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Myopathy as a paraneoplastic manifestation of renal cell carcinoma
BRIEF CLINICAL OBSERVATIONS 6. Warkentin TE, Hayward CPN, Smith CA, et al. Determinants of donor platelet variability when testing for heparin-induced thrombocytopenia. J Lab Clin Med. 1992;120:371-379. 7. Greinacher A, Michels I, Kiefel V, Mueller-Eckhardt C. A rapid and sensitive test for diagnosing heparin-associated thrombocytopenia. Thromb Haemost 1991;66:734-736. 8. Warkentin TE, Levine MN, Roberts RS, et al. Heparin-induced thrombocytopenia is more common with unfractionated heparin than with low molecular weight heparin. Thromb Haemost. 1993;69:911. Abstract. 9. King DJ, Kelton JG. Heparin-associated thrombocytopenia. Ann Intern Med. 1984;100:535-540. 10. Warkentin TE, Soutar RL, Panju A, Ginsberg JS. Acute systemic reactrons to intravenous bolus heparin therapy: characterization and relationship to heparin-induced thrombocytopenia. Blood. 1992;80 (suppl lk160a. Abstract.
Myopathy As a Paraneoplastic Manifestation of Renal Cell Carcinoma Agnes A. Solon, MD, University of Illinois Hospitak and Clinics, Chicago, Illinois, Charles S. Gilbert, MD, Catherine Meyer, MD, Mercy Hospital and Medical Center, Chicago, Illinois
enal cell carcinoma, also known as the internist’s tumor,’ is known to present with a variety of manifestations including fever,lm3 neuropathy,4 congestive heart failure,2,3 amyloidosis,2 enteropathy,” leukocytosis, elevated values on liver function testing,6a7and other metabolic abnormalities. We report a patient who presented with known paraneoplastic manifestations of renal cell carcinoma, as well as proximal muscle weakness, increased serum creatine kinase and aldolase levels, and an electromyogram consistent with a myopathic process.
R
CASEREPORT A 78-year-old white woman with no significant past medical history was admitted for progressive weakness. Over the preceding 6 weeks, she had developed nocturnal temperatures to 39”C, dyspnea, and a cough productive of white phlegm. She also had anorexia, polyarthralgia, and generalized edema. She had taken a week-long course of erythromycin without improvement. Her fevers persisted and her weakness progressed. On admission, her blood pressure was 120/90, pulse rate was 124, respiratory rate was 18, and oral temperature was 37.6%. Notable fmdings on physical examination were rales to the mid-lung fields, anasarca, and proximal muscle weakness. Laboratory data were significant for normochromic, normocytic anemia, leukocytosis without left shift, hyponatremia, elevated transaminases, hypoalbuminemia, and markedly elevated serum creatine kinase and
aldolase levels. Results of renal function testing and urinalysis were normal. Hepatitis profile, blood and sputum cultures, and Legion&a and Chiamydia titers were negative. The results of thyroid function tests were normal. Chest roentgenogram revealed patchy, interstitial densities in both lung fields with blunting of the costophrenic angles. Pleural fluid analysis was consistent with a transudate. Transesophageal echocardiogmn revealed normal left ventricular function. Computed tomography (CT) of the abdomen revealed a low-attenuated enhancing mass around 2 cm in diameter within the superolateral portion of the right kidney. The study was otherwise unremarkable. A CTguided biopsy was scheduled. In the meantime, the patient’s proximal muscle weakness worsened. Electromyogram of the right upper extremity revealed a myopathic process involving the proximal muscles. There were increased polyphasic potentials with decreased amplitude and duration of recruited motor units. After 5 days of prednisone, creatine kinase levels were increased and muscle strength did not improve. A muscle biopsy of the left deltoid showed a predominant finding of type 2 fiber atrophy with minimal perimysial inflammatory infiltrate. Steroids were discontinued. The dimensions of the tumor on three-dimensional CT scan were greater than 2 em and the pathologic appearance was consistent with renal cell carcinoma. A bone scan was negative for metastatic disease and a radical nephrectomy was performed.
TABLE Changes in Blood Variables Before and After Nephrectomy in a Patient With Renal Cell Carcinoma and Concomitant Myopathy Variable (Normal Range) Preoperative Postoperative Hemoglobin 10.7 12.0 (12-15 g/dL) Hematocrit 32 36 (35%-47%) White blood cell count 23.6 9.7 (4.5-10 x 103/L) Sodium 123 135 (135-145 mEq/L) SGOT 120 23 (O-31 L/L) SGPT 140 25 (O-40 IV/L) Alkaline phosphatase 345 107 (39-l 17 M/L) Albumin 1.8 2.6 (3.5-5 g/dL) Creatine kinase 1,034 166 (20-215 N/L) Aldolase 32.7 13.1 (0.0-8.1 U/L) Erythrocyte sedimentation rate 25 12 (O-19 mm/h) SGOT = serum glutamic oxaioacetic tamic pyruvic transaminase.
transaminase;
SGPT = serum glu-
November 1994 The American Journal of Medicine@ Volume 97
491
BRIEF CLINICAL OBSERVATIONS
Postnephrectomy, the patient’s anasarca resolved and muscle weakness improved, with concomitant resolution of laboratory abnormalities (Table).
and a concomitant with nephrectomy.
