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Lupus Erythematosus and Brain Scanning
TO THE EDITOR: We were concerned to read the paper in
the December 1974 issue on the interpretation of a positive brain scan in patients with systemic lupus erythematosus and localising neurologic signs ( 1 ) . While not disputing that the patients described may have had cerebral
vasculitis, we believe that opportunistic infection of the
central nervous system is an equally likely cause of this
clinical feature when such patients are receiving immunosuppressive therapy. This is exemplified by three cases,
(two with cerebral toxoplasmosis, one with brain abscesses
due to nocardial infection) described below and shown in
Figure 1. We believe that delay in diagnosis of infection
may result from the belief that cerebral lupus is by far
the most likely cause of an abnormal brain scan in a patient with systemic lupus erythematosus and neurologic
deficits. We fear that the paper referred to above may
strengthen that belief.
We propose that if the patient is clearly immunosuppressed and the disease well controlled clinically, serologically, and on spinal fluid testing, then exclusion of
infection must be carried out urgently. Depression of cellmediated immune function should particularly be noted,
as the great majority of the ubiquitous opportunistic organisms require cell-mediated immunity for their eradication. If the presence of cerebral infection is determined,
the need for withdrawal of all immunosuppressive therapy
contrasts strongly with the treatment for cerebral vasculitis.
In a subsequent letter ( 2 ) , the need to consider cerebral
lymphoma was pointed out. Although this extremely rare
complication must be kept in mind, its diagnosis does not
require the urgency inherent in the therapeutic dilemma
of infection versus vasculitis.
A 13-year-old girl with biopsy-proved lupus nephritis in 1970
was treated for 2 years with prednisone, 15 to 30 mg, on
alternate days plus azathioprine, 50 to 100 mg/day. Despite
this, the disease process remained active. Azathioprine was
therefore replaced with chlorambucil, 4 mg/day, which resulted
in dramatic improvement in laboratory indices. 18 months
later she was admitted to hospital with severe frontal headache
and vomiting. A brain scan showed a midline area of increased
uptake anteriorly that involved both frontal lobes. A presumptive diagnosis of cerebral lupus was made and dosage
of immunosuppressive agents increased. Despite this, she continued to deteriorate and died a month after admission. At
autopsy, necrotic lesions containing Toxoplasma gondii were
found in both cerebral hemispheres, the thalamus on the right,
and the cerebellum.
Figure 1A. Case 1: technetium-99 pertechnetate brain scan, anterior
view showing a midline area of increased uptake extending into both
hemispheres. Lateral view showed its anterior position in the
frontal lobe region. B. Case 2: anterior view of scan showing abnormal activity inferiorly on the right side. Right lateral view confirmed its presence in the temporal lobe region. C. Case 3: right
lateral scan showing large area of increased uptake in the parietal
lobe region. D. Case 3: anterior view of skull X ray after aspiration
of abscess cavities and instillation of steri-paque contrast medium.
A 25-year-old woman with systemic lupus erythematosus was
treated for 5 years with prednisone, azathioprine, and plaquenil
In 1974 she was admitted with a 4-day history of drowsiness
and right-sided hemiparesis. Apart from an antinuclear factor
titre of 1:100, there was no serologic or spinal fluid evidence
of disease activity. A lesion in the right temporal region was
seen on brain scan that was considered to be consistent with
cerebral lupus, and the dose of prednisone was increased. Although a brain biopsy was done, no organisms were identified,
and, despite the addition of ampicillin, she died a few days
later. Autopsy examination showed extensive cerebritis containing Toxoplasma gondii.
A 31-year-old man presented in 1969 with severe skin, joint,
and pleural manifestations of lupus erythematosus. Prednisone
and azathioprine were required for adequate control of clinical
and laboratory indices of disease activity. After development of
nephritis in 1973, azathioprine was replaced by chlorambucil.
In July 1974 he presented with widespread herpes zoster, followed by grand mal fits. Brain scan showed an abnormality
in the right parietal region, which was shown on aspiration to
be two abscesses due to Nocardia asteroides. Despite intensive
antibiotic therapy and repeated drainage, coupled with reduction in dosage of immunosuppressive agents, he died 3 months
later.
GRAEME STEWART, M.B., M.R.A.C.P.
ANTONY BASTEN, M.B., M.R.C.P.
Department of Clinical Immunology
Royal Prince Alfred Hospital
Camperdonn, N.S.W. 2050, Australia
REFERENCES
1. BENNAHUM DA, MESSNER RP, SHOOP JD: Brain scanfindingsin
central nervous system involvement by lupus erythematosus. Ann
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Intern Med 81:763-765, 1974
2. KRAAG G, RICHARDS AJ, GORDON DA: Brain scanning in lupus
erythematosus. Ann Intern Med 82:594, 1975
Alternate-Day Steroid Therapy
TO THE EDITOR: The study of Hunder and colleagues (Ann
Intern Med 82:613-618, 1975) showed daily administration of corticosteroids to be superior to an alternate-day
regimen in the initial management of giant cell arteritis.
However, it may be premature to totally discard the concept of alternate-day steroid therapy in this disease, for
two reasons.
First, some patients in the alternate-day nonresponder
group apparently derived significant benefit on the days
that they received steroids, since "typically, the patients
receiving alternate-day therapy who did not respond completely felt reasonably well during some portion of the day
on which 90 mg of prednisone was given. . . ." Seybold
and Drachman (1) noticed an increase in weakness on
the "off" day in patients with myasthenia gravis treated
with alternate-day prednisone, who responded to a dose of
5 to 10 mg on that day. This included "several patients
in whom the alteration was marked." While 4 of their 12
patients did develop side effects, it was not necessary to
withdraw the steroids in any case. It is possible that a small
dose (5 to 10 mg) of prednisone on the "off" day might
reduce the loss of control and enable eventual suppression
in patients with giant cell arteritis without an increase in
side effects.
Second, it has been shown that relapse can occur in this
disease either during rapid decrease or after withdrawal of
steroids, even after 2 years of treatment ( 2 ) . Consequently,
treatment with 7.5 to 12.5 mg daily for at least 2 years
has been recommended ( 2 ) . Perhaps, alternate-day steroids, even if not effective in obtaining initial suppression
of this disease, might prove to be as effective a means of
preventing relapses as prolonged daily therapy without
its attendant risks. Therefore, one might consider switching patients to an alternate-day regimen after the disease
has been controlled and then reducing their doses during
the 2 years. This would not seem unreasonable, since the
authors did not present evidence that any patient actually
deteriorated on alternate-day treatment.
