Cancer and other risks of vasectomy.
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Biomedical subjects
Publications and source records attributed to A Alcaraz.
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PURPOSE: Cytogenetic studies of a small number of renal oncocytomas have indicated that loss of chromosomes 1 and Y may be involved in the pathogenesis of this tumor. To evaluate these observations further we selected paraffin embedded renal oncocytoma specimens from 20 male and 10 female patients for fluorescence in situ hybridization analysis. MATERIALS AND METHODS: Isolated nuclei were prepared from paraffin embedded specimens, and fluorescence in situ hybridization was performed with enumeration probes for chromosomes 1, 12, X and Y. RESULTS: Tumors from 10 male (50%) and 4 female (40%) patients demonstrated chromosomal alterations. Loss of chromosome Y was observed in specimens from all 10 male patients, and loss of chromosome 1 or gain of chromosome 12 was noted in 5 and 2 of these specimens, respectively. Of the 4 female patients with chromosomal abnormalities 2 had loss of chromosome 1, 1 had gain of chromosome 1 and 1 had gain of chromosome 12. CONCLUSIONS: Our results confirm that loss of chromosomes Y and 1 is common in renal oncocytoma, and that the alterations are probably involved in the pathogenesis of this tumor.
Presentation of one case of spontaneous retroperitoneal haemorrhage in a 72 year-old male, his first symptom being a left retrothoracic pain of sudden onset. The supplementary studies performed (ultrasound, CAT and MNR) pointed to the adrenal gland as the origin of the haemorrhage. Faced eith the uncertainty of the etiological diagnosis, a left supra-renalectomy was conducted which confirmed the pathological anatomy of the piece and the presence of massive haematoma of the suprarenal gland with no other pathological data. The clinical, diagnostic and therapeutical aspects are discussed.
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Contribution of one case of non-Hodgkin lymphoma (NHL) with vesical involvement, that presented clinically with urological symptomatology. Vesical involvement is typical of NHL, and is becoming more frequent in association with the increased number of AIDS patients under immunosuppressive therapy. It should be expected that this currently unusual entity will become more common in the future.
In an attempt to identify new prognostic markers, we performed fluorescence in situ hybridization (FISH) ploidy analysis of tumor tissue from patients with a targeted stage and histological grade of prostate carcinoma. We identified all 227 patients from the Mayo Clinic radical prostatectomy data base who had a high histological grade pathological stage C (pT3N0M0) tumor removed between 1966 and 1987. After histological review of the paraffin-embedded specimen blocks, 181 cases were suitable for FISH analysis using chromosome enumeration probes for chromosomes 7, 8, 10, 12, X, and Y. FISH detected 80 (44%) diploid, 22 (12%) tetraploid, and 79 (44%) aneuploid tumors. The common aneusomies were of chromosomes 7 and 8, which were present in 51 (28%) and 46 (25%) tumors, respectively. Aneusomies of chromosomes 10, 12, X, and Y were observed in 11 (6%), 15 (8%) 12 (7%) and 16 (9%) tumors, respectively. FISH aneuploid tumors showed a trend of more frequent systemic prostate cancer progression than nonaneuploid tumors (P = 0.060). For individual chromosome anomalies, gains of chromosome 8, aneusomy of chromosome 8, and aneusomy of chromosome Y correlated highly with systemic cancer progression (P = 0.006, 0.013, and 0.021, respectively). Gains of chromosome Y and aneusomy of chromosome Y were associated with an increased prostate cancer death rate (P < 0.001 for both). Multivariate analysis showed that gains of chromosome 8 and aneusomy of chromosome Y were significant independent "predictors" of systemic cancer progression (P = 0.008) and cancer death (P < 0.001), respectively. These results demonstrate that aneuploidy and specific aneusomies detected by FISH are potential markers for a poor prognosis in histological high-grade pathological stage C (pT3N0M0) prostate carcinoma.
