THE WESTERN JOURNAL OF MEDICINE * OCTOBER 1991
* 155 * 4
17. Curtis P: Guitar nipple (Letter). Br Med J 1974; 2:226 18. Murphy JM: Cello scrotum (Letter). Br Med J 1974; 2:335 19. Garland H: The occupational factor in compressive lesions of peripheral nerves. J Univ Leeds Med 1955; 4:63-66 20. Fry HJH: Overuse syndrome, alias tenosynovitis/tendinitis: The terminological hoax. Plast Reconstr Surg 1986; 78:414-417
Cisplatin Therapy-Associated Recurrent Toxic Shock Syndrome ARNOLD C. BERMAN, MD LAWRENCE R. BOLY, MD San Francisco, California
THE IN VITRO RELATIONSHIP of magnesium to the production of toxic shock syndrome toxin- (TSST- 1) has been previously described.'`3 The in vivo relationship of systemic hypomagnesemia to the development of the toxic shock syndrome, however, has not been previously reported. We report a case of recurrent toxic shock syndrome following hypomagnesemia that was induced by cisplatin chemotherapy. Report of a Case
The patient, a 46-year-old woman with non-insulindependent diabetes mellitus, presented with an acute abdomen. During an emergency laparotomy, an 1-cm ruptured "chocolate" cyst of the left ovary was found. Microscopic examination revealed a well-differentiated endometroid adenocarcinoma of the ovary. Primary uterine malignancy was excluded. The postoperative course was complicated by superficial wound infection, necessitating opening and draining.
A week later chemotherapy with cisplatin, 100 mg per mi2, and cyclophosphamide, 600 mg per m2, was initiated. The patient felt well and was afebrile; serous discharge was noted in areas of wound separation. A wound specimen was obtained for culture. The night the patient was discharged home from chemotherapy, fever accompanied by weakness, vomiting, and severe myalgia developed. In the emergency department, a diffuse erythematous rash was obvious. Her blood pressure was 84/50 mm of mercury in the supine position, with a pulse of 120 per minute and a temperature of 39.5°C. Conjunctivitis with purulent discharge and pharyngeal erythema with a strawberry tongue were noted. On abdominal examination, several areas of purulent wound discharge were found; otherwise, the findings were normal. Although lethargic, the patient was easily aroused and neurologic testing was normal. Laboratory tests elicited the following values: glucose 14.9 mmol per liter (normal 3.85 to 6.05); sodium 131 mmol per liter (normal 135 to 148); potassium 3.5 mmol per liter (normal 3.5 to 5.3); chloride 100 mmol per liter (normal 98 to 106); bicarbonate 19 mmol per liter (normal 23 to 30); creatinine 100 .tmol per liter (normal 53 to 124); urea nitrogen 3.2 mmol per liter (normal 2.2 to 8.2); leukocyte count 28 x 109 per liter (28,000 per Al) with neutrophils 0.69 (nor(Berman AC, Boly LR: Cisplatin therapy-associated recurrent toxic shock syndrome. West J Med 1991 Oct; 155:415-416) From the Department of Medicine, Mount Zion Hospital and Medical Center, San Francisco, California. Reprint requests to Arnold C. Berman, MD, 235 Third Ave, Apt I, San Francisco,
CA 94118.