JEFFREY T. KESSLER, M.D.
Department of Neurosciences
College of Medicine and Dentistry of New Jersey
New Jersey Medical School
Newark, New Jersey 07103
REFERENCES
1. SEYBOLD ME, DRACHMAN DB: Gradually increasing doses of
prednisone in myasthenia gravis. N Engl J Med 290:81-84, 1974
2. FAUCHALD P, RYGVOLD O, 0YSTESE B: Temporal arteritis and
polymyalgia rheumatica. Clinical and biopsy findings. Ann Intern
Med 77:845-852, 1972
In comment:
Our study, referred to by Dr. Kessler, showed rather
clearly that at commonly used corticosteroid doses, alternate-day therapy cannot be relied on to control the inflammatory process associated with giant cell arteritis.
But it did not answer the specific question raised by him.
734
We have tried both methods that he has suggested with
several patients who had giant cell arteritis and have not
found them to be generally helpful. However, the questions posed would be answered most convincingly by additional carefully controlled observations.
Regarding his first suggestion, it is not fair to compare
myasthenia gravis to giant cell arteritis. Besides being
vastly different diseases, the aims of treatment are different.
In myasthenia gravis, the aim is to control reversible symptoms, while in giant cell arteritis the major aim is to prevent arterial occlusions or ruptures, which usually cause
irreversible tissue damage. Treatment of giant cell arteritis
is made more difficult by the fact that these vascular complications do not always develop when the patient's symptoms are worst. But the complications seem to be prevented
by suppressing the inflammatory process, as reflected best
by an elevation of the erythrocyte sedimentation rate and
alpha 2 globulins. These factors should be kept in mind
when considering criteria for therapeutic effectiveness of
a drug regimen and the risks of investigating the regimen.
Even though none of our patients on alternate-day drug
therapy seemed to have suffered permanent vascular complications due to inadequate control of the disease, one
had transient blindness and another developed inflammation and dilation of a carotid artery.
Regarding the second question, we found no evidence
to suggest that alternate-day therapy was more effective
in milder cases of giant cell arteritis, and several patients
"late" in the course of the disease were switched to daily
corticosteroid treatment at equivalent total doses to control
more successfully musculoskeletal symptoms.
Although our experience might sound somewhat discouraging, we urge Dr. Kessler to carefully pursue his
questions further in order to more fully define the advantages and limitations of alternate-day therapy.
G E N E G. HUNDER,
SHELDON G. SHEPS,
GEORGE L. ALLEN,
JOHN W. JOYCE,
M.D.
M.D.
M.D.
M.D.
Mayo Clinic
Rochester, Minnesota
Steroid Therapy in Goodpasture's Syndrome
TO THE EDITOR: The recent paper by de Torrente and associates ("Serious Pulmonary Hemorrhage, Glomerulonephritis, and Massive Steroid Therapy," Ann Intern Med
83:218-219, 1975) indicates that massive steroid therapy
may provide an alternative to bilateral nephrectomy as
therapy for life-threatening pulmonary hemorrhage in patients with Goodpasture's syndrome. We wish to report a
second case of lung hemorrhage in Goodpasture's syndrome successfully treated with massive steroid therapy.
A 32-year-old Eskimo woman was admitted to the hospital
because of cough, hemoptysis, and progressive shortness of
breath of 5 days' duration. She gave a history of right upper
lobectomy for therapy of tuberculosis 13 years before admission. One year before admission, therapy with isoniazide and
ethambutol was started because of radiographic recurrence of
her tuberculosis. She had remained asymptomatic with a normal
exercise tolerance until the onset of the acute illness 5 days
before hospitalization.
Her hematocrit was 21% and her prothrombin time, partial
thromboplastin time, and platelet count were within normal
limits. Urinalysis was recorded as within normal limits. Chest
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X ray showed an alveolar infiltrate involving the entire left
lung and the right lower lung. Sputum stains were negative
for acid-fast bacilli. Because of the large quantity of pulmonary
hemorrhage, a pulmonary angiogram was done in an attempt
to localize a bleeding site. None was found.
During the first 36 hours pulmonary hemorrhage continued,
and her arterial Po2 decreased to 37 mm Hg, despite intubation
and positive end-expiratory pressure using 80% inspired oxygen. A repeat urinalysis showed a profusion of erythrocyte
casts and coarse granular casts with 4+ protein. An open
renal biopsy was done under local anesthesia. A proliferative
glomerulonephritis with focal capillary tuft necrosis was seen
by light microscopy. Crescents were present on 18 of 26
glomeruli examined. Immunofluorescent microscopy showed a
linear pattern of immunoglobulin G with a broken pattern for
the third component of complement. Heavy fibrin deposition
was noted in the crescents and locally in several glomerular
tufts. On the basis of clinical and pathologic data, a diagnosis
of Goodpasture's syndrome was made.
At the time of renal biopsy, the patient's creatinine clearance
was approximately 75 ml/min. Despite this, bilateral nephrectomy was considered as a possible means to treat her lifethreatening pulmonary hemorrhage. On the basis of anecdotal
data, methyl prednisolone was begun with a dose of 1 g every
8 hours in an attempt to ameliorate her pulmonary hemorrhage. Other medications included the antituberculous drugs:
streptomycin, isoniazide, and rifampin.
Within 24 hours of beginning methyl prednisolone, the patient's pulmonary hemorrhage ceased and did not recur. Artificial respiration with positive end-expiratory pressure was
necessary for the next 5 days, and her respiratory function
slowly improved. During this time her methyl prednisolone
dose was tapered and replaced with oral prednisone in a dose
of 80 mg/day. Her creatinine clearance stabilized at 60 ml/
min until discharge on her 15th hospital day.
Serum samples assayed for the presence of antiglomerular
basement membrane antibodies by Dr. Curtis Wilson (Scripps
Clinic and Research Foundation) were negative on the first,
third, and seventh hospital day.
