Identification of TNF-alpha and MMP-9 as potential baseline predictive serum markers of sunitinib activity in patients with renal cell carcinoma using a human cytokine array.

BACKGROUND: Several drugs are available to treat metastatic renal-cell carcinoma (MRCC), and predictive markers to identify the most adequate treatment for each patient are needed. Our objective was to identify potential predictive markers of sunitinib activity in MRCC. METHODS: We collected sequential serum samples from 31 patients treated with sunitinib. Sera of six patients with extreme phenotypes of either marked responses or clear progressions were analysed with a Human Cytokine Array which evaluates 174 cytokines before and after treatment. Variations in cytokine signal intensity were compared between both groups and the most relevant cytokines were assessed by ELISA in all the patients. RESULTS: Twenty-seven of the 174 cytokines varied significantly between both groups. Five of them (TNF-alpha, MMP-9, ICAM-1, BDNF and SDF-1) were assessed by ELISA in 21 evaluable patients. TNF-alpha and MMP-9 baseline levels were significantly increased in non-responders and significantly associated with reduced overall survival and time-to-progression, respectively. The area under the ROC curves for TNF-alpha and MMP-9 as predictive markers of sunitinib activity were 0.83 and 0.77. CONCLUSION: Baseline levels of TNF-alpha and MMP-9 warrant further study as predictive markers of sunitinib activity in MRCC. Selection of patients with extreme phenotypes seems a valid method to identify potential predictive factors of response.

[Renal cell carcinoma with sarcomatoid and rhabdoid features: a clinico-pathological series of 74 cases]. / Carcinomas renales con rasgos sarcomatoides y rabdoides: estudio clínico-patológico de 74 casos.

Objetives. Our aim is to analyze and compare the clinico-pathological features in renal cell carcinomas (RCC) with sarcomatoid and rhaboid phenotype. MATERIAL AND METHODS: We reviewed consecutive patients with nephrectomy RCC from January 1988 to January 2015. The subtyping of the RCC followed the recommendations of the College of American Pathologists. Cases with at least 1% of sarcomatoid and/or rhabdoid change were selected. They were classified as sarcomatoid or rhabdoid according with the predominant morphology, considering the global frecuency of both phenotypes as dedifferentiated component. The following variables were collected: sex, age, symptoms and existence of metastases at diagnosis, parameters listed in the protocol of renal carcinoma of the American College of Pathologists, pattern of tumor growth, perineural invasion, percentage of both tumor necrosis and characteristics of the inflammatory infiltrate. They were described by mean / median or percentage, and compared with Student-t / Mann-Whitney U or ? 2 / Fisher, depending on the sample characteristics. RESULTS: From 1,258 RCC, we identified 45 RCC with sarcomatoid predominance (3,6%) and twenty-nine with rhabdoid predominance (2,3%). RCC with sarcomatoid features showed a higher dedifferentiated component and perineural invasion (27.5 vs. 13.5%, p=0.003 and 28.9 vs. 3.4%, p=0.006, respectively) than RCC with rhabdoid features, while the former showed a higher proportion of neutrophilic inflammation (44.8 vs. 22.2%, p=0.04) and arose more frequently over high grade RCC (55.9 vs. 90.5%, p<0,001). CONCLUSIONS: There was overlapping of the clinico-pathological features of RCC with sarcomatoid and rhaboid phenotype, except for the dedifferentiated component, perineural invasion and neutrophilic inflammation. This close relationship could be explained by a common underlying mechanism, the epithelial-mesenchymal transition, with a double morphological expression that, if confirmed, could lead to selecting patients that would benefit from follow-up or treatment depending on their molecular characteristics.

[Fourth branchial cyst within the thyrohyoid membrane: a difficult differential diagnosis with mixed laryngocele]. / Quiste del cuarto arco branquial en la membrana tirohioidea: un difícil diagnóstico diferencial con el laringocele mixto.

We present a case of a 62-year-old female patient with a right latero-cervical mass and an enlarged arytenoepiglottic fold, that caused voice disturbances. Computed tomography of the neck depicted an unilocular and homogeneous well-defined cyst located in the right parapharyngeal space that extended through the thyrohyoid membrane. It was initially diagnosed of mixed laryngocele. During surgical resection, no connexion between the lesion and laryngeal ventricle was detected, so the final diagnosis was branchial cyst. We discuss the pathogenicity and clinical, radiological and histological findings that facilitate differential diagnosis between mixed laryngocele and branchial cysts, mainly those derived from the second and fourth clefts. The radiological and histological findings in both lesions may be similar, so only the communication with the larynx, or its absence, can solve diagnostic doubts, course.