415
mal 0.40 to 0.74) and segmented forms 0.29 (normal 0 to 0.05); hemoglobin 109 grams per liter (normal 120 to 160); platelet count 377 x 109 per liter (normal 150 to 350); uric acid 330 itmol per liter (normal 140 to 355); lactate dehydrogenase 3.75 ltkat per liter (normal 1.33 to 4.03); aspartate aminotransferase 0.58 itkat per liter (normal 0.084 to 0.67); alkaline phosphatase 1.5 ltkat per liter (normal 0.64 to 1.93); bilirubin 1 8 ,tmol per liter (normal 1.7 to 24); total protein 65 grams per liter (normal 60 to 80); albumin 35 grams per liter (normal 32 to 50); calcium 2.17 mmol per liter (normal 2.13 to 2.55); and phosphorus 0.48 mmol per liter (normal 0.8 to 1.5). The prothrombin time was within normal limits; fibrin degradation products, negative; fibrinogen 3.2 grams per liter (normal 1.7 to 4.5). No infiltrate was seen on chest roentgenogram. Arterial blood gas determinations done with the patient receiving 4 liters of oxygen per minute by nasal cannula were pH 7.34 (normal 7.35 to 7.45); Po2 11.2 kPa (normal 10.6 to 13.3); and Pco2 3.8 kPa (normal 4.7 to 6.0). Abdominal wound culture done before admission was positive for Staphylococcus aureus. The serum magnesium level was not measured during this admission. Initial therapy comprised fluids, pressor support, and broad-spectrum antibiotic coverage including antistaphylococcal therapy with vancomycin hydrochloride, later adjusted to nafcillin sodium according to culture sensitivity. Blood cultures were negative for pathogens, and eight days after admission the patient was discharged on a course of oral dicloxacillin sodium. On outpatient follow-up, desquamation of the palms and soles was noted. Assay of the S aureus from the wound specimen cultured during her hospital stay returned positive for the production of TSST-1. Nine days after discharge, the patient returned for her second outpatient chemotherapy course of cisplatin and cyclophosphamide. She was afebrile, and her abdominal wounds were clean. The day after chemotherapy was given, the patient again presented to the emergency department with fever, rigors, myalgia, prostration, and vomiting. On examination she was febrile and hypotensive, with a generalized rash and purulent conjunctivitis. Her abdominal incision wounds had a purulent discharge. The following laboratory values were obtained: glucose 11.4 mmol per liter, sodium 132 mmol per liter, potassium 2.8 mmol per liter, chloride 98 mmol per liter, bicarbonate 20 mmol per liter, calcium 2.02 mmol per liter, magnesium 0.37 mmol per liter (normal 0.7 to 1.0); and liver function studies normal; the leukocyte count was 27 x 109 per liter (27,000 per ILI) with neutrophils 0.80 and segmented forms 0.17. A urinalysis showed trace proteinuria. Coagulation studies were normal. Gram-positive cocci were seen on a specimen taken from the wound. Therapy with fluids, pressor support, and vancomycin was begun. Thrombocytopenia developed on the third day of her hospital stay, with a platelet count nadir of 26 x 109 per liter. Platelets were replenished before extensive surgical wound debridement, but no gross bleeding occurred and the thrombocytopenia resolved. Blood cultures were negative for pathogens, and antibiotic therapy was switched to a cephalosporin, to which the wound bacteria were sensitive. Desquamation of her palms and soles was seen after two weeks of hospital stay. Three weeks after admission, a third course of chemotherapy was administered with the patient continuing to receive oral cephalexin. Magnesium replacement was meticulously monitored. This course was uneventful.
