- Email: [email protected]
A rare case of hepatic injury associated with ovarian hyperstimulation syndrome
AJG - January
BRIEF CASE REPORTS
1998
nervous type as central nervous anosmia. IFN, like various drugs which affect the central or peripheral nervous systems, is thought to impair the olfactory pathway. lFN, administered in cancer patients can cause anosmia (8, 9); however, concomitant chemotherapy or radiation therapy, conducted in these cases, and cancer metastasis to the nervous system cannot be excluded. Prior to IFN therapy, our patient was not known to have any auditory or optical symptoms and ‘there were no abnormal findings on computed tomography, magnetic resonance, or electroencephalography after his symptoms developed. Although the association of anosmia with impaired glucose tolerance in our patient cannot completely be denied, anosmia was likely caused by neurotoxicity induced by IFN, because he complained of anosmia 10 days after the initiation of IFN therapy, and he showed normal blood sugar levels and was without peripheral neuropathy during IFN therapy. Reprint requests and correspondence: Shigeo Maruyama, M.D., Department of Medicine, Saiseikai Gotsu General Hospital, Gotsu-city, 695, Shimane, Japan.
123
pregnancy (2,279-7,353 pg/mL). She was thus diignosed as having ovarian byperstimulation syndrome. Following a period of bed rest, her liver function normalized and tbe ascites disappeared. Based on tbe above findings, tbe patient was considered to have suffered from ovarian byperstimuiation syndrome, complicated by bepatic lujury. (Am J Gastroenterol 1998;93:123-124. 0 1998 by Am. Coll. of Gastroenterology).
INTRODUCTION Infertility is a serious problem for mature women. Therefore, assisted reproductive techniques using ovulation-inducing drugs
have now become popular. However, these are associated with various complications such as hemoconcentration, renal failure, ascites, thromboembolic phenomena, and adult respiratory distress syndrome; collectively, these are referred to as an ovarian hyperstimulation syndrome (OHSS). We herein report a rare case of OHSS associated with hepatic injury.
REFERENCES
CASE REPORT
I. Renault PF, Hoofnagle JH. Side effects of alpha interferon. Semi Liver Dis 1989;9:273-7. 2. Okanoue T, Sakamoto S, Itoh Y, et al. Side effects of high-dose interferon therapy for chronic hepatitis C. J Hepatol 1996;25:283-91. 3. Zusho H, Fukushima Y, Sanada S, et al. A study of olfactory threshold vs. fatigue in intravenous olfaction test. Jpn J Otol 1978;81:562-8 (in Japanese). 4. Shiokawa H. The clinical studies on the olfactory test using standard odorous substances. Jpn J Otol 1975;78:22-34 (in Japanese). 5. Meyers CA, Scheibel RS, Forman AD. Persistent neurotoxicity of systemically administered interferon-alpha. Neurology 1991;41:672-6. 6. Dinarello CA, Bemheim HA, Duff GW, et al. Mechanism of fever induced by recombinant human interferon. J Clin Invest 19&1,74:906-13. 7. Doty RL. A review of olfactory dysfunction in man. Am Otolaryngol 1979;1:57-61. 8. Dorval T, Palangie T, Jouve M, et al. Clinical phase II trial of recombinant DNA interferon (interferon alpha 2b) in patients with metastatic malignant melanoma. Cancer 1986;58:215-8. 9. Cocquyt VFJ, Van Belle SJP. Anosmia associated with alpha-interferon treatment. Anna1 Oncol 1994:5:863-4.
