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LE cells in pleural fluid.

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LETTERS
936
One of 3 patients with normal parotid sialography in 1974 in whom the study was repeated has
now developed punctate sialectasia.
Three of the 4 patients with normal salivary scintiscans in the 1974 study have now become abnormal
with decreased salivary gland radionuclide uptake as
well as *“Tc-pertechnetate excretion in saliva.
It is apparent that with the passage of time, lupus
patients who had subclinical evidence of Sjogren’s syndrome develop sicca symptoms. It is not unlikely that
with longer followup, more or perhaps all of our lupus
patients will develop these symptoms, despite continued
vigilance and treatment. Although none of the 30 patients included in this reevaluation developed acute salivary gland swelling, we have seen this occur in other patients in our lupus clinic who previously had no other
clinical evidence of Sjogren’s syndrome. This occurrence has also been reported by Katz and Ehrlich (3).
All New Zealand black mice and their F, black/
white hybrids, which are animal models of SLE, develop lacrimal and salivary gland inflammatory infiltrates after 4 months of age (4). The reason for the high
prevalence of Sj8gren’s syndrome in human and murine
SLE, as well as in other autoimmune diseases, is not
known, but our findings indicate that in systemic lupus
erythematosus the frequency of sicca symptoms is cumulative and may be heralded by abnormalities in the
more sensitive roentgenographic, radionuclide, or pathologic tests.
MD
FRANCISCO
RAMOS-NIEMBRO,
DONATOALARC6N-SEGOVIA, M D
Department of Immunology and Rheumatology
Instituto Nacional de la Nutricidn
Mkxico 22, DF, Mkxico
REFERENCES
I . Alarc6n-Segovia D, Ibaiiez G, VelAzquez-Forero F,
Hernbdez-Ortiz J, Gonzhlez-Jimtnez Y: Sjogren’s syndrome in systemic lupus erythematosus: clinical and subclinical manifestations. Ann Intern Med 81:557-583, 1974
2. Alardn-Segovia D: Symptomatic Sjogren’s syndrome in
mixed connective tissue disease. J Rheumatol 3:191-195,
1976
3. Katz WA, Ehrlich GE: Acute salivary gland inflammation
associated with systemic lupus erythematosus. Ann Rheum
Dis 31:384-387, 1972
4. Kessler HS: A laboratory model for Sjogren’s syndrome.
Am J Pathol52:671-685, 1978
LE cells in pleural fluid
To the Editor:
The presence of LE cells in pleural fluid of patients with systemic lupus erythematosus (SLE), or procainamide and hydralazine induced lupus (PSLE), has
been previously reported (1-3). Although the association of SLE and PSLE is frequent, the LE phenomenon
in pleural fluid is seldom reported.
We recently published a report of a case (2) of
PSLE in which the initial manifestation of the disease
was the finding of LE cells in pleural fluid. Two further
cases of the in vivo LE phenomenon in pleural fluid
have been subsequently documented.
Case 1. A 71-year-old female experienced an
acute myocardial infarction. She was subsequently
treated with procainamide HC12 gm daily for 5 months.
She then developed right sided pleuritic chest pain.
Chest x-ray revealed pleural effusion. Wright stain of
the pleural fluid documented the presence of LE cells.
LE cells were subsequently found in blood. ANA was
positive in 1/SO00 dilution; however, antibodies to
double-stranded DNA were absent. The pleural fluid
resolved within 2 weeks after cessation of therapy with
procainamide. LE cells in blood were negative a month
later.
Case 2. A 69-year-old female was admitted with
complaints of fever and weakness of one month duration. A left pleural effusion was present on chest x-ray.
LE cells were visible by a Wright stain of the pleural
fluid. The presumptive diagnosis of SLE was confirmed
by the presence of LE cells in the blood, a strongly positive reaction for ANA in a 1/10 dilution, positive reaction for double-stranded DNA antibodies in a 1/1 reaction, and a low serum complement (C’3) of 43 mg%.
Subsequently, treatment with steroids was initiated and
the pleural effusion cleared rapidly.
The documentation of LE cells in pleural fluid of
3 patients over a 1-year period in one general internal
medicine ward suggests that this phenomenon is more
common than has previously been emphasized.
The appearance of LE cells in these effusions
may result from autoincubation of polymorphonuclear
leukocytes in the specific body space. Nucleoprotein is
released from stagnating cells and subsequently phagocytized by viable polymorphonuclear leukocytes. Thus
the specific milieu of the pleural space could explain the
early appearance of LE cells in the pleural fluid in all
our cases. We suggest that searching for LE cells in sus-
LETTERS
937
pected body effusions may be helpful in early diagnosis
of either SLE or PSLE.
