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Successful use of tetracycline pleurodesis to treat massive pleural effusion secondary to systemic lupus erythematosus.

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Successful use of tetracycline pleurodesis to treat
massive pleural effusion secondary to
systemic lupus erythematosus
Systemic lupus erythematosus (SLE)is complicated
by secondary lung or pleural lesions in 4&50% of patients,
with pleuritis or pleural effusions being the most common
clinical manifestations of thoracic involvement ( I ,2)- The
effusions are exudative, often bilateral, and usually responsive to systemic steroid therapy.
Herein we describe a patient with recurrent, rightsided pleural effusion secondary to SLE. The pleural effusion was refractory to systemic steroid therapy, intravenous
pulses of cyclophosphamide, and oral azathioprine. It was
ultimately controlled after tetracycline pleurodesis, which
enabled the patient to discontinue systemic steroid treatment. To our knowledge, this is the first report in the US
literature of tetracycline pleurodesis treatment for a pleural
effusion secondary to SLE.Tetracycline, a sclerosing agent
when applied to the pleural surfaces, has been a wellaccepted method to control malignant pleural effusions,
which are commonly nonresponsive to systemic therapy (3,4).
The patient, a 32-year-old black man, presented in
June 1987 with a 3-month history of fever, fatigue, 20-lb
weight loss, polyarthralgias, malar rash, and dyspnea on
exertion. Laboratory investigations revealed a hemoglobin
level of 90 g d i t e r (normal 140-180), a Westergren erythrocyte sedimentation rate of I I 1 mdhour, positive antinuclear
antibodies (titer > 1:80, speckled pattern), positive antidouble-stranded DNA (anti-dsDNA; Crithidiu method), negative rheumatoid factor by latex fixation, and trace protein
on urinalysis. Chest radiography showed a large left pleural
The patient underwent left-sided thoracentesis,
yielding 1.0 liter of cloudy yellow, sterile fluid. The pleural
fluid had a pH of 7.30. 11 1 red blood celldhigh power field
(HPF), 1,022 white blood cells/HPF, and a glucose level of
3.72 mmoleslliter (plasma glucose 4.77 mmoles/liter; normal
3.9-6.1). The cytologic findings were interpreted as demonstrating nonspecific inflammation.
Renal biopsy showed proliferative glomerulonephritis, and the patient was started on a regimen of prednisone,
60 mglday, followed by 2 subsequent monthly intravenous
pulses of cyclophosphamide. 750 mg. The patient was then
lost to followup due to noncompliance. Three months later,
he preseqted to the clinic with respiratory distress and
bilateral pleural effusions. He was taking prednisone, 10 mg
every other day. A right-sided thoracentesis yielded 2.0
liters of sterile exudative fluid. The prednisone dosage was
increased to 30 mglday, and the patient’s condition improved. Attempts over the next 8 months to taper the
prednisone to <30 mglday were unsuccessful due to recurrent symptoms of dyspnea on exertion accompanied by
persistent pleural effusions (now on the right side more than
the left).
In December 1988, azathioprine, 100 mg/day, was
Arthritis and Rheumatism, Vol. 34, No. 11 (November 1991)
added to the treatment regimen. The azathioprine proved to
not have a significant effect on the steroid dosage required,
the symptoms, or the radiographic appearance of the pleyral
effusions, over a 2-month period. It was discontinued, and
the decision was made to try tetracycline pleurodesis on the
larger, right-sided pleural effusion. The tight hemithorax was
drained after tube thoracostomy, and tetracycline, 20 mdkg,
was instilled. This procedure was repeated 2 weeks later,
because of reaccumulation of fluid. A satisfactory pleurpdesis was then accomplished.
Over the next 18 months, the prednisone was gradually tapered and finally discontinued. Chest radiographic
findings and respiratory symptoms remained stable. The
patient has remained free of steroid treatment for 6 months,
with occasional mild shortness of breath and arthralgias.
