PRIMARY ADRENOCORTICAL CARCINOMA CAUSING ALDOSTERONISM
SEYMOUR L. ALTERMAN, MD, CARLOS DOMINGUEZ, MD, ALFREDO LOPEZ-GOMEZ MD, AND ARNOLD L. LIEBER, MD*
A case of aldosteronism caused by a carcinoma of the adrenal cortex is presented. Plasma renin activity was determined and found to be suppressed. Ten other reported cases of hypermineralocorticism due to primary carcinoma of the adrenal are summarized, and a comparison of the common features is made. Excessive production of 17-hydroxycorticoids and/or 17-ketosteroids was present in most of these patients, but there was very little clinical evidence of the effects of hypercortisolism or hyperandrogenia.
C ONN6 FIRST DELINEATED THE CLINICAL SYN- drome of aldosteronism in 1955. The clinical manifestations of aldosteronism may range from asymptomatic “essential” hyper- tension to the incapacitating symptoms of severe potassium depletion, i.e., periodic muscular weakness and/or paralysis, intermit- tent tetany, paresthesia, headache, polyuria, nocturia, and polydipsia. Although serum electrolytes may be within the normal range,9 most reported cases have demonstrated a hy- pokalemic alkalosis. Hypertension is a consis- tent feature of this syndrome.
The majority of cases of primary adolsteron- sim have been caused by benign adrenocorti- cal adenomata; most of these patients have been cured by removal of their tumor.8 Ma- lignancy is a very rare cause of primary al- dosteronism, as defined by Conn. However, several cases of adrenocortical malignancy manifesting a clinical syndrome caused by the excessive production of aldosterone have been documented. Here we report a case of car- cinoma of the adrenal cortex causing well- documented aldosteronism, and we compare this case with other reported cases of hyper- mineralocorticism due to carcinoma of the adrenal gland.
From the Department of Medicine, Mount Sinai Hospital, Miami Beach, Fla.
* Department of Psychiatry, University of Miami School of Medicine.
1 Hydropres, hydrochlorthiazide and reserpine, Merck Sharp & Dohme.
Address for reprints: Seymour Alterman, MD, 1688 Meridian Avenue, Miami Beach, Fla. 33140.
The authors wish to thank Dr. Lawrence Fishman for his aid in editing the manuscript.
Received for publication March 11, 1969.
CASE HISTORY
A 68-year-old Caucasian man was admitted to the hospital on December 26, 1965 be- cause of a painless swelling in the upper portion of the sternum of 2 weeks’ duration. The patient had a history of hypertension for several years and had been taking one tablet daily of Hydropres.t A left lower lobe lobec- tomy had been performed in 1950 because of bronchiectasis. There was no history of dia- betes, and there had been no recent change in weight. The family history was not con- tributory.
Physical examination revealed an adequately nourished man in no acute distress. The blood pressure in both the recumbent and stand- ing positions was 210/110. A firm, nontender protuberant mass with ill-defined margins was present overlying the upper portion of the sternum. Breath sounds were absent in the lower half of the left hemithorax. There was a Grade II/VI soft apical systolic murmur. The liver and spleen were not enlarged. There were no masses in the abdomen. Rectal ex- amination disclosed a moderately enlarged prostate gland. There was no peripheral edema. Neurologic examination was normal.
A needle biopsy of the sternal mass showed a poorly differentiated carcinoma. A skeletal survey showed no abnormalities in other bones. An intravenous pyelogram was within normal limits. A chest film showed slight cardiomegaly and changes secondary to the remote lobectomy. The serum potassium was persistently low (2.9 to 3.7 meq/1, normal values being 4.3 to 5.6 meq/1). The sternal mass was radiated with the cobalt unit (total dose 4500 rads over a period of 3 weeks). The patient was discharged January 3, 1966
on Aldomet,* Hydropres, and potassium chlo- ride, 15 meq 3 times daily.