Since discharge, the patient has been seen in the outpatient
department, and her steroid dose has been tapered to 60 mg
orally every other day. Her glomerular filtration rate has
remained stable at 60 to 70 ml/min, although her urinary
sediment remains abnormal, showing many granular casts, and
she loses 3 to 5 g of protein in urine per day. Her chest film
is clear except for the evidence of previous tuberculosis.
As in the case reported by de Torrente and colleagues,
this patient had only mild renal impairment, but lifethreatening pulmonary hemorrhage that ceased within 24
hours of starting massive steroid therapy. In case reports
of this type one cannot be certain of the effect of a given
therapeutic maneuver. Yet this case provides the second
instance where massive steroid therapy seemed to provide
a successful alternative to bilateral nephrectomy, which
was being considered. It is reasonable to consider this form
of therapy in future Goodpasture's syndrome patients who
present with life-threatening pulmonary hemorrhage and
relatively intact renal function.
ROBERT KOPELMAN, M.D.
PHILLIP H O F F S T E N , M.D.
SAULO KLAHR, M.D., F.A.C.P.
Department of Medicine
Renal Division
Washington University School of Medicine
St. Louis, Missouri 63110
Asbestos Pleural Effusion?
TO THE EDITOR: I read with interest the paper by Galen
and associates (1) on hemorrhagic pleural effusion in patients undergoing chronic hemodialysis. When pleural effusion is found in a uremic case, one must rule out other
causes. My main interest was in the patient who initially,
before the administration of heparin, had a clear yellow
pleural fluid, a chest X ray confirming the effusion, and
"bilateral pleural thickening with pleural calcification on
the right."
My inquiry is whether this was a benign persistent
pleural effusion associated with asbestosis. Pleural plaques
and calcifications from asbestos exposure may occur without parenchymal asbestosis. As in this patient, asbestos
pleural effusion is a sterile exudate, usually bilateral, and
may be clear fluid or blood tinged ( 2 ) .
The exposure to asbestos dust could have been urban
or occupational. Recent unpublished data have shown that
a good occupational history is not often obtained, and 3.3
histories are taken before past exposure to asbestos is discovered ( 3 ) .
FAYSAL M. HASAN, M.D.
Department of Medicine
American University Hospital
Beirut, Lebanon
REFERENCES
1. GALEN MA, STEINBERG SM, LOWRIE EG, et al: Hemorrhagic
pleural effusion in patients undergoing chronic hemodialysis. Ann
Intern Med 82:359-361, 1975
2. GAENSLER EA, KAPLAN Al: Asbestos pleural effusion. Ann Intern
Med 74:178-191, 1971
3. HASAN FM, NASH G, KAZEMI H: Epidemiological significance of
asbestos-induced and non-asbestos-induced mesothelioma. Unpublished
In comment:
Doctor Hasan has raised an interesting point. While parenchymal disease was absent and we were unable to elicit an
occupational history, we, of course, cannot state with certainty that the patient did not in fact have asbestosis. She
worked as a bookkeeper her entire life and did a substantial fraction of her work within her own home. She
had eight admissions to this hospital and related between
two and three histories with each. N o history of asbestos
exposure is recorded in the chart. Unfortunately, the patient has died and postmortem examination was denied by
the family.
Even if, in fact, the effusion were benign and due to
some cause such as asbestosis, its conversion from nonhemorrhagic to hemorrhagic is well documented. One could
conclude, then, that an otherwise benign effusion may add
to the risks of hemodialysis therapy by mechanisms reviewed in the discussion in the paper.
EDMUND G. LOWRIE, M.D.
Department of Medicine
Peter Bent Brigham Hospital
Boston, Massachusetts
Fluphenazine and Inappropriate Secretion of
Antidiuretic Hormone
TO THE EDITOR: A recent case of inappropriate secretion
of antidiuretic hormone ( A D H ) secondary to the use of
fluphenazine was reported in the June issue. The patient
that was reported suffered two convulsive seizures ( 1 ) .
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Although we have observed a case of inappropriate
ADH secretion in one of our patients treated with fluphenazine ( 2 ) , convulsive seizures can in themselves produce the syndrome "by virtue of an irritable focus that
promotes the secretion of the hormone" (3-5). The case
reported by Dr. de Rivera does not provide sufficient causeeffect relationship between the use of fluphenazine and
inappropriate ADH secretion, particularly when an already
proved causative factor of the syndrome is present.
JORGE S. ZUNIGA, M.D.
TOBY HAZAN, M.D.
Crises Intervention Center
Department of Psychiatry
Sinai Hospital of Detroit
6767 West Outer Drive
Detroit, Michigan 48235
observation of a temporal association, with exclusion beyond reasonable doubt of well-known causes of the syndrome, including intracranial lesions.
There is, however, a wide array of obscure conditions
that may produce this syndrome, including exacerbated
psychosis ( 3 ) . My case report is only suggestive of a possible relationship between fluphenazine (and perhaps other
phenothiazines) and inappropriate secretion of ADH, a
relationship that awaits further elucidation. This may come
from Drs. Zuniga and Hazan, if they report their case;
it would be particularly interesting if they have been able
to study the fluid-electrolyte metabolism of their patient,
with and without medication.
J. L. G. DE RIVERA, M.D.
Psychiatric Consultation Service
Montreal General Hospital
Montreal, PQ H3A 1A1, Canada
REFERENCES
1. DE RIVERA JLG: Inappropriate secretion of antidiuretic hormone
from fluphenazine therapy. Ann Intern Med 82:811-812, 1975
REFERENCES
3. DILLON RS: Handbook of Endocrinology. Philadelphia, Lea and
Febiger, 1973, pp. 201-202
1. WELT LG: Disorders of fluids and electrolytes, in Harrison's
Principles of Internal Medicine, 7th ed., edited by WINTROBE MM
et al. New York, McGraw Hill, 1974, p. 1347
2. ADAMS R: The convulsive state. See Reference 1, p. 135
4. WELT LG, DINGMAN J, THORN G: in Harrison's Principles of
3. DUBOVSKY SL, GRABON S, BERL T, et al: Syndrome of inappro-
2. SHAW R, LQRETTI L: Unpublished
Internal Medicine, 7th ed., edited by WINTROBE MM et al. New
York, McGraw Hill, 1974, chapters 84 and 264
5. SCHWARTZ WB: in Cecil-Loeb Textbook of Medicine, 14th ed.,
priate secretion of antidiuretic hormone with exacerbated psychosis. Ann Intern Med 79:551-554, 1973
edited by BEESON PB, MCDERMOTT W. Philadelphia, W. B.
