The authors report two cases of postradiation angiosarcoma (AS) among 5,100 breast cancer patients treated in the period 1980–1994 at the National Institute of Oncology, Budapest. Relevant data in the literature is also reviewed to analyze the questions of radiogenic origin, diagnosis and treatment. Secondary AS occurred in these cases in a previously irradiated field after a 6- and 8-year latency period, respectively. Detailed histopathological and immunohistochemical examinations from the biopsy specimens confirmed the diagnosis as AS. The first patient was treated successfully with radical surgery. The second patient, with unresectable AS, died of rapid local progression within 4 months. The incidence of chest wall and breast AS after radiotherapy was found to be 0.46 per 1,000 in our patient population, which means an estimated odds ratio of 2.9 for secondary AS. Patients treated with radiotherapy for primary breast cancer are at higher risk for developing secondary AS compared to the healthy population. An etiological relationship between radiotherapy and subsequent AS of the chest wall and breast is likely, but still controversial. Initial radical surgery is the only effective treatment for achieving long-term survival. These very rare cases deserve special attention due to the atypical clinical appearance, difficulties of differential diagnosis and poor prognosis.
The arteriolar changes in renal biopsy samples were studied by light and electron microscopy and immunohistologic observations. Arteriolar hyaline thickening was found to occur in virtually all renal diseases, regardless of whether these were accompanied by hypertension or not. Only amyloidosis and dense deposit glomerulonephritis were accompanied by specific ultrastructural arteriolar changes. The nonspecific "hyalin" was shown ultrastructurally to contain various components: accumulated basement membrane material, fine granular deposit (with filamentous or lipid details), and granulovesicular and threadlike membrane structures. Presumably the material constituting these structures originates partly from the blood and partly from elements of the vascular wall itself.
In 141 cases of glomerulonephritis confirmed by renal biopsy it was demonstrated that foetal glomerular basement membrane antigen caused a migration inhibition most frequently in minimal change glomerulonephritis. Cellular hypersensitivity was less common in membranous nephropathy, membranoproliferative (I-III) glomerulonephritis, IgA nephropathy and lupus nephritis. The correlation between LMT positivity and the occurrence of renal tissue IF activity was a linear one, but in one type, minimal change glomerulonephritis, there was no such correlation. The occurrence of LMT positivity does not show any considerable difference in glomerulonephritis with and without nephrosis.
The clinical course of 30 patients with idiopathic membranous glomerulonephritis has been followed up for 8.1 +/- 3.4 (4-17) years. First, in each case a long-term prednisone treatment was administered. During this therapy 12 (40%) patients improved and 9 had remission. In the 18 (60%) steroid resistant cases the treatment was combined with cytostatic drugs. After a combined regime for 1.9 +/- 0.8 years, 8 patients have improved, 2 of whom remitted. It has been suggested that due to a long-term immunomodulator therapy the level of urinary protein excretion might be reduced in 77% of patients. There was no effect of the applied treatment in 7% of cases, still in 16% a gradual deterioration was observed. Relapsing nephrotic syndrome has occurred in 3 (10%) of the total cases. Side effects requiring cessation of treatment were not observed.
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