RAFAELS.CAREL,MD
MENACHEM
S. SHAPIRO,
MD
OLINDACORDOBA,
MD
ROMAMTI
TARAGAN,
MD
ARONGUTMAN,
MD
Ramat-Gan, Israel
REFERENCES
Pandya MR, Agus B, Grady RF: In vivo LE phenomenon
in pleural fluid. Arthritis Rheum 19:962-963, 1976
Care1 RS, Shapiro MS, Shoham D, Gutman A: Lupus ery-
thematosus cells in pleural effusion. Chest 72:670-672, 1977
Weinstein J: Hypocomplementemia in hydralazine-associated systemic lupus erythematosus.Am J Med 65:553-556,
1978
Adrenocortical carcinoma in a patient with
systemic lupus erythematosus treated with
azathioprine
To the Editor:
We have observed the development of a rare malignancy, adrenocortical carcinoma, in a patient with
systemic lupus erythematosus (SLE) who was treated
with azathioprine. Adrenocortical carcinoma in a patient with SLE has not been described previously, nor
has the presence of this malignancy in a patient receiving azathioprine.
FP, a 47-year-old white male, was referred to the
Brooklyn Veterans Administration Medical Center in
June 1977 with a 4-week history of left flank pain, 4.5
kg weight loss, and fever. SLE had been diagnosed in
1959 at the time of the onset of arthritis and a positive
LE cell test. Over the succeeding years, he had multiple
manifestations of SLE including deforming arthritis,
pleural and pericardial effusions, grand ma1 seizures,
hemolytic anemia, and proteinuria. Eventually he fulfilled 6 of the 14 American Rheumatism Association
criteria for SLE ( I ) . Prednisone (up to a maximum dose
of 40 mg/day) was initiated in 1962. Azathioprine 100
mg three times a day was begun in 1974. From that time
until admission he received the azathioprine, prednisone 10 mg every other day, diphenylhydantoin sodium
300 mg/day, and phenobarbital 30 mg/day.
On physical examination the patient appeared
chronically ill. Blood pressure was 100/70 mm/Hg,
pulse 1OO/minute, respirations 16/minute, and temper-
ature was 38.5OC. There were no stigmata of Cushing's
syndrome. Tenderness and fullness were present in the
left flank, and the spleen and liver were palpated at the
costal margins. Proximal muscle weakness was found in
all extremities. Results of the remainder of the examination were normal.
Laboratory studies showed a hemoglobin of 8.9
gm%, hematocrit of 26%, and white blood count of
16,800 cells/mm-' with 84% polymorphonuclear leukocytes. Urinalysis was normal. Blood urea nitrogen was
38 mg% and serum creatinine was 2.5 mg%. Serum alkaline phosphatase, lactic dehydrogenase, and leucineaminopeptidase levels were elevated. Antinuclear antibody and LE tests were negative at this time; serum
complement levels were normal. Plasma cortisol levels
were normal but did not suppress after 48-hour administration of 2 or 8 mg/day of dexamethasone. Chest xray and skeletal survey were normal. Sonography and
angiography revealed a left solid suprarenal mass with
cystic areas. Liver, spleen, and bone scans revealed no
evidence of metastases.
At surgery, a 12 cm hemorrhagic tumor of the
left adrenal gland was removed. Histologically, the tumor was an undifferentiated carcinoma of the adrenal
cortex. One month after surgery, metastases to the skin,
brain, and ribs became apparent. Despite therapy with
1,l dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)
ethane, the patient's condition deteriorated. A right upper
lobe pulmonary infiltrate appeared, respiratory insufficiency and hypotension developed, and the patient
died. Autopsy permission was denied.
Adrenocortical carcinoma has not been reported
previously in either SLE or in patients receiving
azathioprine. In a study of 484 patients with SLE, a
higher incidence of cancer (3.7%) was found than in a
control population (2). Only 1 of 18 patients developing
malignancy had received an immunosuppressive drug
other than corticosteroids. The malignancies seen did
not differ in type from those occurring in the control
group. Another review of 70 patients with SLE reported
an 1 I .4% incidence of malignancy (3). Three-quarters of
these patients had been treated with immunosuppressive agents. Azathioprine has been implicated in
the 5% incidence of cancer in patients with renal transplants (4). Both the size of the azathioprine dose (300
mg/day in a man weighing 65 kilograms) and the duration of azathioprine therapy (3 years) were exceptional
in the patient reported here. It is not possible to be certain of the contribution of azathioprine to the development of this patient's adrenocortical cancer, however
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