Saunders, 1975, p. 1582
In comment:
After my report on inappropriate secretion of antidiuretic
hormone ( A D H ) from fluphenazine therapy, Drs. Zuniga
and Hazan mention having observed a second case, possibly
similar. It would be of interest to know more details about
their case, unreported until now.
They comment that "convulsive seizures can in themselves produce the syndrome [of inappropriate secretion of
ADH]." Although this may possibly happen, there are no
pertinent data in the literature to support their statement.
There is, however, strong evidence on the opposite relationship, namely, that the syndrome of inappropriate secretion of ADH may produce, through hyponatremia, convulsive seizures ( 1 ) .
The authors quoted by Drs. Zuniga and Hazan do not
refer to convulsions as causative of inappropriate A D H
secretion but to intracranial lesions (infection, trauma, or
tumor), which, independently of their ability to induce
seizures, may produce inappropriate secretion of A D H
"by partial destruction of the posterior [lobe] of the pituitary gland, with escape of hormone; or by virtue of an
irritative focus that promotes the secretion of the hormone" ( 1 ) . There was no evidence in my reported case
of any such intracranial lesion. Brain scan, skull X ray,
and spinal examination were normal; the electroencephalogram showed nonspecific abnormalities, compatible with
the metabolic state, not indicative of intracranial lesion
and certainly not of "irritative focus." There was no
neurologic abnormality after recovery from the acute episode. However, there was strong evidence of water intoxication and hyponatremia, conditions known to be occasionally complicated by generalized motor seizures ( 2 ) , as
was the case in our patient.
I agree that the evidence of a cause-effect relationship
between fluphenazine and the syndrome of inappropriate
secretion of A D H is merely circumstantial, based on an
736
The report by Dr. de Rivera on the possible association
between fluphenazine therapy and the syndrome of inappropriate secretion of antidiuretic hormone is an important
observation and adds a further cause of this syndrome to
the list applying to psychiatric patients. This list now includes schizophrenia itself ( 1 ) , thiothixene ( 2 ) , amitriptyline ( 3 ) , promethazine ( 4 ) , carbamazepine ( 5 ) , emotional
stress, pain, nicotine, barbiturates, morphine, chronic alcoholism, hypofunction of the adrenal, thyroid, and pituitary
glands, acute intermittent porphyria, many tumors, and
miscellaneous nervous system and thoracic disorders ( 6 ) .
The syndrome may be mimicked by psychogenic polydipsia, by syndromes where A D H secretion is appropriate
(for example, heart failure and liver disease), by renal
impairment (which can be intrinsic or due to diuretic
therapy or metabolic disorders), and by a wide range of
other medications (for example, sulphonylureas, acetaminophen, clofibrate, and antineoplastic and antihypertensive drugs [7]).
Two important considerations derive from this ever
expanding list. First, reports that incriminate factors associated with this syndrome should be as completely documented as possible, since one must make the difficult
positive diagnosis of the syndrome and identify the agent
responsible by methodically excluding all other known
possibilities. In this regard the report incriminating fluphenazine warrants further investigation. If fluphenazine
had been responsible for the hypoosmolality, one would
expect osmolality to have fallen again when water restriction was stopped 8 days before the end of the pharmacologic action of fluphenazine, which continues for 14
days after parenteral administration. Second, since the
manifestations of hypoosmolality syndrome are protean,
there may be a place for more frequent measurement of
serum osmolality (or sodium concentration) in neuropsychiatric patients.
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P. J. PHILLIPS, M.B., B.S., M.A. ( O X O N ) ,
M.R.A.CP
R W. PAIN, M.B., B.S., F.R.C.P.A.
Division of Clinical Chemistry,
Institute of Medical and Veterinary Science
Frome Road
Adelaide, South Australia 5000 r Australia
REFERENCES
1. HOBSON J A, ENGLISH JT: Self-induced water intoxication. Ann
Intern Med 58:324-332, 1963
2. AJLOUNI K, KERN MW, TURES JF, et al: Thiothixene-induced
hyponatremia. Arch lnterm Med 134:1103-1105, 1974
3. LUZECKY MH, BURMAN KD, SCHULTZ ER: The syndrome of in-
appropriate secretion of antidiuretic hormone associated with
amitriptyline administration. South Med J 67:495-497, 1974
4. DYBALL REJ: The effect of drugs on the release of vasopressin.
Br J Pharmacol Chemother 33:329-341, 1968
5. KIMURA T, MATSUI K, SATO T, et al: Mechanism of carbamaz-
epine (Tegretol) induced antidiuresis: evidence for release of
antidiuretic hormone and impaired excretion of a water load. J
Clin Endocrinol Metab 38:356-362, 1974
6. MAXWELL MH, KLEEMAN CR: Clinical Disorders of Fluid and
Electrolyte Metabolism, 2nd ed., New York, McGraw Hill, 1972,
chapter 7
7. SCHRIER RW, BERL T: Non-osmolar factors affecting water excretion. N Engl J Med 292:141-145, 1975
paper "Laxative-Induced Hypokalemia, Sodium Depletion
and Hyperreninemia" in the July "Annals." We agree that
a shift of intracellular sodium to the extra cellular space
could have occurred when potassium depletion was specifically corrected. This shift, however, may not occur in the
sodium-deprived subject, as suggested by Cannon, Frazier,
and Hughes (1) on the basis of histologic data but without the intracellular and extracellular electrolyte determinations to confirm it.
In the experimental human studies of potassium depletion and repletion effects on plasma renin ( 2 ) , no direct
measurements of plasma volume were recorded, and unfortunately none are available in our patient. Bull and coworkers ( 3 ) , in studies of potassium repletion after diureticinduced hypokalemia in sodium deprived subjects, noted no
change in blood volume and a slight increase in plasma
volume, but they did not find any significant alteration in
plasma renin activity.
Thus, Dr. Butkus' suggestion can only be tested in future cases similarly studied with the addition of appropriate
fluid volume measurements.
Renin Suppression
BARBARA J. FLEMING, M.D.