[Salivary gland choristoma (hamartoma) of the middle ear: a case report]. / Cas clinique : choristome de glande salivaire au niveau de l'oreille moyenne.

OBJECTIVE: Middle ear salivary gland choristoma are extremly rare. We report a case, describe the clinical management and review the literature. CLINICAL CASE: A 12 year old boy presented with unilateral conductive hearing loss associated with a large inferior retraction pocket on otoscopy. CT scan demonstrated a large mass in the left middle ear cavity. The incus was absent and the stapes was partially eroded. Middle ear exploration demonstrated an 8 mm yellow/red mass in the region of the fallopian canal. This mass was comptly removed and histopathology confirmed salivary gland choristoma. CONCLUSION: These lesions result from an abnormal development of the second branchial arch. It is important to consider these lesions as part of the differential diagnosis for any unilateral hearing loss associated with a middle ear mass in children.

Cytologic and bacteriologic analysis of fluid and pleural biopsy specimens with Cope's needle. Study of 414 patients.

This article describes the results of a dual diagnostic procedure, thoracentesis and pleural biopsy with a Cope's needle, in 414 patients with pleural effusion of unknown origin. A diagnosis of neoplasia or pleural tuberculosis was obtained in 241 subjects (149 with neoplasias and 92 with pleural tuberculosis). In an additional 55 patients, a diagnosis of tuberculosis or neoplasia was obtained using other procedures (15 with tuberculosis and 40 with neoplasias). In 105 subjects, the effusion was neither tuberculosis nor neoplasia. Thirteen patients were excluded from this study due to the impossibility of follow-up. The diagnostic process was repeated in 64 patients. Complications occurred in 46 patients (11%), of which 42 were pneumothorax. The dual diagnostic sensitivity in our series of thoracenteses and pleural biopsies made with a Cope's needle was 86% in tuberculosis and 79% in neoplasia with 100% specificity. The probability of a case being neither tuberculosis nor pleural neoplasia (negative predictive value) when the liquid and the pleural biopsy specimen are nonspecific (each procedure having been applied only once on each patient) is 56%, although a negative result does not exclude these diagnoses. In our opinion, the repetition of the dual procedure is indicated considering the scant morbidity and zero mortality.

Is the regulation of apoptosis altered in smooth muscle cells of adult spontaneously hypertensive rats?

Whereas the protein product of the Bcl-2 gene inhibits apoptosis, the protein product of the Bax gene acts as a promoter of apoptosis. To gain insight into the regulation of apoptosis in vascular smooth muscle cells in arterial hypertension, we investigated the expression of the proteins Bcl-2 and Bax in small intramyocardial arteries of 36-week-old normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). In addition, 16-week-old SHR were treated for 20 weeks with the angiotensin-converting enzyme inhibitor quinapril and killed at 36 weeks of age. We measured the percentages of smooth muscle cells expressing these proteins using monoclonal antibodies and the avidin-biotin immunoperoxidase method. Compared with WKY, untreated SHR exhibited increased (P<.001) Bcl-2 expression and similar Bax expression. Values of Bcl-2 measured in quinapril-treated SHR were significantly lower than values measured in untreated SHR and similar to values measured in WKY. Quinapril-treated SHR showed higher (P<.001) Bax expression than WKY and untreated SHR. Bcl-2 expression was directly correlated with systolic pressure. Inverse correlations were found between the expression of Bax and the activities of both cardiac and circulating angiotensin-converting enzyme. These findings suggest that smooth muscle cell apoptosis might be inhibited in small arteries of adult SHR as a consequence of an excess of the protein Bcl-2. In addition, our results suggest that chronic angiotensin-converting enzyme inhibition might restore the susceptibility to apoptosis in these cells through stimulation of the protein Bax.

Cardiomyocyte apoptosis and cardiac angiotensin-converting enzyme in spontaneously hypertensive rats.