To obtain quantitative information on the in vivo activation of the protein C system during the acute phase of sepsis, several components of the protein C pathway were studied in 18 patients. Blood samples were obtained one day after diagnosis (day 1) and, in 11 patients, also on the fourth and tenth days after diagnosis (days 4 and 10). On day 1, patients showed laboratory signs of haemostatic alterations such as positive fibrinogen/fibrin degradation products, and increased thrombin:antithrombin-III (TAT) complex levels. Compared with the control group, patients on day 1 had significantly decreased (p < 0.001) antigenic protein C (69 +/- 28%) and protein C inhibitor (PCI) (33 +/- 22%) whereas a significant increase in the levels of activated protein C (APC) complexed with alpha 1-antitrypsin (alpha 1AT) (APC:alpha 1AT, 26 +/- 15 ng/mL) and APC:PCI complex (3.0 +/- 2.0 ng/mL), and in the level of plasma kallikrein (KK) complexes with PCI (KK:PCI) (31 +/- 22 ng/mL) was observed. There was a positive correlation between APC:alpha 1AT and TAT complex levels (r = 0.597, p = 0.009). In the follow-up a trend toward normal values in antigenic protein C and PCI, and in APC:PCI and KK:PCI complex levels was found. However, PCI remained significantly decreased compared to normal values. C4b-binding protein, alpha 1AT, and TAT and APC:alpha 1AT complexes did not show any significant variations during the course of the disease, suggesting the contribution of the inflammatory and haemostatic responses, in spite of the good recovery of the patients. This study shows that in the course of sepsis, patients experience a generalized activation of the protein C pathway which was more prominent on day 1, resulting in the consumption of protein C and PCI and in the increase of APC:inhibitor complexes. Moreover, these data provide further evidence that KK:PCI circulating complexes occur in vivo.
Presentation of two clinical cases of spontaneous vesical rupture secondary to bacterial cystitis in elderly patients. One corresponds to an intraperitoneal perforation while the second case was extraperitoneal. The patients were, in both cases, diabetic women admitted in emergency due to acute abdomen. We considered that although vesical perforation secondary to bacterial cystitis is a very uncommon process, it should be taken into account in the differential diagnosis of acute abdomen in predisposed patients (diabetic elderly patients with pyuria). In such instances, a retrograde cystography would provide the diagnosis. Although extraperitoneal vesical perforations can be resolved with a vesical catheter or cystostomy, extravasation of the infected urine may result in a perivesical abscess and septic shock. Early surgical management should be considered in these cases.
A newborn female diagnosed with transposition of the great vessels with restrictive ventricular septal defect presented left facial peripheral nerve paralysis following anatomical surgery correction (arterial switch) by cardiopulmonary bypass. We have not found any causal factor either in the anesthesia or postoperative period. The electromyogram presented signs of peripheral nerve impairment, and the cerebral echography and electroencephalogram were normal. The facial nerve paralysis was almost recovered seven weeks after surgery. This is the first pediatric patient reported with peripheral facial nerve paralysis after cardiac surgery.
Fluorescence in situ hybridization is a new methodology which can be used to detect cytogenetic anomalies within interphase tumor cells. We used this technique to identify nonrandom numeric chromosomal alterations in tumor specimens from the poorest prognosis patients with pathological stages T2N0M0 and T3N0M0 prostate carcinomas. Among 1368 patients treated by radical prostatectomy, 25 study patients were ascertained who died most quickly from progressive prostate carcinoma within 3 years of diagnosis and surgery. Tumors from 25 control patients who survival for more than 5 years and who were matched for age, tumor histological grade, and pathological stage also were evaluated. The tumors from all 25 (100%) poor prognosis patients and from 11 of 25 (44%) control patients were found to be aneuploid by fluorescence in situ hybridization (P < 0.0001). Alterations of chromosome 7 were observed in 24 of the tumors (96%) from the poor prognosis patients versus 3 tumors (12%) from the control group (P < 0.0001). Moreover, a characteristic aneuploidy pattern with multiple abnormal chromosomes and a hypertetrasomic population was generally found in tumors from the poor prognosis patients. This preliminary study suggests that fluorescence in situ hybridization studies of prostate cancer specimens may help to identify those patients at highest risk for early cancer death.