COMMENTS
1. Kiely JM. Hypemephroma-the internist’s tumor. Med Clin North Am. 1966; 50:1067-1083. 2. Berger L, Sinkoff MW. Systemic manifestations of hypernephroma: a review of 273 cases. Am J Med. 1957; 22:791-796. 3. Cronin RE, Kaehny WD, Miller PD, et al. Renal cell carcinoma: unusual systemic manifestations. Medicine. 1976;55:291-371. 4. Thrush DC. Neuropathy, IgM paraproteinemia and autoantibodies in hypernephroma. BMJ. 1970;4:474. 5. Pavelic K, Popovic M. Insulin and glucagon secretion by renal adenocarcinoma. Cancer. 1981;48:98-100. 6. Ramos CV, Taylor HB. Hepatic dysfunction associated with renal carcinoma. Cancer. 1972;29:1287-1291. 7. Shipman KH, Downing SW, Bradfor HA. Hypernephroma presenting as fever of unknown origin associated with elevated serum alkaline phosphatase levels. J Urof. 1993;89:160-163. 8. Takashi M, Zhu Y, Nakano Y, et al. Elevated levels of serum aldolase A in patients with renal cell carcinoma. Ural Res. 1992;20:307-311. 9. lwasaki Y, Mohri 5, Muraki M, et al. A case of interstitial pneumonitis associateli with polymyositis complicated by renal cell carcinoma. NipponKyobuShikkan-Gakkai-Zasshi. 1992;30:1858-1863. Abstract. 10. Kumasaka K, Nomura K, Satoh S, et al. A case of renal cell carcinoma with polymyositis. Hinyokika-Kiyo. 1990;36:1317-1320. Abstract.
Our patient presented with clinical and serologic abnormalities that were initially unexplained. These included fever, leukocytosis, hyponatremia, and elevated values on liver function tests. All of these are known paraneoplastic manifestations of renal cell carcinoma and all resolved after surgical removal of the tumor. This patient also presented with proximal muscle weakness, elevation in serum levels of creatine kinase and aldolase, and had an electromyogram consistent with a myopathic process. There are suggestions in the literature that aldolase levels may be increased in patients with renal cell carcinoma and may even be useful as a tumor marker.8 Though the aldolase may have been of renal origin, in this case where a clear myopathic process was present, it is difficult to speculate on the tissue source(s) of the aldolase. We believe this is the first English language literature report g~loof a patient with renal cell carcinoma
492
November
1994
The American
Journal
of Medicine@
Volume
myopathic
picture that resolved
REFERENCES
Manuscript
97
submitted November 5, 1993 and accepted in revised form January 7, 1994.
Myopathy As a Paraneoplastic Manifestation of Renal Cell Carcinoma Agnes A. Solon, MD, University of Illinois Hospitak and Clinics, Chicago, Illinois, Charles S. Gilbert, MD, Catherine Meyer, MD, Mercy Hospital and Medical Center, Chicago, Illinois
enal cell carcinoma, also known as the internist’s tumor,’ is known to present with a variety of manifestations including fever,lm3 neuropathy,4 congestive heart failure,2,3 amyloidosis,2 enteropathy,” leukocytosis, elevated values on liver function testing,6a7and other metabolic abnormalities. We report a patient who presented with known paraneoplastic manifestations of renal cell carcinoma, as well as proximal muscle weakness, increased serum creatine kinase and aldolase levels, and an electromyogram consistent with a myopathic process.
R
CASEREPORT A 78-year-old white woman with no significant past medical history was admitted for progressive weakness. Over the preceding 6 weeks, she had developed nocturnal temperatures to 39”C, dyspnea, and a cough productive of white phlegm. She also had anorexia, polyarthralgia, and generalized edema. She had taken a week-long course of erythromycin without improvement. Her fevers persisted and her weakness progressed. On admission, her blood pressure was 120/90, pulse rate was 124, respiratory rate was 18, and oral temperature was 37.6%. Notable fmdings on physical examination were rales to the mid-lung fields, anasarca, and proximal muscle weakness. Laboratory data were significant for normochromic, normocytic anemia, leukocytosis without left shift, hyponatremia, elevated transaminases, hypoalbuminemia, and markedly elevated serum creatine kinase and
aldolase levels. Results of renal function testing and urinalysis were normal. Hepatitis profile, blood and sputum cultures, and Legion&a and Chiamydia titers were negative. The results of thyroid function tests were normal. Chest roentgenogram revealed patchy, interstitial densities in both lung fields with blunting of the costophrenic angles. Pleural fluid analysis was consistent with a transudate. Transesophageal echocardiogmn revealed normal left ventricular function. Computed tomography (CT) of the abdomen revealed a low-attenuated enhancing mass around 2 cm in diameter within the superolateral portion of the right kidney. The study was otherwise unremarkable. A CTguided biopsy was scheduled. In the meantime, the patient’s proximal muscle weakness worsened. Electromyogram of the right upper extremity revealed a myopathic process involving the proximal muscles. There were increased polyphasic potentials with decreased amplitude and duration of recruited motor units. After 5 days of prednisone, creatine kinase levels were increased and muscle strength did not improve. A muscle biopsy of the left deltoid showed a predominant finding of type 2 fiber atrophy with minimal perimysial inflammatory infiltrate. Steroids were discontinued. The dimensions of the tumor on three-dimensional CT scan were greater than 2 em and the pathologic appearance was consistent with renal cell carcinoma. A bone scan was negative for metastatic disease and a radical nephrectomy was performed.