Increased apoptosis has been reported in the heart of rats with spontaneous hypertension and cardiac hypertrophy. This study was designed to investigate the relationship between apoptosis and hypertrophy in cardiomyocytes from the left ventricle of spontaneously hypertensive rats (SHR). In addition, we evaluated whether the development of cardiomyocyte apoptosis is related to blood pressure or to the activity of the local angiotensin-converting enzyme (ACE) in SHR. The study was performed in 16-week-old SHR, 30-week-old untreated SHR, and 30-week-old SHR treated with quinapril (10 mg x kg[-1] x d[-1]) during 14 weeks before they were killed. Cardiomyocyte apoptosis was assessed by direct immunoperoxidase detection of digoxigenin-labeled 3'-hydroxyl ends of DNA. Nuclear polyploidization measured by DNA flow cytometry was used to assess cardiomyocyte hypertrophy. Compared with 16-week-old normotensive Wistar-Kyoto rats, 16-week-old SHR exhibited increased blood pressure (P<.001), increased rate of tetraploidy (P<.05), and similar levels of ACE activity and apoptosis. Compared with 30-week-old Wistar-Kyoto rats, 30-week-old SHR showed increased blood pressure (P<.001), increased ACE activity (P<.05), increased rate of tetraploidy (P<.01), and increased apoptosis (P<.01). Untreated 30-week-old SHR exhibited similar values of blood pressure and tetraploidy and higher ACE activity (P<.05) and apoptosis (P<.001) than 16-week-old SHR. A direct correlation (P<.01) was found between ACE activity and the apoptotic index in untreated 30-week-old SHR. The long-term administration of quinapril was associated with the normalization of ACE activity and apoptosis in treated SHR. These results suggest that the timing and mechanisms responsible for apoptosis and hypertrophy of cardiomyocytes are different in SHR. Whereas hypertrophy seems to be an earlier alteration that develops in parallel with hypertension, apoptosis develops later in association with overactivity of the local ACE. Our data suggest that cell death dysregulation may be a novel target for antihypertensive agents that interfere with the renin-angiotensin system in hypertension.

Are mast cells involved in hypertensive heart disease?

OBJECTIVE: To evaluate the potential relationship of mast cells with myocardial fibrosis in the cardiac ventricles of spontaneously hypertensive rats (SHR). DESIGN: Experiments were performed on hearts from 36-week-old SHR with established left ventricular hypertrophy (n = 12) and from 36-week-old normotensive Wistar-Kyoto (WKY) rats (n = 12). Furthermore, to evaluate whether antihypertensive treatment with the angiotensin converting enzyme inhibitor quinapril interferes with the potential relationship between mast cells and fibrosis in SHR, we treated 16-week-old SHR (n = 12) with oral quinapril (10 mg/kg body weight per day) for 20 weeks. METHODS: Mast cells were counted in 25 high-power fields. Toluidine blue-stained sections and avidin staining were used to detect mast cells. The extent of myocardial fibrosis was analysed in samples stained with Masson's trichrome. The amount of collagen was evaluated morphometrically, using an automatic image analyser, and biochemically, using myocardial hydroxyproline concentration. RESULTS: In the left ventricle of untreated SHR compared with age- and sex-matched normotensive WKY rats we found more extensive interstitial and perivascular fibrosis, an increased collagen volume fraction, an increased hydroxyproline concentration and an increased number of mast cells. Similar but less intense abnormalities were observed in the right ventricles of untreated SHR compared with the left ventricles of the same rats. In the left ventricles of quinapril-treated SHR compared with those of untreated SHR we found a marked decrease in fibrosis, a lower collagen volume fraction, a lower hydroxyproline concentration and fewer mast cells. Treatment with quinapril was also accompanied by normalization in the myocardial structure of the right ventricles of SHR. A positive correlation was found between the density of mast cells and the collagen volume fraction in the left ventricles of all of the rats. CONCLUSIONS: The present findings suggest that mast cells can play a part in the development of the myocardial fibrosis that occurs in the cardiac ventricles with hypertensive cardiac hypertrophy. In addition, the present results suggest that the ability of quinapril to interfere with mast cells might be involved in its cardioreparative properties.

Toward the biochemical assessment of myocardial fibrosis in hypertensive patients.

The serum concentrations of amino-terminal procollagen type III and carboxy-terminal procollagen type I-derived peptides, which have been proposed as useful markers of the tissue synthesis of collagen types III and type I, respectively, were abnormally increased in patients with essential hypertension and became normal after angiotensin-converting enzyme (ACE) inhibition. An association was found between baseline serum concentrations of these peptides and left ventricular hypertrophy, diastolic dysfunction, and ventricular arrhythmias in hypertensive patients. On the other hand, increased serum concentration of the carboxy-terminal procollagen type I-derived peptide was found in spontaneously hypertensive rats compared with normotensive Wistar-Kyoto control rats. An association was found between the serum concentration of this peptide and the extent of myocardial fibrosis and the hydroxyproline concentration in the left ventricle of spontaneously hypertensive rats. It is proposed that procollagen-derived peptides in serum may be markers of exaggerated collagen tissue synthesis involved in hypertensive myocardial fibrosis.