He was readmitted on March 6, 1966 be- cause of increasing nocturia. Again, persis- tent low-serum potassium levels were ob- served (2.6 to 3.3 meq/1). The 24-hour urine excretion of potassium and aldosterone, per- formed while the patient was on a kosher diet (containing approximately 3g NaCl per 24 hours), was increased. Arterial blood studies showed a metabolic alkalosis, and a glucose tolerance test showed a diabetic curve (Table 1). Several urine specimens showed a relatively fixed specific gravity in the range of 1.005 to 1.010. The antihypertensive and diuretic medication was discontinued; he was discharged on March 15, on 15 meq KCI 3 times daily.
The patient was readmitted on March 27 because of severe nocturia, pain over the lumbar spine, and weakness. Physical ex- amination was essentially unchanged from the previous admissions. The blood pressure was 200/100.
A needle biopsy of the prostate gland
* Aldomet, methyldopa, Merck Sharp & Dohme.
1 Kindly performed by E. L. Cohen, MD.
showed prostate tissue with focal glandular atypism but no definite evidence of malig- nancy. A bone marrow aspiration from the left iliac crest showed metastatic carcinoma to the bone marrow. Serum postassium con- tinued to be low (2.1 to 2.9 meq/1), despite the fact that the patient was now off diuretic medication and taking potassium supplements. Twenty-four hour urine excretion of potas- sium and aldosterone, with the patient on a kosher diet, was again elevated. Urinary excretion of 17-hydroxycorticosteroids on March 27 showed slightly elevated values. Urinary 17-ketosteroid excretion was normal. Repeat testing on April 9 showed an in- creased level of 17-ketosteroids and 17-hydroxy- corticosteroids. A dexamethasone suppression test was performed from April 7 through April 9. Dexamethasone failed to suppress the abnormally elevated 17-ketosteroids and 17-hydroxycorticosteroids. Plasma renin activ- ityt was not measurable in blood samples obtained in either the recumbent or the up- right posture, with the patient on a low sodium diet (200 mg sodium daily for 3 days prior to the test).
Five-fluorouracil was administered intra-
| Arterial blood studies: (3-10-66) | ||
|---|---|---|
| Normal | Patient | |
| Carbon dioxide tension (mm Hg) | 40 ± 2 | 49.5 |
| pH (units) | 7.40 ± 0.02 | 7.53 |
| Standard Bicarbonate (meq/liter) | 21.3-24.8 | 39.0 |
| Plasma CO2 content (meq/liter) | 23-28 | 41.8 |
| Base Excess. (meq/liter) | ±2 | +16.0 |
| Hematocrit (percent) | 37-50 | 35.0 |
| Blood volume studies: (3-31-66) | Normal | Patient |
|---|---|---|
| Total blood volume (ml) | 4820 ± 465 | 5986 |
| Total plasma volume (ml) | 2676 ± 321 | 4419 |
| Red cell volume (ml) | 2144 ±± 144 | 1567 |
| TBV (ml X kg) | 76 ±8 | 82.3 |
| TPV (ml X kg) | 42 ± 5 | 60.8 |
| RCV (ml X kg) | 30 ± 2 | 21.6 |
Urinary hormone studies: (24-hour excretion) Normal
| 3-14-66 | 3-27-66 | 3-30-66 | 4-9-66 | |
|---|---|---|---|---|
| Aldosterone 3-32 ug/24 hrs | 96 | 131 | 91 | |
| 17 Hydroxyc. 3-10 mg/24 hrs | 16 | 20 | 21 | |
| 17 Ketoster. 9-22 mg/24 hrs | 17.8 | 18 | 28 |
Urinary electrolyte studies: (24-hour excretion) Normal
Patient
| 3-15-66 | 3-29-66 | |
|---|---|---|
| Sodium (meq/24 hr) 130-200 | 81.2 | 8.4 |
| Potassium (meq/24 hr) 40-65 | 150.8 | 92.4 |
| Chloride (meq/24 hr) 170-250 | 46.4 |
Oral glucose tolerance test: (3-11-66)
| FBS | ¿ hr. pp | 1 hr. pp | 2 hr. pp | 3 hr. pp | |
|---|---|---|---|---|---|
| Blood glucose (mg/100 ml) | 130 | 185 | 242 | 292 | 216 |
| Urine glucose | Neg | Neg | Neg | 1+ | 1+ |
venously for the treatment of metastatic car- cinoma in a dose of 1 g daily from April 4 through April 8. Subsequently, the patient developed an ulcerating stomatitis, anemia, thrombocytopenia, and marked granulocyto- penia. A low-grade fever developed on April 17, and the patient’s general condition de- teriorated progressively until April 21 when he expired.