Pleural effusions secondary to SLE are rarely nonresponsive to steroid therapy. A review of the Englishlanguage literature has revealed 3 other reports that discuss
management of steroid-resistant pleural effusions secondary
to SLE;their treatment included talc poudrage, tetracycline
pleurodesis, and pleurectomy, respectively (5-7). Two of the
3 patients described in those reports were similar to our
patient in several respects (5,7). The patients were men in
their early thirties with positive dsDNA antibodies, renal
involvement, and large pleural effusions that were nonresponsive to immunosuppressiveagents, including corticosteroids and azathioprine. The case discussed herein is the third
report of a patient treated successfully with a manipulative
procedure that promotes pleural adhesion; this treatment
enabled discontinuation of systemic steroid therapy in our
patient. Gilleece et al ( 6 ) theorized that steroid-resistant
pleural effusions would be refractory to other types of
immunosuppressive therapy, and this observation was supported by the findings in our patient and those reported by
others (5.7); in our patient, the specific immunosuppressive
agents that were tried were intravenous pulse cyclophosphamide and oral azathioprine.
The pathogenesis of pleural inflammation and effusion in SLE is probably related to immune complexes and
complement consumption at the pleural membrane (8,9).
Thus, removal of the pleural membrane, whether by chemical or surgical means, may suppress inflammation and fluid
accumulation within the pleural space. The fact that pleurectomy, in addition to chemical sclerotherapy, also has been
used successfully to treat SLE pleural effusions and chronic
pleurisy lends credence to this theory on the pathogenesis of
inflammation and fluid accumulation (10).
Although pleural effusions dcre to SLE are usually
managed effectively with antiinflammatory drugs, especially
corticosteroids, there are instances when this therapy fails,
for reasons that are as yet unclear. Pleural sclerotherapy
may then be a very effective treatment option. Patients with
large symptomatic effusionsand relatively limiteq extrapleural manifestations would seem to be the most likely to benefit
from this procedure, potentially allowing the qjscontinuation
of corticosteroid therapy or reduction of the dosage. Tetracycline pleurodesis is especially attractive in these cases,
because it is less invasive compared with the thoracotomy
that is required for pleurectomy or for talc pleurodesis.
Kevin M. McKnight, Y D
Norman E. Adair, MD
Carlos A. Agudelo, MD
Bowman Gray School of Medicine
Winston-Salem, NC
I Matthay RA, Schwarz MI. Petty TL. Stanford RE, Gupta RC.
Sahn SA, Steigerwald JC: Pulmonary manifestations of systemic lupus erythematosus: review of 12 cases of acute lupus
pneumonitis. Medicine (Baltimore) 54:397409, 1974
2. Haupt M, Moore GW.Hutchins GM: The lung in systemic lupus
erythematosus: analysis of the pathogenic phanges in 120 patients. Am J Med 713789-791, 1981
3. Horvath T, Orosz E, Czenkar B: Management of malignant
pleural effusion by tetracycline pleurodesis. Orv Hetil 130: 10511052, 1989
Landvater L, Hix WR. Mills M, Siege1 RS, Aaron BL: Malignant pleural effusion treated by tetracycline sclerotherapy: a
comparison of single vs repeated instillation. Chest 93:1196-
Kaine JL: Refractory massive pleural effusion in systemic lupus
erythematosus treated with talc poudrage. Ann Rheum Dis
1198, 1988
44:6144, 1985
Gilleece MH, Evans CC, Bucknall RC:Steroid resistant pleural
effusion in systemic lupus erythematosus treated with tetracycline pleurodesis. Ann Rheum Dis 47:1031-1032, 1988
7. Elborn JS, Conn P, Roberts SD: Refractory massive pleural
effusion in systemic lupus erythematosus treated by pleurectomy. Ann Rheum Dis 46:77-80, 1987
8. Inour T, Kanayama Y,Ohe A, Kato N, Horiguchi T, lshii M,
Shiota K: Immunopathologic studies of pneumonitis in systemic
lupus erythematosus. Ann Intern Med 91:3&34, 1979
9. Halla JT, Schrohenloher RE, Volanakis JE: Immune complexes
and other laboratory features of pleural effusions. Ann Intern
Med 92:748-752, 1980
10. Bell R. Lawrence DS: Chronic pleurisy in systemic lupus
erythematosustreated with pleurectomy. Br J Dis Chest 793146.