Molecular features in a biphenotypic small cell sarcoma with neuroectodermal and muscle differentiation.

We report a case of a 13-year-old girl with soft tissue sarcoma of the hand, which showed muscle and neuroectodermal immunophenotypes. Molecular studies were performed on RNA collected from fine-needle aspiration (FNA) cytology and peripheral blood samples by nested reverse transcriptase-polymerase chain reaction (RT-PCR) and Southern blot analysis. This biphenotypic tumor showed simultaneous expression of EWS-FLI1 and PAX3-FKHR transcripts, specific of Ewing family tumors and alveolar rhabdomyosarcoma, respectively. Although childhood sarcomas with simultaneous muscle and neural differentiation have been described to have EWS-FLI1 transcripts, there are no reports of tumors with both transcripts. Cytological specimens are a good source of RNA for molecular studies.

Susceptibility to apoptosis measured by MYC, BCL-2, and BAX expression in arterioles and capillaries of adult spontaneously hypertensive rats.

Hypertension results in microvascular rarefaction or disappearance of microvessels. In the present study, we investigated the pathogenic role of apoptosis in hypertension-induced rarefaction of heart arterioles and capillaries of spontaneously hypertensive rats (SHR). Experiments were performed on hearts from 6-week-old, 16-week-old, and 30-week-old SHR (n = 30 rats) (SHR6, SHR16, SHR30). We used as controls 6-week-old, 16-week-old, and 30-week-old normotensive rats (WKY) (n = 30 rats) (WKY6, WKY16, WKY30). We analyzed the expression of c-myc, bcl-2, and bax and in situ end-labeling DNA fragmentation in vascular smooth muscle cells of arterioles and endothelial cells of arterioles and capillaries. Endothelial cells of capillaries and endothelial and smooth muscle cells of arterioles of hypertensive animals (SHR) express more Bax protein and Myc protein than their respective normotensive controls by margins that were statistically significant. The SHR30 group expressed the lowest levels of Bcl-2 protein by a margin that was statistically significantly different from WKY30. We did not find evidence of apoptosis in arterioles or capillaries on the basis of in situ end-labeling. However, our results indicated that alterations in the expression of members of the Bcl-2 family of proteins and Myc protein occurred in smooth muscle cells and endothelial cells of arterioles and capillaries of SHR. In conclusion, although evidence of apoptosis in arterioles and capillaries was not found by in situ end-labeling, our findings suggest that in hypertension they may have a higher susceptibility to apoptosis, and therefore rarefaction may be a consequence of apoptosis.

Quinapril decreases myocardial accumulation of extracellular matrix components in spontaneously hypertensive rats.

In genetic and acquired hypertension, a structural remodeling of the nonmyocyte compartment of myocardium, including the accumulation of fibrillar collagen and other components of the extracellular matrix (ECM) within the interstitium, represents a determinant of pathologic hypertrophy that leads to ventricular dysfunction. Therefore, to evaluate the potential benefit of the angiotensin converting enzyme (ACE) inhibitor quinapril in reversing the interstitial remodeling in spontaneously hypertensive rats (SHR) with established left ventricular hypertrophy (LVH), we treated 16-week-old male SHR with oral quinapril (average dose, 10 mg/kg body weight/day) for 20 weeks. Interstitial fibrosis was determined morphometrically using an automatic image analyzer. The amount of collagen was evaluated by measuring myocardial hydroxyproline concentration. Myocardial deposition of collagen molecules (types I, III, and IV) and other ECM components (fibronectin, laminin) was analyzed by immunohistochemical techniques using specific monoclonal antibodies. The activity of ACE was measured in left ventricular tissue by a fluorometric assay. In quinapril-treated SHR compared with 36-week-old untreated SHR and age- and sex-matched Wistar-Kyoto (WKY) controls, we found 1) a lesser degree of LVH and a lesser level of blood pressure, 2) a lesser degree of interstitial fibrosis, represented by less interstitial collagen volume fraction (5.73 +/- 0.45% v 3.42 +/- 0.28%, P < .05; WKY, 3.44 +/- 0.66%), 3) a lower hydroxyproline concentration (1.09 +/- 0.05 mumol/L/g dry weight/100 g body weight to 0.81 +/- 0.05 mumol/L/g dry weight/100 g body weight, P < .05; WKY, 0.96 +/- 0.06 mumol/L/g dry weight/100 g body weight), 4) a lesser presence of collagen fibers, and 5) a lesser presence of collagen IV, fibronectin, and laminin.(ABSTRACT TRUNCATED AT 250 WORDS)

