
Aerobacter aerogenes, and acetyl sulfisoxazole was
given. A later repeat culture showed no growth.
A daily temperature to 38.6"C continued. On
May 18, a right temporal artery biopsy (specimen
2.5 cm in length) and a right triceps muscle biopsy were performed. The temporal artery was
normal, but the right triceps muscle showed acute
necrotizing panarteritis involving small arteries and
normal striated muscle (Figure 3).
Prednisone was started in a dose of 10 mg every
6 hours. Within 24 hours, the patient became afebrile, the muscle pains diminished, and she rapidly
felt stronger.
She returned on August 5 , 1965, at which time
she was taking 10 mg of prednisone daily. Except
for the slight muscle pain, which developed after
974
Fig 2. Same as left but showing multinucleated giant cell in arterial media (H&E,
X400).
the last reduction in the dose of prednisone, she
felt well. Physical examination was normal. Several
very small breast lumps were noted as before and
considered to represent fibrocystic disease. The
hemoglobin was 12.0 g/lOO ml. leukocyte count
10,000/mm3, ESR (Westergren) 98 mm in 1 hour,
and SGOT level was normal. During the ensuing
months, the dose of prednisone was gradually reduced further and symptoms did not recur. The
patient discontinued prednisone completely in 1968
and was asymptomatic when last seen in December
1973.
DISCUSSION
The specific diagnosis or categorization
of a case of arteritis usually depends on
clinical manifestations and the size and dis-
Arthritis and Rheumatism, Vol. 17, No. 6 (November-December 1974)
VASCULlTlS OF THE BREAST IN POLYARTERITIS
ment of small muscle arteries has not been
reported in temporal arteritis even though
lesions may be widespread (1,2,4).
Arteritis of the breast has been noted at
autopsy when no breast lesions were clinically evident (5,6), but few patients with
prominent symptoms related to arteries of
the breast have been described. Waugh (7)
described a 64-year-old woman in whom a
painful lump in each breast was due to
necrotizing arteritis of medium-sized arteries. Disruption of the internal elastic lamina and thrombosis were seen in both biopsy specimens and giant cells in one. The
patient had a “greatly elevated’ sedimentation rate, but felt well 16 months later.
Waugh (7) concluded that this patient had
a variant temporal arteritis because of her
age, the high erythrocyte sedimentation
rate, involvement of medium-sized arteries
in a random fashion showing giant cells on
histologic examination, and the apparent
self-limited course.
McCarty and co-workers (8) described a
Fig 3. Muscle biopsy showing fibrinoid necrosis 66-year-old woman who had multiple, tenof small muscular artery walls and surrounding der lumps in both breasts due to arteritis.
inflammatory reaction (HBE, Xl60).
Four months previously, a clinical diagnosis of temporal arteritis had been made on
the basis of headaches and scalp tenderness.
tribution of the vessels involved. In ouI The patient had improved on 20 mg of
case, polymyalgia rheumatica with temporal prednisone daily, but later the tender breast
arteritis was suggested because the patient nodules appeared. A biopsied breast nodule
was more than 50 years old and had proxi- showed acute necrotizing panarteritis inmal muscular aching, elevated erythrocyte volving small arteries and arterioles. The
sedimentation rate, and rare giant cells in pain and evidence of inflammation of the
the breast artery wall. The small artery dis- breasts subsided in response to prednisone
ease, but normal temporal artery, shown on therapy (60 mg daily), but returned when
muscle biopsy indicated polyarteritis rather the dose was reduced below 20 mg daily.
than temporal arteritis (used synonymously When seen 17 months later, no clinical eviwith cranial arteritis and giant cell arteri- dence of arteritis had developed elsewhere.
tis). Giant cells are recognized as being most At no time was the sedimentation rate
commonly associated with temporal arteri- elevated. McCarty and co-workers (8) betis, but they are not completely diagnostic lieved that the findings suggested an unof that disease (1-3). I n addition, involve- usual example of focal arteritis rather than
Arthritis and Rheumatism, Vol. 17, No. 8 (November-December 1974)
975
DEGA AND HUNDER
a variant of temporal arteritis or Mondor’s
disease (9). The breast lesion resembled
panarteritis typical of polyarteritis nodosa,
but systemic features were absent. However,
biopsy specimens of other tissues were not
taken.
Two other patients (one man and one
woman) clinically thought to have Mondor’s
disease were described (10). Biopsy of the
vascular cords, however, showed arterial lesions rather than venous involvement. Neither patient had systemic symptoms or findings.
Thus, our patient may be different from
those in the previous reports, but evidence
to completely define the differences is lacking. Waugh (7) believed that his patient
had temporal arteritis, but he did not demonstrate temporal or other artery involvement. His patient’s “systemic reaction,” like
that of our patient, may have been secondary to polyarteritis in spite of the giant cells
seen on one breast biopsy specimen. Similarly, the possibility of systemic arteritis
in the patient reported by McCarty and coworkers (8) was not completely excluded.
The headaches, sweats, numbness, and
“burning” sensations of the extremities
could have been the result of intermittent
fevers and a mild transient peripheral neuropathy on the basis of diffuse polyarteritis.
The symptomatic improvement after 20 mg
of prednisone daily and the subsequent a p
pearance of breast lesions due to arteritis
are compatible with partially suppressed
polyarteritis or a spontaneous exacerbation
of her disease or both. The normal erythrocyte sedimentation rates are valid evidence
against active cranial arteritis, although
normal sedimentation rates have been uncommonly seen in polyarteritis (1 1). Studies
976
of additional cases of arteritis of the breast
with clinically evident lesions using immunofluorescent techniques to search for viral
antigens, immunoglobulins, and complement in sections of these arteries (12) may
help determine whether or not these patients form a separate clinical syndrome.
REFERENCES
1. Hamilton CR Jr, Shelley WM, Tumulty
PA: Giant cell arteritis: including temporal
arteritis and polymyalgia rheumatica. Medicine 5O:l-27, 1971
2. Hamrin B: Polymyalgia arteritica. Acta Med
Scand (Suppl) 533:7-131, 1972
3. Nasu T: Pathology of pulseless disease: a
systematic study and critical review of twentyone autopsy cases reported in Japan. Angiology 14:225-242, 1963
4. Hunder GG, Ward LE, Burbank MK: Giantcell arteritis producing an aortic arch syndrome. Ann Intern Med 66:57&582, 1967
5. Moskowitz RW: Discussion. Arthritis Rheum
11:801-802, 1968
6. Schultz A: Cited by Sokoloff L: Discussion.
Arthritis Rheum 11:802-803, 1968
7. Waugh TR: Bilateral mammary arteritis:
report of a case. Am J Pathol 26:851-861,
1950
8. McCarty DJ, Imbrigia J, Hung JK: Vasculitis of the breasts. Arthritis Rheum 11:796801, 1968
9. Johnson WC, Wallrich R, Helwig EB: Superficial thrombophlebitis of the chest wall:
Mondor’s disease. JAMA 180:103-108, 1962
10. Hatteland K, Kluge T: Mondor’s disease: a
subcutaneous form of periarteritis nodosa?
Acta Chir Scand 129:67-71, 1965
11. Frohnert PR, Sheps SG: Long-term followup study of periarteritis nodosa. Am J Med
43:8-14, 1967
12. Gocke DJ, Hsu K, Morgan C, et al: Association between polyarteritis and Australia
antigen. Lancet 2:1149-1153, 1970
Arthritis and Rheumatism, Vol. 17, No. 6 (November-December 1974)
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