TO THE EDITOR: The paper by Fleming and associates in
the July issue (Ann Intern Med 83:60-62, 1975) understates the possible role of volume repletion in contributing
to the suppression of serum renin levels noted during the
early period of potassium repletion in their patient (Figures 1 and 2, p. 61). During the initial period of potassium
repletion, although external sodium balance was maintained, a positive balance of over 300 meq of potassium
was attained with an increase in body weight of 1 kg.
Potassium depleted states are accompanied by a reciprocal increase in intracellular sodium (1-3). Repletion of the
potassium deficit results in a decrease in intracellular
sodium with a shift of sodium to the extracellular space. In
the patient described by the authors, although external
sodium balance was maintained, it is likely that internal
shifts of sodium as a result of potassium repletion resulted
in at least mild extracellular fluid volume expansion, which
could, in part, explain the observed reduction in serum
renin. That volume expansion was only partial (as documented later in their report) would explain the continued
exaggerated response of serum renin to upright posture.
Concomitant measurements of plasma volume might have
served to distinguish between the direct effect of potassium
repletion and the indirect effect of internal sodium shifts on
the observed reduction in serum renin level in this interesting report.
DONALD E. BUTKUS, M.D., LTC, MC
Nephrology Service
Fitzsimons Army Medical Center
Denver, Colorado 80240
REFERENCES
1. COTLOVE E, HOLLIDAY MA, SCHWARTZ R, et al: Effects of elec-
trolyte depletion and acid-base disturbance on muscle cations.
Am J Physiol 167:665-675, 1951
2. LEAF A, SANTOS RF: Physiologic mechanisms in potassium deficiency. N Engl J Med 264:335-341, 1961
3. FLEAR CTG, FLORENCE T: Muscle biopsy in man: an index of
Division of Medicine
The Mt. Sinai Hospital of Cleveland
Cleveland, Ohio 44106
REFERENCES
1. CANNON PR, FRAZIER LE, HUGHES HR: Sodium as a toxic ion in
potassium deficiency. Metabolism 2:297:313, 1953
2. BRUNNER HR, BAER L, SEALEY JE, et al: The influence of potas-
sium administration and of potassium deprivation on plasma
renin in normal and hypertensive subjects. J Clin Invest 49:21282138, 1970
3. BULL MB, HILLMAN RS, CANNON PJ, et al: Renin and aldoster-
one secretion in man as influenced by changes in electrolyte
balance and blood volume. Circ Res 27:953-960, 1970
Factor VIII Nomenclature
TO THE EDITOR: A task force has recommended to the International Committee on Thrombosis and Haemostasis the
adoption of a new nomenclature for the "factor-VIII-related-activities." An "on-the-line" system of nomenclature
has been recommended for the three major classes of activities related to blood coagulation factor VIII, that is
VIII:C (for the coagulant activity), VIIIR:AG (for the
antigenic activities related to factor VIII), and VIIIR:WF
(for the "von Willebrand factor" activities related to factor
VIII).
Adoption of these recommendations, which are at present
before the International Committee, will be deferred for
at least 1 year while the task force receives and considers
suggestions of modification.
Anyone who wishes a copy of the full report or wishes
to make suggestions to the task force should contact its
chairman: Professor John B. Graham, Department of
Pathology, School of Medicine, University of North Carolina, Chapel Hill, NC 27514, USA.
cellular potassium? Nature (Lond) 199:156-158, 1963
In comment:
We note with interest the comments of Dr. Butkus on our
JOHN B. GRAHAM, M.D.
Department of Pathology
School of Medicine
University of North Carolina
Chapel Hill, North Carolina 27514
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Antiplatelet Antibody
Pulmonary Radiation Reactions
TO THE EDITOR: In their recent paper (Ann Intern Med 83:
190-196, 1975) Lackner and Karpatkin reported that many
patients with the "easy bruising" syndrome have abnormal
platelet function, increased percentages of megathrombocytes, and an elevated prevalence of antiplatelet antibody.
I agree that the easy bruising in these patients reflects a
qualitative platelet defect, but I question whether the defect
is the result of an autoimmune process. Most of the patients
studied were women of child-bearing age and, unless the
target platelets used for platelet antibody testing were autologous, the increased frequency of platelet antibody activity could be explained by the presence of pregnancy-induced (or transfusion-induced) isoantibody. I also question
whether the increased percentage of megathrombocytes in
these patients is evidence for a compensated thrombocytolytic state. This would be more convincingly shown by
platelet survival measurements, since megathrombocytes
may be seen in normal persons, (1, 2) and, as the authors
note, their presence in excess may not always reflect
shortened platelet survival ( 3 ) .
TO THE EDITOR: I have recently described the appearance
of increased clinically symptomatic pulmonary radiation
reactions with adjuvant chemotherapy (1), specifically a
combination of nitrogen mustard, procarbazine, and vincristine. My comments in that paper suggested that "increased reactions be looked for in all organ systems that
are irradiated during combination studies." Further evidence in support of this statement is given by the recent
report of synergistic cardiotoxicity with adriamycin and
radiation in your journal by Merrill and associates (Ann
Intern Med 82:122-123, 1975), and another article by
Cassady and associates (2) on treatment of Wilms tumor
with combined modality therapy.
To expand on my original articles citing increased
pulmonary radiation reactions with adjuvant chemotherapy
(1, 3), I later observed similar symptomatic pulmonary
reactions in patients who received radiotherapy after cyclic chemotherapy with adriamycin, vincristine, and cyclophosphamide.
Evaluation of my data collected while at the National
Cancer Institute, plus preliminary evaluation of patients
recently treated here (present address), indicates that the
degree of symptomatic reaction is related to a number of
factors, including the number of cycles of chemotherapy
before radiotherapy, the size of the radiation field, whether
the radiation is given during or after completion of chemotherapy, and presumably the drug itself.
The main reason for my two papers was to point out that
the big danger in increased symptomatic reactions is that
making an incorrect diagnosis could lead to improper and
perhaps even dangerous therapy. However, it is becoming
more obvious that increased reactions should be looked
for in all organ systems that are irradiated during combination studies, and this possibility should be considered when
protocols are planned.
PHILIP L. CIMO, M.D.