316, 1979
Achromobacfer xylosoxidans septic arthritis in a
patient with systemic lupus erythematosus
Achromobacter xylosoxidans was originally proposed as a distinctive organism in 1971 ( I ) . Since then this
gram-negative, opportunistic, oxidase-positive, flagellated
bacillus has been demonstrated to be the causative agent in
a variety of infections, mainly affecting children and elderly
persons ( 2 4 ) . Achromobacter has been isolated from blood,
cerebrospinal fluid, urine, feces, pleural and peritoneal fluid,
respiratory secretions, wounds, and swab material from
ears, eyes, and pharynx (2). In most reports of A xylosoxiduns infection, the infection has occurred in association with
a nosocomial outbreak (5.7). The organism has never before
been described as a cause of septic arthritis. We report
herein a case of septic arthritis associated with A xylosoxiduns infection in a patient with systemic lupus erythematosus (SLE).
The patient, a 41-year-old woman, had been diagnosed as having SLE when she was 17 years old. She since
had multiple complications, including thrombocytopenia.
pericarditis, nephritis, Raynaud’s phenomenon, arthritis,
and an occipital stroke. She presented to the emergency
room reporting the presence of pain and swelling in her right
extremities, and low-grade fever and chills of 1 night’s
duration. She had been taking long-term antibiotic therapy
for staphylococcal infection of a distal interphalangeal (DIP)
joint. Her history of recent environmental exposure was
pertinent in that she had been drinking well water described
as discolored and odoriferous.
Physical examination revealed decreased visual acuity, cushingoid facies, multiple lip ulcers, bony hypertrophy
of the DIP joint of the left third finger, which was fixed in
flexion, and swelling of the right hand, right wrist, right
ankle, and inner portion of the right knee. Cultures of blood
withdrawn in the emergency room grew A xylosoxidans,
which was sensitive to ceftazidime, mezlocillin, and trimethopridsulfamethoxazole. She was initially prescribed nafcillin and ceftazidime for possible sepsis, and her steroid
dosage was tapered. She remained afebrile for 2 days on this
regimen, but fever recurred on the third hospital day. The
ceftazidime dosage was increased to 2 gm every 8 hours. She
continued to have fevers through 8 days of ceftazidime
therapy, so mezlocillin. 3 gm every 6 hours, was added to the
regimen. She improved clinically and was discharged, having completed a ICday course each of ceftazidime and
Two weeks later, the patient was readmitted with
cellulitis of the right ankle, knee, and wrist. An effusion in
the right knee was noted, and cultures of aspirates grew A
xylosoxidans. The patient underwent serial needle aspirations, which were unsuccessful, and arthroscopic debridement plus a I-month course of intravenous piperacillin.
After 2 months, she returned to the Flinic and reported minimal swelling, pain, and warmth in the knee. The
synovial fluid white blood cell count was 36,000/mm3, with
87% neutrophils, 3% lymphocytes, and 10% macrophages.
Synovial fluid cultures initially gave negative results, but the
organism was detected again before the final report. The
patient required a repeat arthroscopic synovectomy and 6
weeks of ceftazidime therapy, 3 gm intravenously every 6
hours. To date, the knee has remained swollen but not
tender, and the most recent joint aspiration yielded a small
amount of fluid with 700 white blood cells/mm3 and negative
culture results. The most recent radiographs show a joint
effusion and patchy osteoporosis, but no evidence of joint
space narrowing or bony destruction (Figure I).
There have been reports of only 4 cases of community-acquired sepsis with A xylosoxidans (2,8). All 4 patients
were elderly; 2 had bacteremic pneumonia and 2 had metastatic carcinoma. Other features, as well, make our patient’s
case unique: This is the first report of infection with this
organism affecting a joint.
Impaired immune function induced by long-term
immunosuppressive therapy as well as by the underlying
disease makes patients with SLE prime candidates for
infection. However, A xylosoxidans infection has not been
reported previously in a patient with SLE.Our patient was
younger than those previously described and was not acutely
ill at the onset of the infection. She presumably acquired the
infection from her well water. It is notable that, although the
infection was so refractory to treatment, the organism was
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pleural, massivy, lupus, effusion, systemic, tetracyclic, secondary, erythematosus, successful, treaty, pleurodesis, use
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