Herpes simplex encephalitis (HSE) is a life-threatening condition with high mortality. The pathogenesis underlying the reactivation of latent herpes simplex virus (HSV) remains undefined. We present the case of a 55-year-old female who developed HSE type 1 during brain irradiation and antioedematous dexamethasone treatment for leptomeningeal metastasized breast tumor with epileptic seizures. During the radiotherapy (RT), after a total of 32 Gray administrated in 16 fractions, our patient developed cognitive impairment and partial epileptic status without fever. Two days later the patient's clinical conditions had deteriorated and high fever manifested. A diagnosis of HSE type 1 was made by a positive cerebrospinal fluid polymerase chain reaction. Antiviral therapy with high doses of acyclovir was practiced for four weeks but the comatose state persisted. The patient died 59 days after the last RT fraction. The temporal relationship of RT to the occurrence of HSE suggests that cranial irradiation may play a role in the reactivation of latent HSV. Although antiviral therapy resistance is infrequent in immunocompetent patients, it is one of the main problems in immunocompromized patients.
The present study has shown this combination to be active as second-line treatment, and its toxic effects have been well tolerated. It should be considered a reasonable option for patients with metastatic disease who have already been treated with anthracyclines.
Two hundred sixteen patients with unresectable non-small cell lung carcinoma were randomly allocated to receive etoposide (120 mg/m2, days 1-3) either alone or in combination with high-dose cisplatin (60 mg/mz, days 1-2). The patients' distribution and characteristics were similar in the two treatment arms. The objective response rate for etoposide was 7% versus 25.8% for etoposide plus cisplatin ( P < 0.005). Median progression-free survival in etoposide arm was 3.5 months versus 5 months in the combination arm ( P = 0.43). The median survival time for etoposide was 6 months compared with 8 months for etoposide combined with cisplatin (P = 0.87). Significantly more nausea/vomiting (P < 0.005), serum creatinine elevation ( P < 0.0051, hearing loss and/or tinnitus ( P < 0.005), peripheral neuropathy ( P < 0.005), leukopenia ( P < 0.025), and anemia ( P < 0.005) occurred in the etoposide plus cisplatin arm. No statistically significant difference was recorded between the two arms in terms of performance status changes. In conclusion the addition of high-dose cisplatin to single-agent etoposide significantly increases the chance of obtaining tumor response in advanced non-small cell lung cancer at the cost of an increased toxicity without any significant long-term impact on survival and progression-free survival.
Fifty-three cases of metastatic pleural effusion (30 haemorragic and 23 serofibrinous) were treated with 4 mg of Corynebacterium parvum (CP) injected weekly into the pleural cavity after total thoracentesis. Of the 53 effusions, 24 were metastases from lung cancer and 29 from breast cancer. Complete response (CR) was assessed as total resolution of pleural effusion after explorative thoracentesis. The results were as follows: 15 CR after two injections of CP, 30 CR after three, and 5 CR after the fourth administration. Three of 53 cases could not be evaluated because of early death. Of the 30 clearly haemorragic effusions, 25 turned into serofibrinosis after the first intrapleural injection of CP and the other five after the second. These findings indicate that intracavitary CP is the most adequate treatment for the control of neoplastic pleural effusion because it induces a significant clinical improvement with milder side effects with respect to other drugs and/or physical agents commonly used.
Hd-Epi + CTX is very active against both LABC and MBC. The administration of G-CSF allows dose intensification of both drugs (a 59.5% increase of the actual dose intensity) with acceptable clinical tolerance (a lower incidence of neutropenia but a higher incidence of anemia and thrombocytopenia). Only a specifically designed phase III trial will lead to definitive conclusions regarding the greater antitumor activity of accelerated CSF-including regimens as compared to standard chemotherapy for advanced breast cancer.
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