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Inappropriate secretion of ADH in a patient with systemic lupus erythematosus.

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her scalp. trunk, and left leg, indicating hematologic dissemination.
Over the next week her skin rash and joint pains
completely resolved and she has been well since. She has
remained asymptomatic for the last 6 months. Herpes zoster
was confirmed by a greater than fourfold rise in her serum
complement fixation titer.
Discussion. The joint involvement in this patient
probably occurred from spread along nerves arising from the
dorsal root of L2. Both the femoral and obturator nerves
arise from the dorsal root of L2, 3,4. and supply branches to
the hip joint. In the previously reported case ( I ) in which
both knees were involved, it was postulated that arthritis in
one knee resulted from spread along the nerves. However, in
the other knee where there was no vesicular rash in the same
dermatome distribution, hematogenous spread was suspected. If hematogenous spread does occur, it is surprising that
arthritis is not more frequent in generalized herpes zoster
The current patient had obvious hematogenous
spread causing disseminated zoster but there was no involvement of other joints. Disseminated zoster occurs in
2-10% of patients. The incidence increases, especially in
malignancy, usually lymphomas. In a study (3) on the
incidence of herpes zoster with lymphoma, there were 21
disseminated cases in 129 patients. Arthritis was not reported in any of these. If hematogenous spread resulted in
arthritis. it would have been expected to occur more commonly in this group with severe disseminated disease. However, an immune complex mediated mechanism must also be
considered since this may account for those cases where
there is no dermal eruption in contiguous dermatomal distribution to that supplying the joint.
The most likely mechanism remains that of direct
inflammation of the synovium via viral spread along the
nerves arising from the activated dorsal root. In all cases
reported to date. the arthritis has resolved rapidly, with no
sequelae. after the appearance of the skin rash.
Perhaps because of severe pain in the dermatome
involved with herpes zoster, other cases of synovitis have
been masked and not diagnosed. The transient nature of the
arthritis also makes diagnosis difficult. The major difficulty
remains that of excluding a bacterial arthritis in these
patients .
M.D. Devereaux, MB. BS
K.A. Hazelton, MRCP(UK), FRACP
Princess Alexandra Hospitol
Brishane, Australia
1. Cunningham AL. Frdser JKE, Clarris BJ. Hobbs JB: A study of
synovial fluid and cytology in arthritis associated with herpes
zoster. Aust NZ J Med 9:W. 1979
2. Priest JR. Urick J U , Groth KE. Balfour H H Jr: Varicellaarthritis
documented by isolation of virus from joint fluid. J Pediatr
9390. 1978
3. Goffinet DR. Gladsteon EJ. Merigan TC: Herpes zoster varicella
infections and lymphoma. Ann Intern Med 76:235. 1972
Inappropriate secretion of ADH in a patient with
systemic lupus erythematosus
To the Editor:
Inappropriate secretion of antidiuretic hormone
(SIADH) has been reported in a wide variety of disorders,
and in diseases involving the central nervous system (CNS)
in particular (Zerbe R. Stropes L, Robertson G: Vasopressin
function in the syndrome of inappropriate diuresis. Annu
Rev Med 31:315-327, 1980). Surprisingly. there is only one
report of SlADH in a patient with systemic lupus erythematosus with CNS involvement, but that patient had tuberculosis during her illness (Kaplan AP. Curl FD, Decker JL:
Central hyperventilation and inappropriate antidiuretic hormone secretion in systemic lupus erythematosus. Am J Med
48:661-667, 1970). We would like to report a case of SlADH
occurring as a sole consequence of active lupus.
Our patient, a 26-year-old white male homosexual,
was admitted to St. Clare's Hospital on December 29, 1981
with a 3-day history of fever to 103°F. nausea, vomiting.
diarrhea. For the past 6 months he had experienced muscle
and joint pains. In August 1981 he developed a malar rash
after sun exposure at the beach. History was remarkable for
a positive test for syphilis 7 years previously, which, although he was asymptomatic, had resulted in treatment with
penicillin. His father died from multiple sclerosis.
On examination. the patient was lethargic and notably dehydrated. An atrophic, scaly rash was noted on the
malar areas, forehead, eyebrows, bridge of the nose, and
ears. Initial hematocrit count was 33%, erythrocyte sedimentation rate 45 mm/hour, white blood count 2,700, blood
urea nitrogen (BUN) 40 mg%. creatinine 1.2 mg%, serum
sodium 147 mEqlliter; other electrolytes were normal. Intravenous hydration was begun with the patient receiving a
total of 3,000 cc on the first hospital day, 2,000 cc of which
was D5W and 1.OOO cc of normal saline. On the second
hospital day, with the same intravenous intake and an
additional 500 cc orally, the serum sodium fell to I20 mEq/
liter and the BUN to 28 mg%.
On the third hospital day the patient had a grand ma1
seizure. Serum sodium was noted to have fallen to I10 mEql
liter. An additional 500 cc of 3% (hypertonic) saline was
administered. Although the patient was very confused and
disoriented, there were no localizable neurologic signs, and
spinal tap results were negative. Other laboratory values of
note were a platelet count of 13O,OOO,antinuclear antibodies
positive at a titer of 1/80 with a peripheral pattern, 3 positive
lupus preps. latex fixation 1/80, VDRL test positive 112.
fluorescent treponemal antibody-absorption test negative,
C4 and C3 normal, cryoglobulins positive 1/20, and cold
agglutinins. hepatitis-associated antigen. cytomegalovirus.
and Monotest all negative. Urine was 1 + for protein. White
blood count was 2.550 and red blood count, 50-100. Serum
osmolality was 260 mOsm/liter, urine osmalality. 620 mOsm/
liter. Urine electrolytes were normal.