Division of Hematology
University of Texas Medical School
Houston, Texas 77025
REFERENCES
1. O'BRIEN JR, JAMIESON S: A relationship between platelet volume
and platelet number. Thromb Diath Haemorrh 31:363-365, 1974
2. VON BEHRENS WE: Mediterranean macrothrombocytopenia.
Blood 46:199-208, 1975
3. MURPHY S: Hereditary thrombocytopenia. Clin Haematol 1:359368, 1972
In comment:
It is unlikely that the presence of antiplatelet antibody
could be due to isoantibody induced by pregnancy for two
reasons: [1] 7 of our 19 patients (Types I and II) with
positive antiplatelet antibody were childless or unmarried,
or both, and two were men; and [2] we have tested several
normal women with multiple pregnancies and have not
found positive antiplatelet antibody titers.
The presence of increased megathrombocytes does not
prove the existence of a compensated thrombocytolytic
state, and its presence in excess may not reflect shortened
platelet survival in some rare conditions. Nevertheless, we
consider the presence of increased megathrombocytes as
highly suggestive of a compensated thrombocytolytic state,
since the 8 patients whom we studied with this finding had
shortened platelet survival ( 1 , 2 ) .
HENRIETTE LACKNER, M.D., M.R.C.P.
SIMON KARPATKIN, M.D.
New York University Medical Center
550 First Avenue
New York, New York 10016
REFERENCES
1. GARG SK, AMOROSI EL, KARPATKIN S: Use of the mega thrombocyte as an index of megakaryocyte number. N Engl J Med 284:
11-17, 1971
2. KARPATKIN S, GARG SK, SISKIND GW: Autoimmune thrombocytopenic purpura and the compensated thrombocytolytic state.
Am J Med 51:1-4, 1971
738
KENT B. LAMOUREUX
Department of Radiation Therapy
Arnot-Ogden Memorial Hospital
Roe Avenue
Elmira, New York 14901
REFERENCES
1. LAMOUREUX KB: Increased clinically symptomatic pulmonary
rediation reactions with adjuvant chemotherapy. Cancer Chem
Rep 58:705-708, 1974
2. CASSADY JR, MEYER G, JAFFE N, et al: Fever, lethargy and rash
complicating treatment for Wilms' tumor—a new syndrome?
Radiology 115:171-174, 1975
3. LAMOUREUX KB: Diagnostic problems after radiotherapy involving the lung. South Med J 66:1388-1392, 1973
BCG Therapy and Urticaria
TO THE EDITOR: We are presently treating a patient who
developed recurrent urticarial eruptions that were temporally related to the administration of BCG. This systemic
reaction is not described in the recent article by Aungst,
Sokal, and Jager (1) nor in other extensive reviews of the
complications of BCG therapy (2-4).
The patient is a 49-year-old man who was referred to the
New England Medical Center Hospital in November 1974 with
pancytopenia and shortness of breath. He had petechiae, ecchymoses, and splenomegaly. The leukocyte count was 5000 with
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67% myeloblasts, and the bone marrow was diagnostic of
acute myelomonocytic leukemia.
Complete remission was induced with cytosine arabinoside
and 6-thioguanine. His course from aplasia to remission was
complicated by sepsis, candidal esophagitis, jaundice, and a
perirectal abscess with fistula requiring a colostomy. He received a good deal of blood component support, including
granulocytes, and experienced a single episode of urticaria
concomitant with the administration of a unit of packed erythrocytes.
After it was shown that he was not anergic, he was started on
a maintenance regimen consisting of cyclical courses of BCG
and 6-mercaptopurine. BCG, 300 mg, was administered by
scarification on Days 1 and 8. On Days 15 to 20, he received
500 mg/m2 body surface of 6-mercaptopurine orally. He received five and a half courses with two omissions of 6-mercaptopurine because of cytopenias or a transient increase in serum
concentrations of hepatic enzymes. Several days after the fourth
BCG injection, he noted mild urticaria over his extremities and
back that subsided rapidly and spontaneously. With each subsequent injection the urticaria appeared more rapidly and was
more intense and diffusely distributed. An episode of mild
angioneurotic edema occurred in the mouth after the final
dose. These lesions were only minimally responsive to diphenhydramine, were unresponsive to hydroxyzine and chlortrimeton, and gradually resolved within a week. At no time
did he experience any fever or chills after BCG administration.
A local inflammatory response occurred only after the final
dose. Eosinophilia (up to 10%) was noted for the first time
a few days before the initial episode of urticaria and was also
seen once more during his course.
The patient's leukemia has recently relapsed. Since BCG
and 6-mercaptopurine have been withdrawn, urticaria has
not recurred. This supports our impression that the urticaria was an allergic phenomenon related to the BCG.
BRUCE D. CHESON, M.D.
Department of Hematology
New England Medical Center Hospital
Boston, Massachusetts 02111
REFERENCES
to increase the proportion of animals that died in the
convulsive phase. Prophylactic sodium thiosulfate (1 g/kg,
15 minutes before azide) also had no effect on mortality.
Two additional human cases of azide poisoning from the
accidental ingestion of a hematologic laboratory regent (4)
further emphasize the need for an effective antidote.
We will continue to recommend the induction of methemoglobinemia by nitrite for acute poisoning by hydrogen
sulfide or its salts. To our knowledge it has not yet been
tried in acute human sulfide intoxication. As evaluated in
animals, an equivalent methemoglobinemia afforded a
much greater degree of protection against sulfide than
against azide ( 5 ) . Moreover, antidotal effects of nitrite in
sulfide poisoning have also been determined in animals ( 6 ) .
Oxygen and thiosulfate can do no harm, but they had only
marginal effects at best, whether used alone or in combination with nitrite.
ROGER P. SMITH, PH.D.
ROBERT E. GOSSELIN, M.D., PH.D.
ROBERT KRUSZYNA, M . S .