The patient, a 26-year-old married woman, was admitted to our hospital because of massive ascites and hepatic injury in July, 1993. She had no history of blood transfusion, surgery or alcohol consumption. She had experienced spontaneous abortions in January and December, 1992, and her menstrual cycle had been irregular. Therefore, she was put on human menopausal gonadotropin (hMG) therapy on June 1,1993, (hMG 150 IU i.m. injection 8 times from June 1 to July 8). From June 27 to July 8, she also had taken clomiphene citrate, 50 mg/day. On July 9, she noted abdominal fullness. Two days later, upper abdominal pain and vomiting developed. On July 24, she noted dark urine and went to a physician. She was found to have elevated concentrations of serum transaminases and massive ascites on abdominal ultrasound. Accordingly, she was admitted to our hospital on July 30, 1993. Gn admission, she was alert. Her height was 155.2 cm and her body weight was 47.2 kg. Her systolic blood pressure was 132 mmHg and her diastolic blood pressure was 80 mmHg. She did not demonstrate hepato-splenomegaly, but ascites was present. Neither a flapping tremor nor any abnormal neurological findings were noted. Laboratory data were as follows: red blood cell 400 x 103/mm3; hemoglobin 12.0 g/dL; hematocrit 38%; white blood cell 8,300/mm3; platelet count 35,300/mm3; AST 127 III/L; ALT 194 Iv/L; total bilirubin 1.3 mg/dL; total protein 6.4 g/dL; albumin 3.9 g/dL; blood urea nitrogen 7 mg/dL; creatinine 0.6 mg/dL; total bile acid 172.5 @l/L. Immunological examinations were all negative for antinuclear antibody, IgM-hepatitis A antibody, hepatitis B surface antigen, or antibodies to hepatitis C virus, mumps virus, herpes simplex virus, Epstein-Barr virus or cytomegalovirus. The effect of hMG on a mixed lymphocyte proliferation assay was negative. However, her serum estradiol concentration was high at 12,100 pg/mL (the value of early stage of pregnancy ranged 2,279-7,353 pg/mL). An ultrasound also showed massive ascites and multiple ovarian cysts. Paracentesis performed on admission yielded a translucent yellowish fluid. She was diagnosed as having OHSS in association with normal pregnancy (estimated gestational age was 7 wk and 1 day). Following admission, she was treated with bed rest. Thereafter, ascites began to gradually decrease, although the AST concentration peaked at 326 IU/L on August 9
A RARE CASE OF HEPATIC INJURY ASSOCIATED WITH OVARIAN HYPERSTIMULATION SYNDROME Junya Sblmono, M.D., Hlrosbi Tsuji, M.D., Koicbi Azuma, M.D., Mamoru Hasbigucbi, M.D., and Masatosbl Fujisbima, M.D. Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan
A 26-year-old married woman was admitted to our hospital because of massive ascites and bepatic injury. The patient bad been treated with human menopausal gonadotropin and clomipbene citrate to prevent recurrence of spontaneous abortions. About 1 month later, she developed upper abdominal pain and noticed dark urine. On admission, she bad elevated concentrations of serum transaminases with an asparate aminotransferase of 127 IU/L and alanlne aminotransferase of 194 Iv/L. An abdominal ultrasound showed massive as&es. Her serum concentration of estradiol was high at 12,100 pg/mL, which was much greater than the value of early stage of
Received May 20, 1997: accepted Sep. 22, i997.
124
BRIEF CASE REPORTS
and then slowly decreased. Moreover, her serum concentration of estradiol also decreased to 3,720 pglmL on August 23. She was diagnosed as having had a spontaneous abortion with intrauterine fetal death (gestational age was 9 wk) on September 2; dilatation and curettage were performed on the following day. During the follow-up after discharge at outpatient clinic, her liver function has been normal and the ascites. have not recurred.