Quinapril inhibits c-Myc expression and normalizes smooth muscle cell proliferation in spontaneously hypertensive rats.

A number of data suggest that angiotensin II-dependent activation of the protooncogene c-myc participates in the proliferative response of smooth muscle cells (SMC) of rats with spontaneous hypertension (SHR). We therefore investigated the effects of chronic treatment with the angiotensin converting enzyme (ACE) inhibitor quinapril on the oncoprotein c-Myc and the proliferating cell nuclear antigen cyclin A in SMC of small intramyocardial arteries from the left ventricle of SHR. The expression of c-Myc and cyclin A was assessed by immunocytochemical analysis. The number of smooth muscle cells was assessed by morphometrical analysis. As compared to normotensive Wistar-Kyoto (WKY) rats, untreated SHR exhibited an increased percentages of cells expressing c-Myc (33% +/- 4% v 19% +/- 2%, mean +/- SEM, P < .005) and cyclin A (25 +/- 2 v 11% +/- 1%, P < .001). In quinapril-treated SHR compared with untreated SHR, we found decreased expression of c-Myc (22% +/- 2%, P < .005) and cyclin A (13% +/- 1%, P < .001). No significant differences were found between WKY rats and quinapril-treated SHR in the above parameters. Cyclin A was directly correlated with the number of SMCs in each group of rats. These results suggest that an enhanced expression of c-Myc may be involved in the increased proliferation seen in SMCs from small arteries of SHR. Quinapril administration normalizes proliferation in the SMCs of SHR, possibly by inhibiting the expression of the oncoprotein c-Myc and its effects on the cell cycle.

Mast cells in chronic rejection of human renal allografts.

An increased number of mast cells (MCs) is found in renal specimens of patients with diseases associated with persistent chronic inflammation. MCs proliferation is partly dependent on the presence of T lymphocytes. Both chronic inflammation and T-lymphocytes are essential in the development of chronic rejection (CR), and probably for the infiltration of MCs. MC-derived products such as heparin, histamine, and serine proteases may be responsible for endothelial proliferation and excess collagen production by fibroblasts. In this study, a quantitative evaluation of the MCs infiltration in kidney allografts with CR is performed. The extent of renal fibrosis was analysed in samples stained with Masson's trichrome. To evaluate the potential relationship between MCs and fibrosis in CR we analysed 30 kidneys with CR (25 from nephrectomies and 5 from autopsies). Ten transplanted kidneys obtained from patients died by causes not related with rejection were used as controls. CR was graded according to the Banff schema, which assesses the degree of vasculopathy, tubular atrophy, interstitial fibrosis and transplantation glomerulopathy. Giemsa-stained sections and immunohistochemistry using anti-MC tryptase and c-kit monoclonal antibodies were used to detect MCs. The mean number of MCs per 20 high-power fields (HPF) in the transplanted kidney with CR was 101.8+/-15.3 in the renal cortex and 46.60+/-6.52 in the medulla. MCs were significantly more numerous in CR with respect to normal kidneys, both in the cortex (P<0.01; Mann-Whitney U test) and in the medulla (P<0.01; Mann-Whitney U test). There was a positive correlation between the number of MCs and extent of fibrosis (P<0.01; Kruskal-Wallis one-way anova test) and tubular atrophy (P<0.01). These results suggest that MCs may play a role in the process of development of interstitial fibrosis in CR.

PTEN protein expression correlates with PTEN gene molecular changes but not with VEGF expression in astrocytomas.