ALERTS, NOTICES, AND CASE REPORTS
416
416
Discussion The epidemiologic and clinical identification of the toxic shock syndrome according to the Centers for Disease Control rests on the following criteria4: Fever, rash, hypotension, and desquamation that occurs within two weeks after the disease starts must all be present. Three organ systems must be involved. Diseases that can mimic the syndrome, such as bacterial sepsis as in the case presented here, must be appropriately excluded. Clinical and laboratory manifestations of the syndrome have been recently reviewed.5 All four major criteria as well as evidence of multisystem involvement were met in both episodes of the toxic shock syndrome that followed chemotherapy in our patient. Cultures of blood were negative for pathogens, consistent with the diagnosis. Renal toxicity of cisplatin has been well described,6 along with metabolic abnormalities that include hypomagnesemia, which is common and may be profound. The hypomagnesemia is dose dependent and correlates with the cumulative cisplatin dose.7-9 It has been reported to occur in some patients, however, after the first course of chemotherapy even with lower doses of cisplatin at 50 mg per m2.8 9 Profound hypomagnesemia was documented when symptoms were present during the recurrent toxic shock syndrome episode that followed the second course of chemotherapy. Our patient received cisplatin at 100 mg per m2, and, in addition, she had non-insulin-dependent diabetes that may have contributed to the degree of hypomagnesemia. Subclinical hypomagnesemia has been associated with poorly controlled diabetes mellitus and correlated with high levels of fasting blood glucose and an increased level of glycosylated hemoglobin.'0 The patient did not have evidence of renal disease or documented hypomagnesemia before the first course of chemotherapy, and, unfortunately, her serum magnesium level was not measured during the episode that followed the initial administration of cisplatin. The hypomagnesemia documented during the second episode required parenteral replacement. Many studies indicate a central role for TSST-1 in the pathogenesis of the toxic shock syndrome." The in vitro production of TSST-1, an exotoxin, by S aureus has been intensively investigated, in particular in regard to the effect of trace metals. The toxin is produced in excess in hypomagnesemic environments.`3 The role of foreign bodies, particularly tampons, in menstrual toxic shock syndrome is well known.4'5 The postulated mechanisms of tampcns in the pathogenesis include a foreign body effect with alteration of the vaginal microfloral2 and the binding of magnesium by tampon fibers, producing a magnesium-deficient local environment.3 Epidemic menstrual toxic shock syndrome was linked to the use of tampons composed of polyacrylate rayon that is thought to function as an ion exchange resin. 13 Recurrent toxic shock syndrome in our patient was temporally related to repeated courses of chemotherapy. The symptoms occurred far too early to invoke immunosuppression by chemotherapy. Moreover, there was no evidence of leukopenia during the episodes of toxic shock. We propose that hypomagnesemia due to cisplatin chemotherapy created conditions favorable to TSST- 1 production by existing S aureus in the wound, precipitating the toxic shock syndrome in our patient.
ALERTS,
NOTICES,
AND
CASE
REPORTS
We emphasize the need to monitor serum magnesium levels and to correct hypomagnesemia, if present, during episodes of this syndrome. REFERENCES 1. Bergdoll MS: Regulation and control of toxic shock syndrome toxin-I: Overview. Rev Infect Dis 1989; 1 1:S142-143 2. Reeves MW: Effect of trace metals on the synthesis of toxic shock syndrome toxin-I. Rev Infect Dis 1989; 1 1:S145-149 3. Kass EH: Magnesium and the pathogenesis of toxic shock syndrome. Rev Infect Dis 1989; ll :S167-172 4. Reingold AL, Hargrett NT, Shands KN, et al: Toxic shock surveillance in the United States, 1980 to 1981. Ann Intern Med 1982; 96 (Pt 2):875-880 5. Chesney PJ: Clinical aspects and spectrum of illness of toxic