DISCUSSION OHSS is a complication of assisted reproductive techniques using ovulation-inducing drugs. OHSS is characterized by a marked ovarian enlargement and acute third-space fluid shifting, resulting in increased body weight, ascites, hydrothorax, and anasarca. The symptoms can range from mild to severe. Navot er al. (1) proposed to define the severest degree of OHSS as critical or life-threatening stage. The criteria for critical OHSS include tense ascites, severe hemoconcentration, profound leukocytosis, oliguria, renal failure, thromboembolic phenomena, and adult respiratory distress syndrome. They also described liver dysfunction as a component of severe OHSS, as seen in our case. The hepatic injury in this case may have been caused by several factors including pregnancy, drugs, and OHSS. Bacq et al. (2) have reported that in the first trimester of normal pregnancy, the sentm concentrations of AST, ALT, gamma-glutamyl transpeptidase, alkaline phosphatase, lactate dehydrogenase, total bilirubin, direct bilirubin, and total bile acid are all lower than those of the matched controls. Drugs such as hMG and clomiphene citrate may have also caused hepatic injury: however, in our case, the effect of hMG on a mixed lymphocyte proliferation assay was negative. To our knowledge, there have only been six previous reports in which OHSS was complicated by hepatic injury (3-8). The first patient, reported by Sueldo et al. (4). sequentially received clomiphene citrate, hMG, and hCG. and suffered from clinically severe OHSS with a pleural effusion. Our patient had a high concentration of serum estradiol at 12,100 pg/mL and therefore, estrogen released by hMG, which has a follicle-stimulating hormone-like action, might have caused the hepatic injury. Another study by Wakim and Fox (8) did not show a relationship between the severity of hepatic injury and the peak estradiol concentration. In contrast, Sueldo et al. (4) and Ryley ?I [I/. (7). who performed liver biopsies on patients with OHSS. found a normal lobular pattern and normal portal triads. Paracristalline inclusions within the mitochondria and a dilatation of the endoplasmic reticulum were seen on electron microscopy. Such changes usually are not seen in the hepatic injury induced by estrogen. which commonly causes cholestatic hepatic injury. The mechanism of hepatic injury in OHSS remains unclear, but as described by Wakim and Fox (8). increased permeability of the hepatic vasculature induced by several vasoactive substances seems to be a cause. For example, it has been known that the renin-angiotensin system causes hepatic edema and injury. As a result, we suggest that the main source of hepatic injury in this case was an abnormal permeability induced by OHSS. Recently, Friedlander et al. (9) have reported an increased concentration of interleukin-6 in the ascites and serum from women with OHSS. suggesting that it may mediate OHSS. Interleukin-6 increases in the acute phase response to hepatic injury and is an inhibitor of hepatic protein production. Further investigations, including studies of hormonal substances and cytokines, are needed to understand the mechanism for hepatic injury in OHSS.
AJG - Vol. 93, No. I, 1998 Reprint requests and correspondence: Junya Shimono, M.D., Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Maidashi 3- 1- 1, Higashi-ku, Fukuoka 8 12-82. Japan. REFERENCES 1. Navot D, Bergh PA, Laufer N. Ovarian hyperstimulation syndrome in novel reproductive technologies: Prevention and treatment. Fettil Stetil 1992;58:249-61. 2. Bacq Y. Zarka 0, Brechot JF, et al. Liver function tests in normal pregnancy: A prospective study of 103 pregnant women and 103 matched controls. Hepatology 1996;23: 1030-4. 3. Forman RG, Frydman R, Egan D, et al. Severe ovarian hyperstimulation syndrome using agonists of gonadotropin-releasing hormone for in vitro fertilization: A European series and a proposal for prevention. Fertil Steril 1990;53:502-9. 4. Sueldo CE, Price HM, Bachenberg K, et al. Liver dysfunction in ovarian hyperstimulation syndrome. J Reprod Med 1988;33:387-90. 5. Younis JS, Zeevi D, Rabinowitz R, et al. Transient liver function tests abnormalities in ovarian hyperstimulation syndrome. Fertil Steril 1988; 50:176-g. 6. Balasch 1, Carmona F, Llach J, et al. Acute prerenal failure and liver dysfunction in a patient with severe ovarian hyperstimulation syndrome. Hum Reprod 1990;5:348-51. 1. Ryley NG, Forman R, Barlow D, et al. Liver abnormality in ovarian hyperstimulation syndrome. Hum Reprod 1990;5:938-43. 8. Wakim AN, Fox SD. Elevated liver function tests in a case of moderate ovarian hyperstimulation syndrome. Hum Reprod 1996; 11588-9. 9. Friedlander MA, Loret de Mola JR, Goldfarb JM. Elevated levels of interleukin-6 in ascites and serum from women with ovarian hyperstimulation syndrome. Fertil Steril 1993;60:826-33.
