A case of primary retroperitoneal mucinous cystic tumor of borderline malignancy is reported. A 36-year-old, nulliparous woman complained of abdominal fullness. Physical examination revealed a cystic mass 12-cm x 8-cm in size. At laparotomy, a cystic tumor was observed in the right retroperitoneal space. Both ovaries appeared normal and the uterus was almost normal except for small myomatous nodules. Removal of the retroperitoneal tumor, an appendectomy, and a myomectomy were performed. The histologic diagnosis was a primary retroperitoneal mucinous cystic tumor of borderline malignancy, similar to findings for ovarian tumor. There was no evidence of disease 6 months after the surgery.
Sarcoidosis is characterized by multisystemic granulomatous lesions of unknownetiology. A 62-year-old womandeveloped sarcoidosis after treatment with oc-2a interferon (IFN) for 24 weeks (total dose: 522 million units) for chronic hepatitis C. She developed complete atrioventricular block and multiple noncaseating granulomatous lesions in the lung. IFN therapy, which may disturb cellular immuneactivation in some patients, may have contributed to the onset and progression of sarcoidosis.
SUMMARYThe therapeutic effects of interferon in chronic hepatitis C and many of its adverse effects have been well documented. However, there are only a few reports regarding its adverse effects on the cardiovascular system. The aim of this study was to clarify the clinical features of the adverse effects of interferon on the cardiovascular system in patients with chronic hepatitis C. We monitored 295 patients with chronic active hepatitis C during 312 courses of interferon therapy and for 1 year after the end of treatment for the presence of cardiovascular adverse effects. We found 6 patients with cardiovascular adverse effects during interferon therapy and 4 more patients within 1 year after the end of therapy (10/312, 3.2%). The adverse effects of interferon on the cardiovascular system included arrhythmia (n=4), ischemic heart disease (n=4) and myocardial disease (n=2). None of the clinical factors, including history of cardiovascular disease, were related to these cardiovascular adverse effects. In all instances the patient's condition improved after discontinuation of interferon and adequate therapy. The cardiovascular adverse effects of interferon occurred frequently in patients with chronic hepatitis C, even after the end of therapy and they were unpredictable. Thus, all patients undergoing interferon therapy should be monitored not only during but also after the end of treatment. (Jpn Heart J 1996; 37: 905-915)
We aimed to evaluate whether there was a difference in the arterial stiffness assessed by the cardio-ankle vascular index (CAVI) between patients with acute coronary syndrome (ACS) and those with stable angina pectoris (SAP). A total of 199 consecutive patients, 79 with ACS and 120 with SAP, who underwent emergency or elective coronary revascularization were enrolled. The CAVI was measured within 2 days after the procedures, and was compared between the ACS and SAP patients. As parameters related to arteriosclerosis, carotid intima-media thickness (IMT) and number of stenotic coronary vessels were also evaluated. Although IMT was significantly greater in SAP patients (2.1 ± 1.1 vs. 2.4 ± 0.9; P¼0.022), CAVI was significantly higher in ACS patients (10.0±1.7 vs. 9.3±1.3; P¼0.0012). After an adjustment for the clinical parameters with a significant difference between the two patient groups, CAVI remained significantly higher in ACS patients than in SAP patients (odds ratio 1.92, 95% confidence interval 1.30-3.02; P¼0.0023). A multiple linear regression analysis revealed that age (b¼0.44; Po0.0001) and ACS (b¼0.3; Po0.0001) were the independent determinants of CAVI. A significant decrease in CAVI was observed at 6 months of follow-up as compared with the acute phase in 18 patients with ACS (10.9±1.6 vs. 10.0±1.5; P¼0.019). In conclusion, CAVI was significantly and independently higher in patients with ACS than in those with SAP, which might result from a transient increase in the CAVI caused by acute myocardial ischemia.
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