Department of Pharmacology and Toxicology
Dartmouth Medical School
Hanover, New Hampshire 03755
REFERENCES
1. ABBANAT RA, SMITH RP: The influence of methemoglobinemia
on the lethality of some toxic anions. I. Azide. Toxicol
Pharmacol 6:576-583, 1969
Appl
2. GLEASON MN, GOSSELIN RE, HODGE HC, et al: Clinical Toxic-
ology of Commercial Products, 3rd ed. Baltimore, Williams &
Wilkins, 1969, pp. 11-20, 111-122
3. EMMETT EA, RICKING JA: Fatal self-administration of sodium
azide. Ann Intern Med 83:224-226, 1975
4. RICHARDSON SGN, GILES C, SWAN CHJ: TWO cases of solium
azide poisoning by accidental ingestion of Isoton. / Clin Pathol
28:350-351, 1975
5. SMITH RP, GOSSELIN RE: On the mechanism of sulfide inactiva-
tion by methemoglobin. Toxicol Appl Pharmacol 8:159-172, 1966
6. SMITH RP, KRUSZYNA R, KRUSZYNA H: Management of acute
sulfide poisoning: effects of oxygen, thiosulfate and nitrite. Arch
Environ Health, in press
1. AUNGST CW, SOKAL JE, JAGER BV: Complications of BCG vac-
cination in neoplastic diseases. Ann Intern Med 82:666-669, 1975
2. SPARKS FC, SILVERSTEIN MJ, HUNT JS, et al: Complications of
BCG vaccination in patients with cancer. N Engl J Med 289:
827-830, 1973
3. BAST RC JR, ZBAR B, BORSOS T, et al: BCG and cancer. N Engl
J Med 290:1413-1420, 1458, 1974
4. NATHANSON L: Use of BCG in the treatment of human neoplasms: a review. Semin Oncol 1:337, 1974
Sodium Azide Poisoning
TO THE EDITOR: Since we (RS, R G ) were responsible for
the suggestion that the therapeutic induction of methemoglobinemia might be of value in acute azide poisoning ( 1 ,
2), we are naturally disappointed that it was not effective
in its first human trial ( 3 ) . That recommendation will not
appear in the fourth edition of our reference manual,
which is now in press ( 2 ) .
Recent observations by one of us ( R K ) suggest that
there are two distinctive mechanisms of death in mice
acutely poisoned by sodium azide. If death in convulsions
does not occur within 10 minutes, survivors may die during
the phase of collapse an hour or more after azide administration. Although the prophylactic and therapeutic administration of oxygen (100% at 1 atmosphere) had no effect
on the overall mortality of azide-poisoned mice, it seemed
Furosemide Screening Test and Pheochromocytoma
TO THE EDITOR: It was recently suggested in this journal
that the measurement of peripheral plasma renin activity
after the administration of oral furosemide is a reliable
screening test in hypertension to rule out a surgically correctable lesion ( 1 ) . Plasma renin activity above 5 ng/ml • h
was associated with a renovascular cause of hypertension
in five patients. We wish to report on two additional patients who had markedly elevated plasma renin activity in
the furosemide screening test and no evidence of any
renovascular abnormalities.
Patient 1 was a 54-year-old white woman who had hypertension and superimposed hypertensive paroxysms responsive
to intravenous phentolamine. The hypertension was unresponsive to all conventional medications except phenoxybenzamine.
Urinary vanillylmandelic acid was elevated between crises
(16.3 mg/g creatinine), as well as during the paroxysms (69.2
mg/0.2 g creatinine). The norepinephrine and epinephrine
were within normal limits. Arteriography did not show evidence of any adrenal or renovascular lesion. A laporotomy did
not identify an abdominal chromaffin tumor, and postoperatively the patient continued to save the same hypertensive
episodes. Preoperatively and postoperatively, the plasma volume was constricted at 31.08 ml/kg (ideal, 47.43). Plasma
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renin activity postfurosemide was 11.1 ng/ml • hr, clearly elevated in the renovascular range.
Patient 2 was a 28-year-old black woman who presented with
pulmonary edema and normotension. During hospitalization,
she had several hypertensive crises. Urinary vanillymandelic
acid, norepinephrine, and epinephrine were elevated at 116
mg/g creatinine, 210.6 /xg/24 h, and 82.2 fig/24 h, and 82.2
/xg/24 h, respectively. Laporotomy showed a solitary pheochromocytoma and no evidence of a renovascular lesion. Preoperatively, the plasma volume was diminished at 36.47 ml/kg
(ideal, 47.43). Plasma renin activity postfurosemide was 13.6
ng/ml • h. Postoperatively, the plasma volume returned to normal, the patient was normotensive, and plasma renin activity
returned to a normal value of 1.2 ng/ml • h.
From these data it becomes obvious that elevated plasma
renin activity postfurosemide not only may implicate
renovascular hypertension (1) but also pheochromocytoma. The plasma volume is obviously a major determinant ( 2 ) , and the circulating catecholamines play a role
as well (2, 3 ) . We believe that in the presence of elevated
plasma renin activity postfurosemide, a pheochromocytoma
should be given special consideration, since radiologic
procedures used in the delineation of renovascular hypertension are potentially dangerous in patients with chromaffin tumors ( 4 ) .
ZEV M. M U N K , M.D.C.M.
GEORGE TOLIS, M.D., M . S C , C.S.P.Q. ( C )
Douglass would be much greater than in the cooked (and
presumably processed) diet taken previously by those two
patients. We suggest that the insulin requirement of both
these patients fell because the postprandial rises of blood
sugar were not as great after raw food as after processed
and cooked food.
ANTHONY R. LEEDS,
DAVID J. A. JENKINS,
MIGUEL A. GASSULL,
BERNARD COCHET,
LAWRENCE M. BLENDIS,
M.D.
M.D.
M.D.
M.D.
M.D.
Medical Research Council Gastroenterology Unit
Central Middlesex Hospital
London N.W.10 7 N.S., England
REFERENCES
1. DOUGLASS JM: Raw diet and insulin requirements. Ann Intern
Med 82:61-62, 1975
2. HORWITZ DL, SLOWIE L: Raw diet in diabetes mellitus. Ann
Intern Med 82:853-854, 1975
3. JENKINS DJA, LEEDS AR, GASSULL MA, et al: Reduction in
postprandial glycaemia by guar and pectin. Unpublished
Fever, Flashbulbs, Humps, and Spikes
TO THE EDITOR: A letter {Ann Intern Med 83:84, 1975)
adds a new phrase to medical jargon in addition to "fever
spike." In its accompanying figure, the depicted febrile
bout resembles a dagger more than a goalpost or a spike
REFERENCES
(daggerfever?). A spike is a large untapered nail. It is
doubtful if fever ever rises and falls like the flash of a
1. WALLACH L, NYARAI I, DAWSON KG: Stimulated renin: a screening test for hypertension. Ann Intern Med 82:27-34, 1975
flashbulb. The "highest daily temperatures" shown in the
2. DAVIS JO: The control of renin release. Am J Med 55:333-350,
graph obviously do not portray the whole febrile reaction.