A CASE OF ISCHEMIC COLITIS ASSOCIATED PHEOCHROMOCYTOMA
WITH
Chong II Sohn, Jae-Jun Khn, Young Hee Lim, Poong Lyul Rhee, Kwang Chul Koh, Seung Woon Paik, Jong Chul Rhee, Jae Hoon Chung, Myung Shik Lee, and Jung Hyun Yang Division of Gastroenterology, Division of Endocrinology and Metabolism, and Department of General Surgery, Samsung Medical Center, Seoul, Korea
A 40-year-old woman was admitted because of abdominal pain and diarrhea. She sometimes experienced paroxysmal hypertension, sweating, headache, and palpitation. Sigmoidoscopic findings showed well-demarcated diffuse mucosal edema, hyperemia, and easy touch bleeding from distal descending colon up to the splenic flexure area. Barium x-ray showed loss of haustral marking, thumb printing appearance, and diffuse luminal stenosis in the transverse, descending, and sigmoid colon. On the abdominal computed tomogram, a 3%cm sized well-enhanced right adrenal mass was incidentally found. Twenty-four hour urinary excretion of vanillyl mandelic acid, norepinephrine, and normetanephrine were inscan showed hot creased. Iodine”’ metaiodobenzylguanidine uptake on the right adrenal gland compatible with pheochromocytoma. Exploratory laparotomy was done under the impression of ischemic colitis associated with pheochromocy toma. Adrenalectomy and resection of the stenotic left colon were performed. After surgery, pain subsided, blood pressure fell gradually, blood sugar and catecholamine level became Received Jan. 28, 1997; accepted Sep. 22, 1997.
BRIEF CASE REPORTS
1998
nervous type as central nervous anosmia. IFN, like various drugs which affect the central or peripheral nervous systems, is thought to impair the olfactory pathway. lFN, administered in cancer patients can cause anosmia (8, 9); however, concomitant chemotherapy or radiation therapy, conducted in these cases, and cancer metastasis to the nervous system cannot be excluded. Prior to IFN therapy, our patient was not known to have any auditory or optical symptoms and ‘there were no abnormal findings on computed tomography, magnetic resonance, or electroencephalography after his symptoms developed. Although the association of anosmia with impaired glucose tolerance in our patient cannot completely be denied, anosmia was likely caused by neurotoxicity induced by IFN, because he complained of anosmia 10 days after the initiation of IFN therapy, and he showed normal blood sugar levels and was without peripheral neuropathy during IFN therapy. Reprint requests and correspondence: Shigeo Maruyama, M.D., Department of Medicine, Saiseikai Gotsu General Hospital, Gotsu-city, 695, Shimane, Japan.
123
pregnancy (2,279-7,353 pg/mL). She was thus diignosed as having ovarian byperstimulation syndrome. Following a period of bed rest, her liver function normalized and tbe ascites disappeared. Based on tbe above findings, tbe patient was considered to have suffered from ovarian byperstimuiation syndrome, complicated by bepatic lujury. (Am J Gastroenterol 1998;93:123-124. 0 1998 by Am. Coll. of Gastroenterology).
INTRODUCTION Infertility is a serious problem for mature women. Therefore, assisted reproductive techniques using ovulation-inducing drugs
have now become popular. However, these are associated with various complications such as hemoconcentration, renal failure, ascites, thromboembolic phenomena, and adult respiratory distress syndrome; collectively, these are referred to as an ovarian hyperstimulation syndrome (OHSS). We herein report a rare case of OHSS associated with hepatic injury.