Fluorescence in situ hybridization (FISH) with centromere-specific probes for chromosomes 7, 8, 11, and 12 was used to evaluate multiple 18-gauge needle biopsy cores from 50 randomly selected radical prostatectomy specimens. FISH analysis detected 26 diploid (52%), 7 tetraploid (14%), and 17 aneuploid tumors (34%). The FISH results were concordant with flow cytometric (FCM) DNA content measurements of the corresponding prostatectomy specimens for 31 tumors. For the 19 FISH/FCM discordant tumors, FISH was more sensitive than FCM for detecting ploidy anomalies. Common numerical chromosome alterations were gains of chromosomes 7 and 8, which were found in 13 (76%) and 10 (59%) aneuploid tumors, respectively. Gain of chromosome 7 was strongly associated with higher Gleason score (> or = 8) (P < 0.0001) and with advanced tumor pathological stages (stages T3 + T4; P < 0.01). Gain of chromosome 8 also correlated with higher Gleason score (P < 0.01). FISH showed intratumoral ploidy heterogeneity in 3 of 41 (7%) studied tumors. Among 17 noncancerous adjacent tissue specimens, chromosome alterations were observed in one, which contained high-grade prostatic intraepithelial neoplasia. Combined FISH and fluorescent leukocyte common antigen staining showed that infiltrating leukocytes do not contribute to the observed gains of chromosomes 7 and 8 in prostate cancer tissue. These results demonstrate that (a) FISH analysis of prostate needle biopsy-sized specimens can be a practical, sensitive method for determination of nuclear ploidy and numerical chromosome alterations; and (b) gains of chromosomes 7 and 8 are common numerical alterations of prostate cancer cells and may be potential markers of tumor behavior and patient prognosis.
Fluorescent in situ hybridization using 12 chromosome enumeration probes (for chromosomes 4, 6, 7, 8, 9, 10, 11, 12, 17, 18, X and Y) was used to evaluate fresh tumor touch preparations from 40 randomly selected radical prostatectomy specimens. Of the tumors 16 (40%) contained chromosomal aneusomies. Chromosome 8 was aneusomic in 9 tumors (23%). Gain of chromosome 7 was observed in 8 tumors (20%). Chromosome 17 was aneusomic in 4 cases, and chromosomes 10, 11, 12, 18 and Y were each aneusomic twice. Loss of chromosome 9 was observed in 1 tumor. Chromosomes 4, 6, and X were never aneusomic. The percentage of monosomy 17 nuclei was 2 to 4 times the amount noted with the other autosomes for tumor and benign tissue. Computer analysis demonstrated that these signals contained twice the signal density and were significantly different (p < 0.0001) than the single diploid chromosome 17 signals. This result is consistent with homologous pairing of chromosome 17 in benign and neoplastic prostate tissue. Anomalies of chromosomes 8 and/or 7 were present in 14 of the 16 cases (88%) aneusomic by fluorescent in situ hybridization. High grade tumors were more likely to be aneuploid on fluorescent in situ hybridization (p < 0.001). Tumors with chromosome 8 aneusomies were of higher stage (p < 0.05). Fluorescent in situ hybridization is more sensitive than flow cytometry for the detection of aneusomy/aneuploidy. The prognostic relevance of these findings will require further investigation.
Xanthogranulomatous pyelonephritis can become clinically apparent in a variety of manners. The paper contributes a very infrequent presentation; a picture of acute peritonitis following non-focal generalized toxic syndrome and haematuria episodes.
BACKGROUND: MVAC is considered the most effective chemotherapy regimen for transitional cell bladder carcinoma. However, due to its significant toxic effects we substituted carboplatin for cisplatin and epirubicin for adriamycin in an attempt to produce the same response with less toxicity. PATIENTS AND METHODS: Twenty-seven patients with invasive transitional cell bladder carcinoma received Carbo-MVE: carboplatin (300 mgr/m2 d2), methotrexate (30 mgr/m2 d1, 15, 22), vinblastine (3 mgr/m2 d2, 15, 22) and epirubicin (30 mgr/m2 d2) every 4 weeks. RESULTS: There were 2 complete clinical responses (8.4%), 5 partial clinical responses (20.8%), 8 stabilizations (33.3%) and 9 progressions (37.5%). The overall clinical response rate was 29.2% (11%-47.4%, 95% CI), but 2 partial clinical remissions were not pathologically confirmed; were they to be considered as non-responses the response rate would fall even lower (20.8%). Toxicity was moderately severe, with 77.8% developing WHO grade III-IV granulocytopenia, 22.2% grade III-IV thrombocytopenia and 59.3% grade II-III vomiting. There were no toxic deaths nor any renal toxicity. CONCLUSIONS: Our results suggest that Carbo-MVE is less active and at least as hematotoxic as multiagent CDDP-based regimens.
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