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and resulted in normal systemic arte Moreover, subjects with the highest reason, captopril should be used with

rial pressure readings after many renin levels showed the greatest caution inpatients with renal insuffi
other drugs had been ineffective. increment in serum and body potas ciency, in patients receiving potas
Although there were no short-term sium levels.2 The fact that our patient sium-sparing diuretics, or perhaps in
untoward effects on plasma creati had markedly elevated plasma re patients whose pretreatment potas
nine levels, hyperkalemia occurred nin activity before captopril therapy sium levels generous. The effect of
are
within days. This was not explainable is consistent with such an observa captopril renal function in man
on

by increased potassium intake, acido- tion. must also be clarified before the drug
sis, discontinuation of kaliuretic drug The second important issue in this can be used with impunity in the
therapy, or worsening renal function. case is the occurrence of marked presence of renal failure.
It seems likely that captopril effected hyponatremia encountered the day
a state of hypoaldosteronism through after the initiation of captopril thera This study was supported by the Veterans
inhibition of angiotensin-converting Administration and by grant HL-18095 from the
py (Table 1). Though the diuretic dose National Institutes of Health.
enzyme, reducing levels of angioten- was tapered at that time, the level of Ms Annie Chen gave technical assistance.
sin II, which in turn resulted in less serum sodium continued to decline,
stimulation of adrenal release of probably attributable to continued Nonproprietary Names and
aldosterone. The evidence for drug- water intake with impaired free- Trademarks of Drugs
induced hypoaldosteronism is compel water clearance. Without refuting CaptoprilCapoten.
ling: urinary aldosterone levels fell that the initial diuresis may have Clonidine hydrochlorideCatapres.
Prazosin hydrochlorideMinipress.
dramatically with accompanying re been vigorous, some attempt at fluid
versal of the urinary sodium-potas removal in this patient who showed References
sium ratio. Captopril alone has not weight gain, heart failure, and ad 1. Case DB, Atlas SA, Laragh JH, et al:
been sufficient to cause hyperkalemia vanced renal insufficiency was indi Clinical experience with blockade of the renin\x=req-\
in patients with milder degrees of cated. The original report of captopril angiotensin-aldosterone system by an oral con-
renal dysfunction and scleroderma use for scleroderma renal and hyper verting enzyme inhibitor (SQ 14225, captopril) in
hypertensive patients. Prog Cardiovasc Dis 1978;
hypertension.3 In our patient, it is tensive crisis implied that diuretics 21:195-206.
likely that the functional hypoal might be avoided; nevertheless, the 2. Atlas SA, Case DB, Sealey JE, et al:
dosteronism summated with the po Interruption of the renin-angiotensin system in
patient in that case did not have hypertensive patients by captopril induces sus-
tassium-retaining tendency of ad advanced renal failure, as was pres tained reduction in aldosterone secretion, potas-
vanced renal insufficiency to produce ent in our patient. It is necessary to sium retention, and natriuresis. Hypertension
1979;1:274-280.
clinically important hyperkalemia. recall the etiologic importance of 3. Lopez-Ovejero JA, Saal SD, D'Angelo WA,
Previous experimental work by Atlas volume excess in hypertension in et al: Reversal of vascular and renal crises of
scleroderma by oral angiotensin-converting\x=req-\
et al2 has shown that captopril pro patients with severe renal insuffi enzyme blockade. N Engl J Med 1979;300:1417\x=req-\
duces an increase in the amount of ciency.4 1419.
serum potassium and positive potas The potentially adverse effects of 4. Lazarus JM, Hampers CL, Merrill JP:
sium balance in subjects with mild to even slight potassium retention in
Hypertension in chronic renal failure: Treat-
ment with hemodialysis and nephrectomy. Arch
moderate essential hypertension. renal failure are well known. For this Intern Med 1974;133:1059-1066.

Dysphagia in a Patient With Hodgkin's Disease


Bruce W. Trotman, MD; John H. Glick, MD; Sergio G. S. deBarros, MD; Barbara F. Atkinson, MD

DYSPHAGIA owing to lymphoma- the esophagus and confirmed by a neously overthe next few weeks. Five
tous involvement of the esophagus is lymph node biopsy specimen. We months before admission, he experienced
uncommon and usually occurs late in emphasize the importance of exfoli- anorexia, malaise, and progressive dys-
the course of the disease, followed by ative cytology and the careful ap-
phagia for solid food and then liquids. This
was accompanied by a 20-kg weight loss.
death within six to 12 months.1,2 A proach to management and staging of He denied fever, night sweats, or pruri
patient with Hodgkin's lymphoma this uncommon clinical presentation. tus.
initially manifested dysphagia. The Case
A physical examination revealed a
diagnosis was suspected by the pres- Report of a
chronically ill, afebrile man in no acute
ence of Sternberg-Reed cells in the A 33-year-old man was admitted to the distress. Prominent, firm, bilateral lower
exfoliative cytological examination of Hospital of the University of Pennsylvania cervical and supraclavicular lymphade-
From the Gastrointestinal Section (Drs Trotman
complaining of progressive dysphagia and nopathy was present. The trachea was
weight loss for the past five months. The deviated to the right. No hepatospleno-
and deBarros) and the Hematology-Oncology
Section (Dr Glick), Department of Medicine; and patient was healthy until 12 months megaly or lymphadenopathy below the
the Department of Pathology (Dr Atkinson), before admission when he experienced diaphragm was noted.
School of Medicine, University of Pennsylvania, occasional nocturnal nausea relieved by Laboratory data showed a normal hemo
Philadelphia. bilious vomiting. An upper gastrointesti- globin level and platelet count and a
Reprint requests to 570 Maloney Bldg, Hospital
of the University of Pennsylvania, 3400 Spruce St, nal (GI) tract series was normal at that moderate leukocytosis (16,000/cu mm,
Philadelphia, PA 19104 (Dr Trotman). time, and his symptoms subsided sponta- with a shift to the left [8% band forms]).