REFERENCES
CASE REPORT
I. Renault PF, Hoofnagle JH. Side effects of alpha interferon. Semi Liver Dis 1989;9:273-7. 2. Okanoue T, Sakamoto S, Itoh Y, et al. Side effects of high-dose interferon therapy for chronic hepatitis C. J Hepatol 1996;25:283-91. 3. Zusho H, Fukushima Y, Sanada S, et al. A study of olfactory threshold vs. fatigue in intravenous olfaction test. Jpn J Otol 1978;81:562-8 (in Japanese). 4. Shiokawa H. The clinical studies on the olfactory test using standard odorous substances. Jpn J Otol 1975;78:22-34 (in Japanese). 5. Meyers CA, Scheibel RS, Forman AD. Persistent neurotoxicity of systemically administered interferon-alpha. Neurology 1991;41:672-6. 6. Dinarello CA, Bemheim HA, Duff GW, et al. Mechanism of fever induced by recombinant human interferon. J Clin Invest 19&1,74:906-13. 7. Doty RL. A review of olfactory dysfunction in man. Am Otolaryngol 1979;1:57-61. 8. Dorval T, Palangie T, Jouve M, et al. Clinical phase II trial of recombinant DNA interferon (interferon alpha 2b) in patients with metastatic malignant melanoma. Cancer 1986;58:215-8. 9. Cocquyt VFJ, Van Belle SJP. Anosmia associated with alpha-interferon treatment. Anna1 Oncol 1994:5:863-4.
The patient, a 26-year-old married woman, was admitted to our hospital because of massive ascites and hepatic injury in July, 1993. She had no history of blood transfusion, surgery or alcohol consumption. She had experienced spontaneous abortions in January and December, 1992, and her menstrual cycle had been irregular. Therefore, she was put on human menopausal gonadotropin (hMG) therapy on June 1,1993, (hMG 150 IU i.m. injection 8 times from June 1 to July 8). From June 27 to July 8, she also had taken clomiphene citrate, 50 mg/day. On July 9, she noted abdominal fullness. Two days later, upper abdominal pain and vomiting developed. On July 24, she noted dark urine and went to a physician. She was found to have elevated concentrations of serum transaminases and massive ascites on abdominal ultrasound. Accordingly, she was admitted to our hospital on July 30, 1993. Gn admission, she was alert. Her height was 155.2 cm and her body weight was 47.2 kg. Her systolic blood pressure was 132 mmHg and her diastolic blood pressure was 80 mmHg. She did not demonstrate hepato-splenomegaly, but ascites was present. Neither a flapping tremor nor any abnormal neurological findings were noted. Laboratory data were as follows: red blood cell 400 x 103/mm3; hemoglobin 12.0 g/dL; hematocrit 38%; white blood cell 8,300/mm3; platelet count 35,300/mm3; AST 127 III/L; ALT 194 Iv/L; total bilirubin 1.3 mg/dL; total protein 6.4 g/dL; albumin 3.9 g/dL; blood urea nitrogen 7 mg/dL; creatinine 0.6 mg/dL; total bile acid 172.5 @l/L. Immunological examinations were all negative for antinuclear antibody, IgM-hepatitis A antibody, hepatitis B surface antigen, or antibodies to hepatitis C virus, mumps virus, herpes simplex virus, Epstein-Barr virus or cytomegalovirus. The effect of hMG on a mixed lymphocyte proliferation assay was negative. However, her serum estradiol concentration was high at 12,100 pg/mL (the value of early stage of pregnancy ranged 2,279-7,353 pg/mL). An ultrasound also showed massive ascites and multiple ovarian cysts. Paracentesis performed on admission yielded a translucent yellowish fluid. She was diagnosed as having OHSS in association with normal pregnancy (estimated gestational age was 7 wk and 1 day). Following admission, she was treated with bed rest. Thereafter, ascites began to gradually decrease, although the AST concentration peaked at 326 IU/L on August 9
A RARE CASE OF HEPATIC INJURY ASSOCIATED WITH OVARIAN HYPERSTIMULATION SYNDROME Junya Sblmono, M.D., Hlrosbi Tsuji, M.D., Koicbi Azuma, M.D., Mamoru Hasbigucbi, M.D., and Masatosbl Fujisbima, M.D. Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan
A 26-year-old married woman was admitted to our hospital because of massive ascites and bepatic injury. The patient bad been treated with human menopausal gonadotropin and clomipbene citrate to prevent recurrence of spontaneous abortions. About 1 month later, she developed upper abdominal pain and noticed dark urine. On admission, she bad elevated concentrations of serum transaminases with an asparate aminotransferase of 127 IU/L and alanlne aminotransferase of 194 Iv/L. An abdominal ultrasound showed massive as&es. Her serum concentration of estradiol was high at 12,100 pg/mL, which was much greater than the value of early stage of
Received May 20, 1997: accepted Sep. 22, i997.