The patient began a treatment program of fluid
restriction, prednisone 100 mg daily, and Dilantin 300 mg
daily. Urine output increased from 600 cc to 1,800 cc daily.
The serum sodium rose to 142 mEq/liter. His mental status
improved dramatically, and there was no further seizure
activity. The subsequent course was complicated by a
proximal myopathy that involved the shoulder and pelvic
girdles and was attributed to high-dose corticosteroid therapy, but the patient was discharged in good condition on
February 9, 1982, with his prednisone decreased to 30 mg
Bertrand Agus, MD
Sudha Nayar, MD
Dipti J. Patel, MD
Michael McGrath, MD
St. Clare’s Hospital
New York, N Y
Systemic lupus erythematosus, gout, and Paget’s
To the Editor:
Two short communications concerning the occurrence of crystal induced deposition disease as a cause of
arthritis in patients with systemic lupus erythematosus
(SLE) have been published (Moidel RA, Good AE: Coexistence of gout and systemic lupus erythematosus. Arthritis
Rheum 24:967-971, 1981), (Rose EP, Alves LE: Coexistent
gout and systemic lupus erythematosus. Arthritis Rheum
25:713-714, 1982). By and large the majority of articular
flare-ups in patients with SLE can be accounted for by the
disease itself. However, other etiologies should be ruled out
in the usual fashion especially if the patient lacks other
manifestations suggestive of active SLE. We wish to report
another patient with SLE and gout, who also happened to
have Paget’s disease of bone, which made the interpretation
of her symptoms more complicated.
A 52-year-old black woman was admitted to the
hospital on January 7, 1982 with a 2-day history of chest
pain. Medical history was pertinent for hypertension, hypertensive cardiovascular disease, insulin dependent diabetes
metlitus, hyperparathyroidism secondary to parathyroid adenoma (removed in 1978), and hyperuricemia. Cholecystectomy and hysterectomy had been performed in the past. The
diagnosis of SLE was made when at age 38 she was admitted
to another hospital with fever, polyarthralgias, pleurisy, skin
rash, photosensitivity, and positive antinuclear antibody.
Treated with various doses of prednisone ever since,
she was first admitted to our medical center at age 48; bone
pains were a prominent part of her complaints. Her SLE was
inactive. Hyperparathyroidism was diagnosed and she
underwent parathyroidectomy; her bone survey showed
skull and pelvic lesions diagnostic of Paget’s disease of bone.
She was found to be hyperuricemic. It was believed that her
bony aches were primarily related to her Paget’s disease and
thus a trial of calcitonin gave relief from pain. However,
calcitonin had to be stopped because of the cost involved. At
age 49, and ever since, the patient experienced episodes of
acute oligoarthritis in addition to persisting bone pain. Her
SLE remained quiescent.
Two weeks before admission the patient developed
chest pain which was believed to be skeletal in origin and,
because of persistence of that symptom, she was admitted.
Shortly afterward acute left ankle arthritis was noted; aspiration yielded a yellow turbid fluid with a white blood cell
count of 22,400, negative Gram stain and cultures, and no
crystals. Three days later minimal effusion developed in the
right knee. A few drops of synovial fluid were obtained and
typical urate crystals were observed under the polarized
scope. Serum urate was 18 mg/100 dl and a 24-hour uric acid
excretion was 448 mg. Because the patient was already
taking 50 mg Indocin twice daily, she was given 1 mg
intravenous colchicine to which she responded dramatically.
Thereafter she was placed on oral colchicine with complete
resolution of her arthritis. It was thought that her SLE was
not responsible for her present symptoms and thus prednisone was tapered. Her problems illustrate the complexity of
patients with systemic lupus erythematosus.
Graciela S. Alarcon, MD
Gene V. Ball, MD
Paul M. Goldfarb, Jr, MD
University of Alabama
Birmingham, Alabama
Pancreatitis and systemic lupus erythematosus: a case
To the Editor:
Pancreatitis may sometimes be seen in the course of
systemic lupus erythematosus (SLE), but the role of
SLE in the pathophysiology of the pancreatitis is often
obscured by the concomitant use of drugs that are known to
cause pancreatitis or by coexistent medical problems. We
report a case of recurrent pancreatitis in a young woman
with SLE. In this patient, there appeared to be a direct
relationship between episodes of pancreatitis and SLE activity. Endoscopic retrograde cannulation of her pancreatic
duct revealed normal pancreatic anatomy.
The patient is a 30-year-old white woman who has
had SLE since 1971. In early 1980, while she was receiving
prednisone 10 mg per day, intermittent diarrhea and recurrent episodes of severe coexistent abdominal pain occurred.
During one such episode in May 1980, her serum amylase
was elevated (Figure I). Results of an oral cholecystogram
and an ultrasound study of the gall bladder and pelvis were
normal, and computerized tomogram of the abdomen
showed diffuse pancreatic enlargement. She responded well
to conservative therapy with nasogastric suction and intravenous hydration. Prednisone was continued at 10 mg per
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adh, lupus, patients, systemic, erythematosus, secretion, inappropriate
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