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I.ivpr function test results were normal. diotherapy, and is clinically well 18
A chest roentgenogram demonstrated a months later.
mass in the superior mediastinum with The cytological diagnosis of Hodg
displacement of the trachea. A thyroid kin's disease has been reported previ
scan was normal. An upper GI tract series
showed an 11-cm narrowed segment in the ously on sputum and gastric speci
mens, and the malignant cells from
proximal esophagus with effacement of this patient resemble those previous
mucosa.
Endoscopy with a pdiatrie endoscope ly described. Cytologically similar
revealed a narrowed area at 22 cm from cells have been observed in several
the incisors. There was extrinsic compres benign and malignant conditions oth
sion associated with ulcration of the er than Hodgkin's lymphoma.1 Thus,
overlying mucosa. The result of brush a lymph node biopsy specimen is
cytology was initially interpreted as
necessary to confirm the diagnosis of
adenocarcinoma but on review was found
to be classic Sternberg-Reed cells. A
Hodgkin's disease.
supraclavicular lymph node biopsy speci Laparotomy and splenectomy are
men confirmed the diagnosis of Hodgkin's
important for the staging and man
disease, nodular sclerosis type. A bipedal agement of Hodgkin's disease. Thirty-
lymphogram was normal, but the high eight percent of patients with clinical
para-aortic lymph nodes were not well stage IIB will have disease below the
visualized. Percutaneous bilateral bone diaphragm at surgery.4 However,
marrow biopsy specimens were normal. acute life-threatening complications
Because of the risk of esophageal perfo (bronchospasm, inability to extubate
ration and dangers associated with intu patients, and respiratory arrest) have
bation anesthesia in mediastinal Hodg occurred during intubation anesthe
kin's disease, the patient received mantle sia for staging laparotomy in un
radiotherapy to 3,950 rads in cautiously treated patients with moderate to
increasing fractions. A repeated barium
swallow one month after the conclusion of large mediastinal masses.5 Reversing
his mantle radiotherapy demonstrated the usual sequence of staging laparot
complete resolution of the esophageal Fig 1.Barium swallow demonstrates nar omy followed by treatment should not
lesion that was confirmed by endoscopy. rowed segment of upper esophagus with notably affect the eventual overall
The mediastinal mass did not appear on a mucosal effacement. management of the majority of
repeated chest roentgenogram, and his patients with mediastinal disease.
weight returned to normal. Our patient was treated with subtotal
The patient later underwent staging nodal radiotherapy without adjuvant
laparotomy and splenectomy that were chemotherapy. This approach is re
negative for Hodgkin's disease below the
diaphragm. The final pathological stage ported to result in 80% disease-free
was IItB. He then received an additional survival.6
3,600 rads to the uninvolved para-aortic The good prognosis of our patient's
lymph nodes and splenic pedicle. He has esophageal involvement with Hodg
remained asymptomatic and free of recur kin's disease is due to secondary
rence for 18 months. His swallowing is extension of the mediastinal node
normal. disease rather than primary involve
Comment Classic Sternberg-Reed cell ob ment.
Fig 2.
Dysphagia is a serious symptom of tained by esophageal brushing.

References
esophageal disease and requires ra
diological and endoscopie evaluation. disease.' In extensive clinicopatho-
an 1. Ehrlich AN, Stadler G, Geller W, et al:
The usual causes of dysphagia are logical report on GI involvement in Gastrointestinal manifestations of malignant
lymphoma. Gastroenterology 1968;54:1115-1121.
esophageal motor disorders, stricture, lymphoma, the presence of dysphagia 2. Hambly CK, Blundell JE: Hodgkin's disease
tumor, or inflammatory lesions. was a poor prognostic symptom cul of the oesophagus. Aust Radiol 1968;12:43-48.
3. Strum SB, Park JK, Rappaport H: Observa-
There were unique aspects in this minating in death within one year in tion of cells resembling Sternberg-Reed cells in
case: (1) Dysphagia was the symptom Hodgkin's or non-Hodgkin's lympho conditions other than Hodgkin's disease. Cancer
of Hodgkin's disease. (2) Diagnosis ma.' The clinical impression that dys 1970;26:187-190.
4. Gamble JF, Fuller LM, Martin RG, et al:
was presumed to be Hodgkin's disease phagia is a late manifestation is sup Influence of staging celiotomy in localized pre-
by esophageal exfoliative cytology. ported by a report of three patients in sentations of Hodgkin's disease. Cancer 1975;
whom dysphagia developed after 6, 35:818-825.
(3) Careful radiotherapy management 5. Piro AJ, Weiss ER, Hellman S: Mediastinal
was necessary to avoid complications 10, and 11 years of Hodgkin's dis Hodgkin's disease: A possible danger for intuba-
of mediastinal lymph node involve ease. Death occurred within one year tion anesthesia. Int J Radiat Oncol Biol Phys
ment. in these patients.2 In contrast, the 1976;1:415-420.
6. Rosenberg SA, Kaplan HS, Brown BW: The
Postmortem studies have shown patient of this report initially mani role of adjuvant MOPP in the therapy of Hodg-
fested dysphagia owing to lymphoma- kin's disease: An analysis after ten years, in
esophageal involvement in 2% to 6% Jones SE, Salmon SE (eds): Adjuvant Therapy of
of patients with Hodgkin's disease tous involvement of the esophagus, Cancer II. New York, Grune & Stratton Inc,
usually associated with disseminated attained complete remission with ra- 1979, pp 109-117.

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