shock syndrome: Overview. Rev Infect Dis 1989; 1 1:SI -7 6. Schilsky RL, Anderson T: Hypomagnesemia and renal magnesium wasting in patients receiving cisplatin. Ann Intern Med 1979; 90:929-931 7. Vogelzang NJ, Torkelson JL, Kennedy BJ: Hypomagnesemia, renal dysfunction and Raynaud's phenomenon in patients treated with cisplatin, vinblastine and bleomycin. Cancer 1985; 56:2765-2770 8. Lam M, Adelstein DJ: Hypomagnesemia and renal magnesium wasting in patients treated with cisplatin. Am J Kidney Dis 1986; 8:164-169 9. Buckley JE, Clark VL, Meyer TJ, Pearlman NW: Hypomagnesemia after cisplatin combination chemotherapy. Arch Intern Med 1984; 144:2347-2348 10. Pun KK, Ho PWM: Subclinical hyponatremia, hyperkalemia and hypomagnesemia in patients with poorly controlled diabetes mellitus. Diabetes Res Clin Pract 1989; 7:163-167 1 1. Schlievert PM: Role of toxic shock syndrome toxin- I in toxic shock syndrome: Overview. Rev Infect Dis 1989; 1 1:S107-109 12. Chow AW, Bartlett KH: Sequential assessment of vaginal microflora in healthy women randomly assigned to tampon or napkin use. Rev Infect Dis 1989; 11 :S68-73 13. Kass EH: Magnesium, Staphylococcus aureus and toxic shock syndrome. Magnesium 1988; 7:315-319
Hepatocellular Carcinoma Coexisting With Hepatic Adenoma Incidental Discovery After Long-Term Oral Contraceptive Use JACOB KORULA, MD ALBERT YELLIN, MD GARY KANEL, MD GAIL CAMPOFIORI, MD PETER NICHOLS, MD Los Angeles, California
THE CAUSAL RELATIONSHIP between oral contraceptive use and hepatic adenoma is well documented,1 though the evidence for the mechanism of the transformation of adenomas to hepatocellular carcinoma is not conclusively established.2
Recently Gyorffy and colleagues reported the development of hepatocellular carcinoma in a woman in whom hepatic adenoma was diagnosed 18 months earlier when she presented with abdominal pain.3 We report a case where a hepatic adenoma with coexistent hepatocellular carcinoma was diagnosed in an asymptomatic woman in whom the hepatic neoplasm was identified by incidental hepatic ultrasonography. Report of a Case The patient, a 40-year-old woman, was referred to the University of Southern California (Los Angeles) Liver Unit (Korula J, Yellin A, Kanel G, Campofiori G, Nichols P: Hepatocellular carcinoma coexisting with hepatic adenoma-Incidental discovery after long-term oral contraceptive use. West J Med 1991 Oct; 155:416-4 18) From the Departments of Medicine (Hepatology) (Drs Korula and Campofiori), Surgery (Dr Yellin), and Pathology (Drs Kanel and Nichols), University of Southern California School of Medicine, and the USC Liver Unit, Rancho Los Amigos Medical Center (Drs Korula and Kanel), Los Angeles, California. Reprints are not available.
* 155 * 4
17. Curtis P: Guitar nipple (Letter). Br Med J 1974; 2:226 18. Murphy JM: Cello scrotum (Letter). Br Med J 1974; 2:335 19. Garland H: The occupational factor in compressive lesions of peripheral nerves. J Univ Leeds Med 1955; 4:63-66 20. Fry HJH: Overuse syndrome, alias tenosynovitis/tendinitis: The terminological hoax. Plast Reconstr Surg 1986; 78:414-417
Cisplatin Therapy-Associated Recurrent Toxic Shock Syndrome ARNOLD C. BERMAN, MD LAWRENCE R. BOLY, MD San Francisco, California
THE IN VITRO RELATIONSHIP of magnesium to the production of toxic shock syndrome toxin- (TSST- 1) has been previously described.'`3 The in vivo relationship of systemic hypomagnesemia to the development of the toxic shock syndrome, however, has not been previously reported. We report a case of recurrent toxic shock syndrome following hypomagnesemia that was induced by cisplatin chemotherapy. Report of a Case
The patient, a 46-year-old woman with non-insulindependent diabetes mellitus, presented with an acute abdomen. During an emergency laparotomy, an 1-cm ruptured "chocolate" cyst of the left ovary was found. Microscopic examination revealed a well-differentiated endometroid adenocarcinoma of the ovary. Primary uterine malignancy was excluded. The postoperative course was complicated by superficial wound infection, necessitating opening and draining.