124
BRIEF CASE REPORTS
and then slowly decreased. Moreover, her serum concentration of estradiol also decreased to 3,720 pglmL on August 23. She was diagnosed as having had a spontaneous abortion with intrauterine fetal death (gestational age was 9 wk) on September 2; dilatation and curettage were performed on the following day. During the follow-up after discharge at outpatient clinic, her liver function has been normal and the ascites. have not recurred.
DISCUSSION OHSS is a complication of assisted reproductive techniques using ovulation-inducing drugs. OHSS is characterized by a marked ovarian enlargement and acute third-space fluid shifting, resulting in increased body weight, ascites, hydrothorax, and anasarca. The symptoms can range from mild to severe. Navot er al. (1) proposed to define the severest degree of OHSS as critical or life-threatening stage. The criteria for critical OHSS include tense ascites, severe hemoconcentration, profound leukocytosis, oliguria, renal failure, thromboembolic phenomena, and adult respiratory distress syndrome. They also described liver dysfunction as a component of severe OHSS, as seen in our case. The hepatic injury in this case may have been caused by several factors including pregnancy, drugs, and OHSS. Bacq et al. (2) have reported that in the first trimester of normal pregnancy, the sentm concentrations of AST, ALT, gamma-glutamyl transpeptidase, alkaline phosphatase, lactate dehydrogenase, total bilirubin, direct bilirubin, and total bile acid are all lower than those of the matched controls. Drugs such as hMG and clomiphene citrate may have also caused hepatic injury: however, in our case, the effect of hMG on a mixed lymphocyte proliferation assay was negative. To our knowledge, there have only been six previous reports in which OHSS was complicated by hepatic injury (3-8). The first patient, reported by Sueldo et al. (4). sequentially received clomiphene citrate, hMG, and hCG. and suffered from clinically severe OHSS with a pleural effusion. Our patient had a high concentration of serum estradiol at 12,100 pg/mL and therefore, estrogen released by hMG, which has a follicle-stimulating hormone-like action, might have caused the hepatic injury. Another study by Wakim and Fox (8) did not show a relationship between the severity of hepatic injury and the peak estradiol concentration. In contrast, Sueldo et al. (4) and Ryley ?I [I/. (7). who performed liver biopsies on patients with OHSS. found a normal lobular pattern and normal portal triads. Paracristalline inclusions within the mitochondria and a dilatation of the endoplasmic reticulum were seen on electron microscopy. Such changes usually are not seen in the hepatic injury induced by estrogen. which commonly causes cholestatic hepatic injury. The mechanism of hepatic injury in OHSS remains unclear, but as described by Wakim and Fox (8). increased permeability of the hepatic vasculature induced by several vasoactive substances seems to be a cause. For example, it has been known that the renin-angiotensin system causes hepatic edema and injury. As a result, we suggest that the main source of hepatic injury in this case was an abnormal permeability induced by OHSS. Recently, Friedlander et al. (9) have reported an increased concentration of interleukin-6 in the ascites and serum from women with OHSS. suggesting that it may mediate OHSS. Interleukin-6 increases in the acute phase response to hepatic injury and is an inhibitor of hepatic protein production. Further investigations, including studies of hormonal substances and cytokines, are needed to understand the mechanism for hepatic injury in OHSS.