At autopsy, the left adrenal gland was re- placed by a nonencapsulated mass, measur- ing 4.5 × 4.5 x 3 cm and weighing 30 g (Fig. 1). The tumor infiltrated the peri- adrenal fat. Cross section revealed numerous areas of necrosis and hemorrhage. Histologi- cally, the pattern was that of a solid carcinoma composed of pleomorphic cells, with vacu- olated granular eosinophilic cytoplasm and prominent nuclei. Some of the cells were multinucleated. There was local invasion of vascular spaces and lymphatics (Fig. 2). The right adrenal gland showed marked autolysis. Metastases were found in the capsule of the pituitary gland (adjacent to the pars nervosa and the pituitary stalk), right lung and pleura, and bones (sternum, vertebrae, iliac bones). In the kidneys, the juxtaglomerular cells showed degranulation of cytoplasm, and there was hydropic degeneration of some of the cells in the proximal convoluted tubules (Fig. 3). No Crooke’s changes were noted in the pituitary gland.
DISCUSSION
We have reported a case of adrenal carci- noma causing a clinical syndrome of hyper- tension and hypokalemic alkalosis. Urinary
excretion of aldosterone was markedly ele- vated on several occasions and plasma renin activity was suppressed.
Conn,8 in considering the problem of diag- nosis of primary aldosteronism, states that evi- dence of excessive production of adrenal steroids other than aldosterone rules out the diagnosis of primary aldosteronism. In re- viewing the literature, we have found only 10 other documented cases of carcinoma of the adrenal cortex with primary clinical man- ifestations of excessive mineralocorticoid se- cretion and without evidence of clinical hyper- cortisolism .* Of these 10 cases1, 3, 4, 10, 12, 13, 14, 16, 19, 20, 22 only one20 purports to have established that the excretion of 17-hydroxy- corticoids and 17-ketosteroids were normal. Examination of this report, however, reveals that only one measurement of each of these substances was documented and that no actual measurements of aldosterone excretion were made. In all other cases where steroid studies were performed, excessive production of a steroid other than aldosterone was demon- strated, despite absence of clinical evidence of hypercortisolism or hyperandrogenia. Ap- parently then, adrenal carcinomas are almost invariably associated with a mixed hyper- secretion of steroid elements. Such findings preclude their classification as cases of primary aldosteronism according to the criteria pro- posed by Conn8
Hypertension and hypokalemic alkalosis, the characteristic signs of aldosteronism, can also be produced by hypersecretion of cortisol.7 Crane and Harris,11 based on their extensive steroid analyses, suggest that the hypo- kalemic alkalosis in patients with adrenocor- tical malignancies may be caused by an ex- cess of desoxycorticosterone (DOC). This is
* Conn8 cited a case of adrenocortical carcinoma caus- ing primary aldosteronism but did not present suffi- cient data to warrant its inclusion in Table 2.
supported by the case reported by Marquezy,19 in which hyperaldosteronuria was absent and DOC and its congeners were demonstrated in excessive amounts. The studies by Biglieri et al.2 confirm that excessive production of DOC and/or corticosterone (B) can produce a syndrome of hypertension and hypo- kalemic alkalosis. Leutscher17 has proposed that the term “syndrome of mineralocorticoid excess” be used when hypertension and hypo- kalemic alkalosis cannot be attributed to ex- cessive production of aldosterone.
Secretions of DOC and B were not mea- sured in our patient. Because of the finding of increased excretion of steroids other than aldosterone, the case described here does not fit within the boundaries of Conn’s definition of primary aldosteronism, although it is doubt- ful that the very slight increase in the 17- hydroxycorticoid excretion played any role in the clinical or biochemical picture. We
have, therefore, classified our case, along with others showing a definite excess production of aldosterone, simply as aldosteronism due to primary adrenocortical carcinoma. These cases are summarized in Table 2. The cases of adrenal carcinoma in which aldosterone was either normal or was not measured will be referred to as cases of mineralocorticoid excess syndrome due to primary adrenocorti- cal carcinoma, and these are summarized in Table 3.