1973
If more measurements had been recorded, the fever
3. ASSAYKEEN TA, GANONG WF: The sympathetic neuron system
and renin secretion, in Frontiers in Neuro-Endocrinology, edited curve, no doubt, would appear blunted or humped (humpby MARTININ L, GANONG WF. New York, Oxford University
fever?).
Press, 1971, p. 67
Two items of information are missing: [1] how long did
4. ROSSE P, YOUNG IS, PANKE WF: Techniques, usefulness and
the febrile bouts last; [2] did recurrences cease after the
hazards of arteriography of pheochromocytoma. Review of 99
cases. JAMA 205:547-553, 1968
drug was permanently withdrawn? If they then resumed
at "5 to 7 days" intervals, periodic fever with "unrevealing"
laboratory data, excepting occasional.leukopenia, might be
considered. In that case, short febrile episodes may have
Unabsorbable Carbohydrates and Insulin Need
recurred spontaneously regardless of medication (Am J
Med Sci 243:729, 1962).
TO THE EDITOR: We compliment Dr. Douglass on his reHOBART A. REIMANN, M.D., F.A.C.P.
freshing approach to the dietary control of two diabetic
patients who wished to reduce their insulin therapy ( 1 ) .
Department of Medicine
While accepting that the effect of the raw food diet in
Hahnemann Medical College and Hospital
Philadelphia, Pennsylvania 19102
reducing insulin requirements may be due, at least partly,
to trapping of otherwise absorbable carbohydrate within
intact cellulose cell walls ( 2 ) , we think that other factors
In reply:
may be important. For example, we have shown that
unabsorbable carbohydrate reduces post prandial rises of
blood sugar ( 3 ) .
The duration of the two febrile "bouts" shown in our figure
illustrating the "goalpost" fever pattern was approximately
The addition of Guar gum (a storage polysaccharide
18 to 20 hours. Fever has not recurred since the offending
obtained from the cluster bean, Cyamopsis tetragonoloba)
drug was withdrawn.
to the bread, and pectin (a polymer of galacturonic acid
We suspect that Dr. Reimann is not a football fan. The
obtained from apples) to the marmalade of a breakfast
illustration depicts two fever "spikes" connected by a
test meal resulted in significant reductions of the mean
horizontal (crossbar) line and, as such, is not unlike the
postprandial rise of blood sugar in 7 subjects at 15 minutes
top half of a set of football goalposts.
(97.1 ± 2.6 mg/dl and 116.9 ± 5.1 mg/dl, P < 0.002)
We agree that had the patient's temperatures been
and at 30 minutes (108.9 ± 7.8 mg/dl and 138.2 ± 13.8
plotted every 4 hours, the result would have been a
mg/dl, P < 0.001).
"double humpfever" (? "camel back fever") pattern. But
The total quantity of unabsorbable carbohydrates and
who would have published a letter entitled "Humpfever"?
"dietary fibre" in the raw foods diet prescribed by Dr.
Division of Endocrinology
Royal Victoria Hospital
Montreal, PQ H3A 1A1, Canada
740
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HENRY W. MURRAY, M.D.
JOHN J. MANN, M.D.
Johns Hopkins Hospital
Baltimore, Maryland 21205
Medical Care for the Elderly
TO THE EDITOR: I have followed with interest the paper of
Dr. Brickner and colleagues concerning his program for
care of the elderly at home (Ann Intern Med 82:1-6,
1975) and the editorials and letters engendered by it.
Doctor Mumford and associates' letter of July 1975 (Ann
Intern Med 83:125-126, 1975) was most interesting and
delineated programs long in existence for the chronically
ill elderly patients of New York City through the New
York City Health & Hospitals Corporation. Doctor Brickner's reply to this letter was inaccurate in that he apparently is under the impression that services delivered to
patients in these programs are limited to those allowed by
legislation, and that "there are limiting factors as to the
type of patient included. Most of the patients in homecare programs are people previously known to the hospital." Many services that are not covered by payment
from fiscal intermediaries are provided to patients on a
need, rather than reimbursable, basis. Patient's needs have
been, and continue to be, the primary determinants of
types of services provided. Twenty percent or more of our
patients had not been known to the hospital before acceptance on home care. Case finding in the community is
done by community residents and visiting nurses, as well
as by local hospital staffs. Referrals come from these and
a multiplicity of other sources, and evaluations and care
are then provided, as needed and acceptable to each patient. I would refer Dr. Brickner and staff to the Columbia
Study on Home Health Agencies done in 1967 for a clear
picture of the Corporation programs.
JOSEPHINE A. LOCKWOOD, M.D.
Department of Community Medicine
New York Medical College
New York, New York
TO THE EDITOR: I suspect that your problems in copy
editing are not yet solved. Why in the world would hypercalcemia be "indicated as preferred in American usage to"
hypercalcinuria? It is one thing to insert an extra "n" in
making neologisms. It is quite another thing to convert
urine into blood.
ALVAN R. FEINSTEIN, M.D.
Department of Internal Medicine
School of Medicine
Yale University
New Haven, Connecticut
TO THE EDITOR:
at least dr feest
and dr wrong are right
when the editors pen
inserted an en
in front of their uria
though the calcium was there
it did not disintegrate
but did precipitate
causing pain to the recipient
and an ache to the redactient
which all goes to show
how much we should know
about how many angels
with all of their spangels
can dance on the head of a pin
apologies to edward estlin cummings and see
ann int med aug 1975 p 288
K E N N E T H B. OLSON, M.D.
810 Oakview Drive
New Smyrna Beach, Florida 32019
And with apologies to the anonymous author of the famous
Ginsberg story:
Milk or mud, urine or blood,
Calcium strikes again.
This one we can hang on the printer—small consolation!
The Editor
Scene in Print: Wife-Beaters?
Correction: Apology for "Hypercalcinuria"
In the August 1975 issue, lines 21 and 22 of column 2 on
page 288 should have read: ". . . hypercalciuria" is indicated as preferred in American usage to "hypercalcinuria."
Distinguished leaders in the field of policy and decisionmaking have been invited to share opinions, information
and action strategies to address the national problem of
the increasing population of female substance abusers.
[From an announcement of a conference in Miami Beach,
issued by the National Institute of Drug Abuse.]
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