AJG - Vol. 93, No. I, 1998 Reprint requests and correspondence: Junya Shimono, M.D., Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Maidashi 3- 1- 1, Higashi-ku, Fukuoka 8 12-82. Japan. REFERENCES 1. Navot D, Bergh PA, Laufer N. Ovarian hyperstimulation syndrome in novel reproductive technologies: Prevention and treatment. Fettil Stetil 1992;58:249-61. 2. Bacq Y. Zarka 0, Brechot JF, et al. Liver function tests in normal pregnancy: A prospective study of 103 pregnant women and 103 matched controls. Hepatology 1996;23: 1030-4. 3. Forman RG, Frydman R, Egan D, et al. Severe ovarian hyperstimulation syndrome using agonists of gonadotropin-releasing hormone for in vitro fertilization: A European series and a proposal for prevention. Fertil Steril 1990;53:502-9. 4. Sueldo CE, Price HM, Bachenberg K, et al. Liver dysfunction in ovarian hyperstimulation syndrome. J Reprod Med 1988;33:387-90. 5. Younis JS, Zeevi D, Rabinowitz R, et al. Transient liver function tests abnormalities in ovarian hyperstimulation syndrome. Fertil Steril 1988; 50:176-g. 6. Balasch 1, Carmona F, Llach J, et al. Acute prerenal failure and liver dysfunction in a patient with severe ovarian hyperstimulation syndrome. Hum Reprod 1990;5:348-51. 1. Ryley NG, Forman R, Barlow D, et al. Liver abnormality in ovarian hyperstimulation syndrome. Hum Reprod 1990;5:938-43. 8. Wakim AN, Fox SD. Elevated liver function tests in a case of moderate ovarian hyperstimulation syndrome. Hum Reprod 1996; 11588-9. 9. Friedlander MA, Loret de Mola JR, Goldfarb JM. Elevated levels of interleukin-6 in ascites and serum from women with ovarian hyperstimulation syndrome. Fertil Steril 1993;60:826-33.
A CASE OF ISCHEMIC COLITIS ASSOCIATED PHEOCHROMOCYTOMA
WITH
Chong II Sohn, Jae-Jun Khn, Young Hee Lim, Poong Lyul Rhee, Kwang Chul Koh, Seung Woon Paik, Jong Chul Rhee, Jae Hoon Chung, Myung Shik Lee, and Jung Hyun Yang Division of Gastroenterology, Division of Endocrinology and Metabolism, and Department of General Surgery, Samsung Medical Center, Seoul, Korea
A 40-year-old woman was admitted because of abdominal pain and diarrhea. She sometimes experienced paroxysmal hypertension, sweating, headache, and palpitation. Sigmoidoscopic findings showed well-demarcated diffuse mucosal edema, hyperemia, and easy touch bleeding from distal descending colon up to the splenic flexure area. Barium x-ray showed loss of haustral marking, thumb printing appearance, and diffuse luminal stenosis in the transverse, descending, and sigmoid colon. On the abdominal computed tomogram, a 3%cm sized well-enhanced right adrenal mass was incidentally found. Twenty-four hour urinary excretion of vanillyl mandelic acid, norepinephrine, and normetanephrine were inscan showed hot creased. Iodine”’ metaiodobenzylguanidine uptake on the right adrenal gland compatible with pheochromocytoma. Exploratory laparotomy was done under the impression of ischemic colitis associated with pheochromocy toma. Adrenalectomy and resection of the stenotic left colon were performed. After surgery, pain subsided, blood pressure fell gradually, blood sugar and catecholamine level became Received Jan. 28, 1997; accepted Sep. 22, 1997.