Where we are here concerned chiefly with primary adrenocortical carcinomas, there have also been reports of metastatic carcinoma to the adrenal causing aldosteronism.18-21 Koh- ler15 reported a case of metastatic carcinoma of the prostate associated with adrenal hyper- plasia and aldosteronism; there was no evi- dence of metastasis to the adrenal at autopsy. Brorson5 described the case of a 46-year-old woman with hypokalemic alkalosis and hy-
pertension in whom a right adrenal cortical adenoma was found and removed. Nine months later this patient had a recurrence of her previous symptoms. Autopsy revealed a carcinoma in the region of the right adrenal gland with metastasis to the liver. Levels of aldosterone in the plasma and in the tumor tissue of this patient were normal.
While we do not wish to add to the seman- tic confusion surrounding endocrine syn- dromes associated with malignancy of the adrenal cortex, we feel that the system of clas- sification used here is a reasonable one at least for the present. Aldosteronism, as used here, means simply that an excessive secre- tion of aldosterone has been demonstrated and that we consider this as the cause of the clinical syndrome. A more meaningful classi-
fication of primary adrenocortical carcinoma must await the precise measurement of in- dividual steroids.
SUMMARY
A case of aldosteronism caused by a car- cinoma of the adrenal cortex is presented. Plasma renin activity was determined and found to be suppressed. Ten other cases of hypermineralocorticism due to primary car- cinoma of the adrenal are summarized, and a comparison of the common features is un- dertaken. Excessive production of 17-hydro- xycorticoids and/or 17-ketosteroids was pres- ent in most of these patients, but there was very little clinical evidence of the effects of hypercortisolism or hyperandrogenia.
| CASE REPORTED BY | AGE | RACE | SEX | SYMPTOMS | BLOOD PRESSURE | PHYSICAL EXAMINATION | X-RAY | EKG | NA | K | LABORATORY CL CO2 URINE PH | |
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| FOYE 1955 | 60 | N | M | THIRST, POLYURIA, POLYDIPSIA, GENERALIZED WEAKNESS. | 176/110 TO 200/135 | OBESE, GENERALIZED MUSCULAR WEAKNESS, ENLARGED HEART. RETINOSCOPY SHOWED AV NICKING AND ARTERIOLAR NARROWING. | CHEST: LVH, IVP: NORMAL, RETROPHEUMO :* TRIANGULAR MASS IN RIGHT SUPRARENAL AREA. | LVH AND PERSISTENT U WAVES | 150 | 18 | 90 | 53 6.5 |
| BROOKS 1957 | 40 | - | M | NOCTURNAL POLYURIA, ORTHOPNEA, ANKLE SWELLING. | 205/120 TO 230/120 | ANKLE EDEMA, EARLY HYPERTENSIVE CHANGES IN THE RETINA. | CHEST: LVH, IVP: LEFT KIDNEY LOW IN POSITION, RETROPHEUMO: MASS ABOVE LEFT KIDNEY. | 138 | 2.5 | 98 | 40 | |