A week later chemotherapy with cisplatin, 100 mg per mi2, and cyclophosphamide, 600 mg per m2, was initiated. The patient felt well and was afebrile; serous discharge was noted in areas of wound separation. A wound specimen was obtained for culture. The night the patient was discharged home from chemotherapy, fever accompanied by weakness, vomiting, and severe myalgia developed. In the emergency department, a diffuse erythematous rash was obvious. Her blood pressure was 84/50 mm of mercury in the supine position, with a pulse of 120 per minute and a temperature of 39.5°C. Conjunctivitis with purulent discharge and pharyngeal erythema with a strawberry tongue were noted. On abdominal examination, several areas of purulent wound discharge were found; otherwise, the findings were normal. Although lethargic, the patient was easily aroused and neurologic testing was normal. Laboratory tests elicited the following values: glucose 14.9 mmol per liter (normal 3.85 to 6.05); sodium 131 mmol per liter (normal 135 to 148); potassium 3.5 mmol per liter (normal 3.5 to 5.3); chloride 100 mmol per liter (normal 98 to 106); bicarbonate 19 mmol per liter (normal 23 to 30); creatinine 100 .tmol per liter (normal 53 to 124); urea nitrogen 3.2 mmol per liter (normal 2.2 to 8.2); leukocyte count 28 x 109 per liter (28,000 per Al) with neutrophils 0.69 (nor(Berman AC, Boly LR: Cisplatin therapy-associated recurrent toxic shock syndrome. West J Med 1991 Oct; 155:415-416) From the Department of Medicine, Mount Zion Hospital and Medical Center, San Francisco, California. Reprint requests to Arnold C. Berman, MD, 235 Third Ave, Apt I, San Francisco,
CA 94118.
415
mal 0.40 to 0.74) and segmented forms 0.29 (normal 0 to 0.05); hemoglobin 109 grams per liter (normal 120 to 160); platelet count 377 x 109 per liter (normal 150 to 350); uric acid 330 itmol per liter (normal 140 to 355); lactate dehydrogenase 3.75 ltkat per liter (normal 1.33 to 4.03); aspartate aminotransferase 0.58 itkat per liter (normal 0.084 to 0.67); alkaline phosphatase 1.5 ltkat per liter (normal 0.64 to 1.93); bilirubin 1 8 ,tmol per liter (normal 1.7 to 24); total protein 65 grams per liter (normal 60 to 80); albumin 35 grams per liter (normal 32 to 50); calcium 2.17 mmol per liter (normal 2.13 to 2.55); and phosphorus 0.48 mmol per liter (normal 0.8 to 1.5). The prothrombin time was within normal limits; fibrin degradation products, negative; fibrinogen 3.2 grams per liter (normal 1.7 to 4.5). No infiltrate was seen on chest roentgenogram. Arterial blood gas determinations done with the patient receiving 4 liters of oxygen per minute by nasal cannula were pH 7.34 (normal 7.35 to 7.45); Po2 11.2 kPa (normal 10.6 to 13.3); and Pco2 3.8 kPa (normal 4.7 to 6.0). Abdominal wound culture done before admission was positive for Staphylococcus aureus. The serum magnesium level was not measured during this admission. Initial therapy comprised fluids, pressor support, and broad-spectrum antibiotic coverage including antistaphylococcal therapy with vancomycin hydrochloride, later adjusted to nafcillin sodium according to culture sensitivity. Blood cultures were negative for pathogens, and eight days after admission the patient was discharged on a course of oral dicloxacillin sodium. On outpatient follow-up, desquamation of the palms and soles was noted. Assay of the S aureus from the wound specimen cultured during her hospital stay returned positive for the production of TSST-1. Nine days after discharge, the patient returned for her second outpatient chemotherapy course of cisplatin and cyclophosphamide. She was afebrile, and her abdominal wounds were clean. The day after chemotherapy was given, the patient again presented to the emergency department with fever, rigors, myalgia, prostration, and vomiting. On examination she was febrile and hypotensive, with a generalized rash and purulent conjunctivitis. Her abdominal incision wounds had a purulent discharge. The following laboratory values were obtained: glucose 11.4 mmol per liter, sodium 132 mmol per liter, potassium 2.8 mmol per liter, chloride 98 mmol per liter, bicarbonate 20 mmol per liter, calcium 2.02 mmol per liter, magnesium 0.37 mmol per liter (normal 0.7 to 1.0); and liver function studies normal; the leukocyte count was 27 x 109 per liter (27,000 per ILI) with neutrophils 0.80 and segmented forms 0.17. A urinalysis showed trace proteinuria. Coagulation studies were normal. Gram-positive cocci were seen on a specimen taken from the wound. Therapy with fluids, pressor support, and vancomycin was begun. Thrombocytopenia developed on the third day of her hospital stay, with a platelet count nadir of 26 x 109 per liter. Platelets were replenished before extensive surgical wound debridement, but no gross bleeding occurred and the thrombocytopenia resolved. Blood cultures were negative for pathogens, and antibiotic therapy was switched to a cephalosporin, to which the wound bacteria were sensitive. Desquamation of her palms and soles was seen after two weeks of hospital stay. Three weeks after admission, a third course of chemotherapy was administered with the patient continuing to receive oral cephalexin. Magnesium replacement was meticulously monitored. This course was uneventful.
