[Palliative radiation treatment for superior mediastinal lymph nodes of a patient with recurrent laryngeal nerve palsy-a case report of advanced lung cancer].

The recurrent laryngeal nerve is a branch of the vagus nerve. On the right side, it branches anteriorly to the subclavian artery in the neck. In cases of malignant diseases, lymph node metastasis can lead to recurrent laryngeal nerve palsy. Patients with this condition often suffer from aspiration pneumonia, which requires tube feeding. In this case of an advanced lung cancer, we treated the involved lymph node in the neck with palliative radiotherapy, which restored normal nerve function.

Neoadjuvant LHRH analog plus estramustine phosphate combined with three-dimensional conformal radiotherapy for intermediate- to high-risk prostate cancer: a randomized study.

OBJECTIVE: The objective of this study is to assess the safety and efficacy of a treatment regimen comprising neoadjuvant conventional androgen deprivation therapy (ADT) plus estramustine phosphate (EMP) combined with three-dimensional conformal radiotherapy (3D-CRT) for patients with intermediate- to high-risk prostate cancer. METHODS: Thirty-nine patients with intermediate- to high-risk prostate cancer classified according to the NCCN practice guidelines recurrence risk group were randomly allocated into two groups: neoadjuvant LHRH agonist plus EMP for 6 months until completion of the 3D-CRT (EMP group, n = 20), or neoadjuvant LHRH agonist alone (LHRH group, n = 19). Both groups received 3D-CRT in daily fractions of 2 Gy for a total dose of 70 Gy. PSA relapse was defined according to the Phoenix definition. RESULTS: The median duration of follow-up was 27.1 months. None of the patients died during the follow-up period, but three patients in the LHRH group developed distant metastasis. The 4-year PSA relapse-free survival outcomes for the EMP group and LHRH group were 61.2 and 49.4%, respectively (P = 0.04). Multivariate Cox regression model analyses of the pretreatment PSA level (>20 ng/ml n = 16 vs. < or =20 ng/ml n = 23), grade (G8 or more n = 11 vs. G7 or less n = 28) and modality (LHRH group n = 19 vs. EMP group n = 20) revealed these factors to be independent predictors of PSA relapse after treatment: pretreatment PSA had a relative risk of 3.84 (95% CI: 1.003-14.722), grade had a relative risk of 4.29 (95% CI: 1.093-16.824), and modality had a relative risk of 8.01 (95% CI: 1.867-34.361). No severe toxicities were observed in either group. CONCLUSIONS: The present results indicate that the combination of neoadjuvant ADT plus EMP combined with 3D-CRT sustains freedom from PSA relapse in patients with intermediate- to high-risk prostate cancer. However, this regimen is insufficient for preventing biochemical failure, and an additional intervention such as adjuvant ADT, radiation dose escalation, or both, is required, especially for patients with a pretreatment PSA level of more than 20 ng/ml and high-grade cancer.

Unusual petal-like fibromuscular dysplasia as a cause of acute abdomen and circulatory shock.

Fibromuscular dysplasia (FMD) is a nonatherosclerotic, noninflammatory segmental arterial occlusive disorder that involves primarily the renal and carotid arteries, and less often the coronary, iliac, and visceral arteries. We report the case of 78-year-old Japanese woman who presented with acute abdomen complicated by shock. Autopsy revealed hemorrhagic necrosis of the small intestine due to severe narrowing of the mesenteric arteries. Histologically, smooth muscles showed in-bundle hyperplasia surrounding the adventitia together with medial and perimedial fibrodysplasia of these arteries, forming the characteristic petal-like appearance of FMD. No occlusive thrombus was observed. Further, another medial fibrodysplasia type of FMD was also seen in the renal and left circumflex coronary arteries. Unusual proliferation of smooth muscles resulted in the petal-like atypical FMD at the superior mesenteric artery.

[Clinical significance of plasma concentration of macrophage colony-stimulating factor in patients with vasospastic angina].

OBJECTIVES: The concentration of macrophage colony-stimulating factor (M-CSF), an inflammatory cytokine, increases with the progression of coronary lesions, but no clinical investigations have evaluated the relationship to coronary vascular tone. The present study investigated the relationship between M-CSF and vasoreactivity of the coronary arteries in patients with vasospastic angina. METHODS: Vasospastic angina (VSA) was characterized by transient chest pain and ischemic ST segment changes at rest, or by a positive result in spasm provocation testing with acetylcholine. The subjects were 24 patients with stable VSA(inactive VSA group) treated on an outpatient basis, 31 VSA patients hospitalized with unstable angina (active VSA group), and 13 healthy subjects(control group). The sensitivity of determination of plasma M-CSF in blood was 40 pg/ml. The levels of this factor in each group were compared. Based on the findings of the acetylcholine vasospasm-induction test, patients were divided into those with single-vessel vasospasm and those with multivessel vasospasm, and, according to the dose of acetylcholine required to induce spasm, into high- and low-dose groups. Plasma M-CSF levels in each group were compared. RESULTS: Mean plasma M-CSF was 598 +/- 180 pg/ml in the inactive VSA group, 775 +/- 194 pg/ml in the active VSA group, and 632 +/- 103 pg/ml in the control group. The mean plasma M-CSF level in the active VSA group was significantly higher than that in the inactive VSA group(p < 0.01). Mean plasma M-CSF level in the single-vessel and multivessel vasospasm groups was highest for active VSA patients with multivessel vasospasm (872 +/- 173 pg/ml). The relationship with the acetylcholine induction dose clarified that plasma M-CSF levels were highest in patients with active VSA in the acetylcholine low-dose group (825 +/- 177 pg/ml, p < 0.001). CONCLUSIONS: Plasma M-CSF concentration reflects the vasoreactivity of coronary spasm in the VSA group, and may be an indicator of the severity of coronary endothelial dysfunction.