| KANDRAC 1957 | 44 | W | F | NOCTURIA, WEAKNESS, EASY FATIGABILITY, MUSCULAR PAIN ON EXERTION. | 200/110 | EXOPHTHALMIC GOITER. | RETROPHEUMO: MASS ABOVE LEFT KIDNEY COMPRESSING IT DOWNWARDS. | DEPRESSION OF ST SEGMENTS IN LEADS I, II, AVF AND V5. | 3.8 | 86.2 | ||
| BLEHA (7A) 1956 | ||||||||||||
| ZIMMERMAN 1959 | 38 | - | F | POLYURIA, NOCTURIA, TWO EPISODES OF TETANY, GENERALIZED MUSCLE WEAKNESS. | 200/130 | POSITIVE TROUSSEAU SIGN, PALPABLE RIGHT KIDNEY LATER FEVER, RIGHT FLANK PAIN, INCREASE IN SIZE OF RIGHT FLANK MASS. | IVP: DEPRESSED RIGHT KIDNEY. | 145 | 2.1 | 35 6-7 | ||
| CRANE 1965 | 64 | - | F | WEAKNESS IN LOWER EXTREMETIES, NOCTURIA, FEVER, VOMITING, PAIN IN LEFT UPPER QUADRANT. | 200/102 | FEVER, LEFT UPPER QUADRANT TENDERNESS, MASS IN LEFT UPPER QUADRANT. | CHEST: ENLARGED LEFT AND RIGHT VENTRICLES, IVP: NORMAL ARTERIOGRAM: NORMAL | 139 | 2.3 | 38 | ||
| ALTERMAN 1967 | 68 | W | M | NOCTURIA, WEAKNESS PAINLESS SWELLING IN UPPER PART OF STERNUM OF TWO WEEKS DURATION. | 210/110 | FIRM, NON TENDER MASS OVER UPPER PART OF STERNUM, GRADE 2/6 SOFT APICAL SYSTOLIC MURMUR, PROSTATIC ENLARGEMENT. | CHEST: CARDIOMEGALY, CHANGES SECONDARY TO OLD LEFT LOWER LOBECTOMY, IVP: NORMAL BONE SURVEY: NORMAL | LVH | 139 | 2.9 | 92 | 37 ACID |
| CASE REPORTED BY (CONT.) | 17-HYDROXY- CORTICOIDS (mg/24hr) URINARY | STEROID 17-KETO- STEROIDS | STUDIES | SURGERY | AUTOPSY | MISCELLANEOUS | |
|---|---|---|---|---|---|---|---|
| (mg/24hr) | ALDOSTERONE | GROSS | HISTOLOGY | ||||
| FOYE | 31 (N: 9.6 to 19.2) | 278 (N: 6 to 15) | 12mcg. x IOOmin (N: 4.8) | RIGHT ADRENAL REPLACED BY TUMOR. | CARCINOMA CONSISTING OF THREE DIFFERENT CELLULAR PATTERNS. | THREE MONTHS AFTER SURGERY. RETROPERITONEAL TUMOR WITH METASTASES TO LUNG, LIVER, BONE MARROW | |
| BROOKS | 46 to 86 (N: 5 to 18} | 29 to 53 (N: 5 to 21) | 20 to 30 mcg/24hr (N: 2) | LARGE TUMOR SURROUNDING GREAT VESSELS AND INVOLVING | WELL DIFFERENTIATED NODULAR CARCINOMA WEIGHING 1400 gm. | DIABETIC GLUCOSE TOLERANCE CURVE, PLASMA CORTISOL 8.3 TO IOmcq (N: 2-8). ROSE TO 23 mcg ON STIMULATION WITH ACTH. | |
| LEFT KIDNEY. | |||||||
| KANDRAC | 14 to 19.8 | 24.4 to 34.3 | 98 gamma/24 hr. | OVOID TUMOR | CARCINOMA OF ADRENAL | PLASMA CORTISOL, UPPER LIMITS OF NORMAL. | |
| (N: - IO) | (N: 6 to 15) | (N: - 10) | SUPERIOR TO | CORTEX, HIGHLY | NO RISE ON ACTH STIMULATION. AFTER | ||
| LEFT KIDNEY. | ANAPLASTIC CELLS INVADING THE BLOOD VESSELS. | SURGERY ACTH STIMULATION PRODUCED THE EXPECTED RISE IN PLASMA AND URINARY HYDROXYCORTICOIDS. | |||||