ALERTS, NOTICES, AND CASE REPORTS
416
416
Discussion The epidemiologic and clinical identification of the toxic shock syndrome according to the Centers for Disease Control rests on the following criteria4: Fever, rash, hypotension, and desquamation that occurs within two weeks after the disease starts must all be present. Three organ systems must be involved. Diseases that can mimic the syndrome, such as bacterial sepsis as in the case presented here, must be appropriately excluded. Clinical and laboratory manifestations of the syndrome have been recently reviewed.5 All four major criteria as well as evidence of multisystem involvement were met in both episodes of the toxic shock syndrome that followed chemotherapy in our patient. Cultures of blood were negative for pathogens, consistent with the diagnosis. Renal toxicity of cisplatin has been well described,6 along with metabolic abnormalities that include hypomagnesemia, which is common and may be profound. The hypomagnesemia is dose dependent and correlates with the cumulative cisplatin dose.7-9 It has been reported to occur in some patients, however, after the first course of chemotherapy even with lower doses of cisplatin at 50 mg per m2.8 9 Profound hypomagnesemia was documented when symptoms were present during the recurrent toxic shock syndrome episode that followed the second course of chemotherapy. Our patient received cisplatin at 100 mg per m2, and, in addition, she had non-insulin-dependent diabetes that may have contributed to the degree of hypomagnesemia. Subclinical hypomagnesemia has been associated with poorly controlled diabetes mellitus and correlated with high levels of fasting blood glucose and an increased level of glycosylated hemoglobin.'0 The patient did not have evidence of renal disease or documented hypomagnesemia before the first course of chemotherapy, and, unfortunately, her serum magnesium level was not measured during the episode that followed the initial administration of cisplatin. The hypomagnesemia documented during the second episode required parenteral replacement. Many studies indicate a central role for TSST-1 in the pathogenesis of the toxic shock syndrome." The in vitro production of TSST-1, an exotoxin, by S aureus has been intensively investigated, in particular in regard to the effect of trace metals. The toxin is produced in excess in hypomagnesemic environments.`3 The role of foreign bodies, particularly tampons, in menstrual toxic shock syndrome is well known.4'5 The postulated mechanisms of tampcns in the pathogenesis include a foreign body effect with alteration of the vaginal microfloral2 and the binding of magnesium by tampon fibers, producing a magnesium-deficient local environment.3 Epidemic menstrual toxic shock syndrome was linked to the use of tampons composed of polyacrylate rayon that is thought to function as an ion exchange resin. 13 Recurrent toxic shock syndrome in our patient was temporally related to repeated courses of chemotherapy. The symptoms occurred far too early to invoke immunosuppression by chemotherapy. Moreover, there was no evidence of leukopenia during the episodes of toxic shock. We propose that hypomagnesemia due to cisplatin chemotherapy created conditions favorable to TSST- 1 production by existing S aureus in the wound, precipitating the toxic shock syndrome in our patient.