TABLE Changes in Blood Variables Before and After Nephrectomy in a Patient With Renal Cell Carcinoma and Concomitant Myopathy Variable (Normal Range) Preoperative Postoperative Hemoglobin 10.7 12.0 (12-15 g/dL) Hematocrit 32 36 (35%-47%) White blood cell count 23.6 9.7 (4.5-10 x 103/L) Sodium 123 135 (135-145 mEq/L) SGOT 120 23 (O-31 L/L) SGPT 140 25 (O-40 IV/L) Alkaline phosphatase 345 107 (39-l 17 M/L) Albumin 1.8 2.6 (3.5-5 g/dL) Creatine kinase 1,034 166 (20-215 N/L) Aldolase 32.7 13.1 (0.0-8.1 U/L) Erythrocyte sedimentation rate 25 12 (O-19 mm/h) SGOT = serum glutamic oxaioacetic tamic pyruvic transaminase.
transaminase;
SGPT = serum glu-
November 1994 The American Journal of Medicine@ Volume 97
491
BRIEF CLINICAL OBSERVATIONS
Postnephrectomy, the patient’s anasarca resolved and muscle weakness improved, with concomitant resolution of laboratory abnormalities (Table).
and a concomitant with nephrectomy.
COMMENTS
1. Kiely JM. Hypemephroma-the internist’s tumor. Med Clin North Am. 1966; 50:1067-1083. 2. Berger L, Sinkoff MW. Systemic manifestations of hypernephroma: a review of 273 cases. Am J Med. 1957; 22:791-796. 3. Cronin RE, Kaehny WD, Miller PD, et al. Renal cell carcinoma: unusual systemic manifestations. Medicine. 1976;55:291-371. 4. Thrush DC. Neuropathy, IgM paraproteinemia and autoantibodies in hypernephroma. BMJ. 1970;4:474. 5. Pavelic K, Popovic M. Insulin and glucagon secretion by renal adenocarcinoma. Cancer. 1981;48:98-100. 6. Ramos CV, Taylor HB. Hepatic dysfunction associated with renal carcinoma. Cancer. 1972;29:1287-1291. 7. Shipman KH, Downing SW, Bradfor HA. Hypernephroma presenting as fever of unknown origin associated with elevated serum alkaline phosphatase levels. J Urof. 1993;89:160-163. 8. Takashi M, Zhu Y, Nakano Y, et al. Elevated levels of serum aldolase A in patients with renal cell carcinoma. Ural Res. 1992;20:307-311. 9. lwasaki Y, Mohri 5, Muraki M, et al. A case of interstitial pneumonitis associateli with polymyositis complicated by renal cell carcinoma. NipponKyobuShikkan-Gakkai-Zasshi. 1992;30:1858-1863. Abstract. 10. Kumasaka K, Nomura K, Satoh S, et al. A case of renal cell carcinoma with polymyositis. Hinyokika-Kiyo. 1990;36:1317-1320. Abstract.
Our patient presented with clinical and serologic abnormalities that were initially unexplained. These included fever, leukocytosis, hyponatremia, and elevated values on liver function tests. All of these are known paraneoplastic manifestations of renal cell carcinoma and all resolved after surgical removal of the tumor. This patient also presented with proximal muscle weakness, elevation in serum levels of creatine kinase and aldolase, and had an electromyogram consistent with a myopathic process. There are suggestions in the literature that aldolase levels may be increased in patients with renal cell carcinoma and may even be useful as a tumor marker.8 Though the aldolase may have been of renal origin, in this case where a clear myopathic process was present, it is difficult to speculate on the tissue source(s) of the aldolase. We believe this is the first English language literature report g~loof a patient with renal cell carcinoma
492
November
1994
The American
Journal
of Medicine@
Volume
myopathic
picture that resolved
REFERENCES
Manuscript
97
submitted November 5, 1993 and accepted in revised form January 7, 1994.