| ZIMMERMAN | 4.7 to 5.0 | 29.2 to 37.5 | 17 to 180mcg/24 hr. (N: 2-5) | TUMOR WEIGHING | 583 CARCINOMA. | METASTESES TO LUNG AND SPINE. | ON STIMULATION WITH 40mg ACTH GIVEN IV |
| (Normal) | (N: - 20) | gm ADHERENT TO LIVER AND INVADING INFERIOR VENA CAVA, | OVER AN 8 HOUR PERIOD, ALDOSTERONE EXCRETION ROSE FROM 17 mcg. TO 173 mca. | ||||
| CRANE | 18.6 to 22.3 (N: 5 to18) | 8.6 to 12.7 | 32 to 60mg/24 hr. (N: 4 to 12) | TUMOR OF LEFT ADRENAL WEIGHING | LOBULES AND NODULES | TWELVE WEEKS AFTER SURGERY. METASTASES TO LUNGS, LIVER, | EXTENSIVE STEROID ANALYSES DONE ALL DURING THE |
| (N: 6 to 15) | WITH SCATTERED AREAS | HOSPITAL COURSE. INITIALLY: 17 KETOGENIC STEROIDS- | |||||
| 1010 gm. LIVER METASTASES. | OF HEMORRHAGE AND NECROSIS. CELLS | PERIAORTIC NODES. | ELEVATED, 17 KETOSTEROIDS- ELEVATED, URINARY | ||||
| CORTISOL - NORMAL, TETRAHYDRO-S- MARKED ELEVATION, | |||||||
| ARRANGED IN CORDS. | TETRAHYDRO-E- NORMAL, DOC & THDOC SECRETION- MARKED ELEVATION. | ||||||
| ALTERMAN | 16 to 21 | 17.8 to 28 | 96 to 13/mcg/24ht (N: 3 10 32) | NEEDLE BIOPSY OF | POORLY DIFFERENTIATED | THIRTY gm TUMOR REPLACING LEFT ADRENAL AND MEASURING 4.5 x 4.5 x 3 cm. HISTOLOGICALLY A SOLID CARCINOMA WITH NO DISTINCTIVE CELL TYPE, METASTASES TO LUNG, PLEURA, BONES AND PITUITARY STALK. | DIABETIC GLUCOSE TOLERANCE CURVE. PLASMA |
| (N: 3 to 10) | (N: 9 to 22) | STERNUM MASS. | CARCINOMA. | RENIN ACTIVITY REPORTED AS UNMEASURABLE IN BOTH RECUMBENT AND UPRIGHT POSTURES. ARTERIAL BLOOD STUDIES SHOWED A METABOLIC ALKALOSIS. |
* Nephrograms following retropneumoperitoneum
ADRENOCORTICAL. CA AND ALDOSTERONISM
Alterman et al.
| CASE REPORTED BY | AGE | RACE | SEX | SYMPTOMS | BLOOD PRESSURE | PHYSICAL EXAMINATION | X-RAY | EKG | NA | LABORATORY URINE K CL CO2 PH | ||
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| FELDMAN 1961 | 26 | - | M | HEADACHE, POLYDIPSIA, POLYURIA. | 170/120 | RETINAL CHANGES INDICATIVE OF ARTERIOLAR SCLEROSIS. | CHEST LVH, ELONGATION OF AORTA. IVP CALCIFI- CATION, UPPER POLE OF RIGHT KIDNEY AND DIS- PLACEMENT OF RIGHT KIDNEY. ARTERIOGRAM: MASS AT UPPER POLE OF RIGHT KIDNEY. | |||||
| KNAPTON 1965 | 59 | - | F | THIRST, POLYURIA, WEIGHT LOSS. | 160/85 to 210/130 | FLORID FACIES, PETECHIAE OVER LEGS AND TRUNK, EDEMA OF LEGS | CHEST NORMAL | 112 | 18 | 81 41 (ALK RES | ||
| SANTANDER 1965 | 50 | - | F | ONE YEAR PRIOR TO ADMISSION- POLYURIA, POLYDIPSIA, PARALYSIS OF LOWER EXTREMETIES FOR ONE MONTH. LATER NOTED HEADACHE, WEAKNESS, PALPITATIONS, NOCTURIA, PARESTHESIAS. | 160/110 | ARTERIOLAR NARROWING OF OCULAR FUNDI, SIGNS OF CARDIAC FAILURE, LIVER ENLARGEMENT, NODULE IN RIGHT LOBE OF THYROID. | CHEST: LVH. IVP: WITH RETRO- PHEUMOPERITONEUM, SOFT TISSUE DENSITY IN UPPER POLE OF RIGHT KIDNEY. | LVH | 148 | 26 | 80 | 36 64 |