ALERTS,
NOTICES,
AND
CASE
REPORTS
We emphasize the need to monitor serum magnesium levels and to correct hypomagnesemia, if present, during episodes of this syndrome. REFERENCES 1. Bergdoll MS: Regulation and control of toxic shock syndrome toxin-I: Overview. Rev Infect Dis 1989; 1 1:S142-143 2. Reeves MW: Effect of trace metals on the synthesis of toxic shock syndrome toxin-I. Rev Infect Dis 1989; 1 1:S145-149 3. Kass EH: Magnesium and the pathogenesis of toxic shock syndrome. Rev Infect Dis 1989; ll :S167-172 4. Reingold AL, Hargrett NT, Shands KN, et al: Toxic shock surveillance in the United States, 1980 to 1981. Ann Intern Med 1982; 96 (Pt 2):875-880 5. Chesney PJ: Clinical aspects and spectrum of illness of toxic shock syndrome: Overview. Rev Infect Dis 1989; 1 1:SI -7 6. Schilsky RL, Anderson T: Hypomagnesemia and renal magnesium wasting in patients receiving cisplatin. Ann Intern Med 1979; 90:929-931 7. Vogelzang NJ, Torkelson JL, Kennedy BJ: Hypomagnesemia, renal dysfunction and Raynaud's phenomenon in patients treated with cisplatin, vinblastine and bleomycin. Cancer 1985; 56:2765-2770 8. Lam M, Adelstein DJ: Hypomagnesemia and renal magnesium wasting in patients treated with cisplatin. Am J Kidney Dis 1986; 8:164-169 9. Buckley JE, Clark VL, Meyer TJ, Pearlman NW: Hypomagnesemia after cisplatin combination chemotherapy. Arch Intern Med 1984; 144:2347-2348 10. Pun KK, Ho PWM: Subclinical hyponatremia, hyperkalemia and hypomagnesemia in patients with poorly controlled diabetes mellitus. Diabetes Res Clin Pract 1989; 7:163-167 1 1. Schlievert PM: Role of toxic shock syndrome toxin- I in toxic shock syndrome: Overview. Rev Infect Dis 1989; 1 1:S107-109 12. Chow AW, Bartlett KH: Sequential assessment of vaginal microflora in healthy women randomly assigned to tampon or napkin use. Rev Infect Dis 1989; 11 :S68-73 13. Kass EH: Magnesium, Staphylococcus aureus and toxic shock syndrome. Magnesium 1988; 7:315-319
Hepatocellular Carcinoma Coexisting With Hepatic Adenoma Incidental Discovery After Long-Term Oral Contraceptive Use JACOB KORULA, MD ALBERT YELLIN, MD GARY KANEL, MD GAIL CAMPOFIORI, MD PETER NICHOLS, MD Los Angeles, California
THE CAUSAL RELATIONSHIP between oral contraceptive use and hepatic adenoma is well documented,1 though the evidence for the mechanism of the transformation of adenomas to hepatocellular carcinoma is not conclusively established.2
Recently Gyorffy and colleagues reported the development of hepatocellular carcinoma in a woman in whom hepatic adenoma was diagnosed 18 months earlier when she presented with abdominal pain.3 We report a case where a hepatic adenoma with coexistent hepatocellular carcinoma was diagnosed in an asymptomatic woman in whom the hepatic neoplasm was identified by incidental hepatic ultrasonography. Report of a Case The patient, a 40-year-old woman, was referred to the University of Southern California (Los Angeles) Liver Unit (Korula J, Yellin A, Kanel G, Campofiori G, Nichols P: Hepatocellular carcinoma coexisting with hepatic adenoma-Incidental discovery after long-term oral contraceptive use. West J Med 1991 Oct; 155:416-4 18) From the Departments of Medicine (Hepatology) (Drs Korula and Campofiori), Surgery (Dr Yellin), and Pathology (Drs Kanel and Nichols), University of Southern California School of Medicine, and the USC Liver Unit, Rancho Los Amigos Medical Center (Drs Korula and Kanel), Los Angeles, California. Reprints are not available.