| ANDRADE 1965 | 24 | W | M | HEADACHE, ASTHENIA, EDEMA OF LOWER EXTREMETIES. | 140/IIO to 180/130 | HEPATOMEGALY, SPLENOMEGALY, ASCITES. | CHEST: NORMAL IVP: DISPLACEMENT OF RIGHT KIDNEY BY EXTERNAL COMPRESSION. | LVH | 139 | 39 | 104 | 40 ACID ALK (RES, |
| MARQUEZY 1965 | 15 | - | F | HEADACHE, POLYDIPSIA, POLYURIA, TETANY, VÍRILISM. | 140/80 to 200/100 | RETROPHEUMO: MASSIVE TUMOR, RIGHT ADRENAL AREA. | LVH, PROLONGED QT INTERVAL, U WAVES. | 136 | 2.6 | 100 | 51 | |
| CASE REPORTEO BY (CONT) | URINARY STEROID STUDIES | SURGERY | AUTOPSY | MISCELLANEOUS | |||
|---|---|---|---|---|---|---|---|
| 17-HYDROXY- CORTICOIDS (mg/24 hr) | 17-KETO- STEROIDS (mg/24 hr) | ALDOSTERONE | |||||
| GROSS | HISTOLOGY | ||||||
| FELDMAN | 32.8 (UPPER NORMAL) | TUMOR ABOVE RIGHT KIDNEY. | CARCINOMA OF ADRENAL | POSTOPERATIVE STEROID EXCRETION: 17-KETOSTEROIDS 7.9 mg/24hr. 17-HYDROXYCORTICOIDS: 0.20mg /24 hr. | |||
| KNAPTON | VASCULARIZED TUMOR OF RIGHT ADRENAL INVADING LIVER AND INFERIOR VENA CAVA. | CARCINOMA OF ADRENAL | THIRTEEN DAYS AFTER SURGERY. METASTASES TO SECOND LUMBER VERTEBRA AND PUBIS. | PLASMA 17-HYDROXYCORTICOIDS: 46.5 mcg % AT MIDNIGHT (N: LESS THAN 6) 571mcg % AT 9:00 A. M. (N: 6 to 24) | |||
| SANTANDER | 9.3 (Normal) | 11.5 (NORMAL) | RETROPERITONEAL MASS ON RIGHT FUSED WITH LIVER. | CARCINOMA OF ADRENAL | ONE MONTH AFTER SURGERY. RIGHT ADRENAL TUMOR WEIGHING 90 qm METASTASES TO LIVER AND LUNG. | KIDNEY LESIONS AT AUTOPSY COMPATIBLE WITH HYPOKALEMIC NEPHROPATHY | |
| ANDRADE | 74 morked elevation! | TUMOR OF RIGHT ADRENAL INVADING INFERIOR VENA CAVA. | CARCINOMA OF ADRENAL | SEVERAL DAYS AFTER SURGERY. ADRENAL TUMOR 12 x 15 cm UNDIFFERENTIATED CARCINOMA, METASTASES TO LUNG AND LIVER | II -OXYSTEROIDS 74 mg/24 hr. (elevated) | ||
| MARQUEZY | 16.2 to 22.4 (elevated) | 24.6 to 27.6 (elevated) | LESS THAN 2mcg/ 24 hx (NORMAL) | TUMOR WEIGHING 370gm REPLACING RIGHT ADRENAL. | CARCINOMA OF ADRENAL. | PATIENT ALIVE AND WELL 18 MONTHS AFTER ABLATION OF TUMOR. STEIN-LEVINTHAL OVARIES NOTED DURING PREVIOUS APPENDECTOMY. MARKEDLY ELEVATED LEVELS OF DOC AND THOOC IN URINE PRIOR TO SURGERY, AND | |
| 17-HYDROXY | (23.4 711.4 | mg/24 hr | WITH ACTH |
|---|---|---|---|
| WITH DECADRON | |||
| 17-KETO | (40.7 | 14 | WITH ACTH |
| 1209 11 | WITH DECADRON | ||
LABORATORY VALUES RETURNED TO NORMAL FOLLOWING SURGERY.
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