PTEN gene (10q23) is a relevant tumor suppressor gene whose protein is a phosphatase involved in the control of angiogenesis of some tumors including astrocytomas. There are no studies correlating molecular changes of PTEN and the immunohistochemical expression of its protein (pPTEN) with the expression of vascular endothelial growth factor (VEGF) in astrocytomas. Fifty-six surgically resected brain gliomas, 10 grade 2, 16 grade 3, and 30 grade 4, were studied by a combined approach, consisting of (1) PCR analysis using four microsatellite markers against the PTEN gene region (10q23), (2) the FISH technique to test chromosome 10 using a pericentromeric probe, and (3) immunohistochemical evaluation of pPTEN and VEGF. Loss of heterozygosity (LOH) of PTEN was observed in 10% of fibrillary grade 2 astrocytomas and all gemistocytic ones. In high-grade tumors, LOH was more frequent in grade 4 than in grade 3 (> or =2 loci deleted, 83% and 56%, respectively). Monosomy for chromosome 10 was observed especially in high-grade tumors (6% of grade 3 and 50% of grade 4) and in 20% of grade 2 tumors, corresponding to gemistocytic astrocytomas. Results with both antibodies against PTEN were concordant: loss of cytoplasmic immunoreactivity was frequently observed according to homogeneous or heterogeneous patterns in 70% and 50% of grades 4 and 3, respectively, but not in grade 2. Immunonegativity of pPTEN was associated with PTEN gene deletion (> or =2 loci deleted) (P = 0.04) but not with monosomy. Cytoplasmic immunoreactivity against VEGF was observed in high-grade and in gemistocytic astrocytomas, but not in conventional grade 2 tumors. Tumor expression of pPTEN was not associated with immunoreactivity against VEGF when the same areas were considered. In conclusion, loss of PTEN expression is frequent in high-grade astrocytomas, but not in grade 2 tumors, and correlates with PTEN deletion and loss of chromosome 10. PTEN immunoreactivity does not correlate with VEGF expression in astrocytomas when similar areas are considered.

Apoptotic cell death and genetic control in graft coronary artery disease in heart transplant.

AIM: Apoptosis is a type of programmed cell death whereby, immunologic, genetic and biochemical mechanisms are involved in its control. On the other hand, graft coronary artery disease is the most important restrictive factor for the long-term survival of heart transplantation. The purpose of this study is to analyse both apoptotic cell lesions in transplanted patients that present coronary artery disease. METHODS: From August 1984 until December 1996, 148 heart transplants were carried out in the Clínica Universitaria de Navarra. In 102 patients, annual coronary angiography was performed, reaching a diagnosis of coronary artery disease in 30 patients. Study of apoptotic cell death was done in the tissue of endomyocardial biopsies on all patients by means of the TUNEL technique. Procedures of immunohistochemistry with antibodies antic-myc, p53 and bcl-2 were carried out and results were compared with a control group of 30 patients with homogeneous characteristics. RESULTS: All patients with coronary artery disease showed apoptotic cardiomyocytes, 13 patients to a mild degree, 14 to a moderate degree and 3 to a severe degree, while in the control group apoptosis was found only to a mild degree in 8 patients, obtaining a very significant statistical difference (p<0.0001). The expression of analysed oncoproteins was null in the 2 groups. CONCLUSION: Myocardial apoptosis is a constant finding in transplanted patients with coronary artery disease. We have not seen any correlation between the apoptotic process and genetic mechanisms.

FNAC guided by computed tomography in the diagnosis of primary pancreatic adenosquamous carcinoma. A report of three cases.

BACKGROUND: Pancreatic adenosquamous carcinoma (ASqC) is an unusual histologic subtype of nonendocrine neoplasia of the pancreas. Although fine needle aspiration cytology (FNAC) is now accepted as a reliable procedure for the diagnosis of pancreatic malignancies, many of these unusual tumors are still diagnosed after surgery or at necropsy. CASES: Between January 1995 and July 1996, 3 of 35 primary pancreatic malignant tumors were diagnosed as ASqC based on computed tomography-guided FNAC. After cytologic diagnosis, all three patients were treated with neoadjuvant chemotherapy and radiotherapy. Two patients completed the treatment and underwent a surgical pancreatic-duodenectomy with antrectomy. The remaining patient is currently under treatment. That patient had a highly infiltrative pancreatic mass that affected the muscular small bowel wall. An endoscopic biopsy was performed. The cytologic diagnosis was confirmed by histology in all cases. Immunohistochemically both components, squamous and glandular, showed reactivity for several keratins, while only the glandular pattern was reactive with carcinoembryonic antigen (CEA). CONCLUSION: FNAC is an accurate, rapid and sensitive tool in the diagnosis of ASqC of the pancreas. We recommend a careful search for both malignant components. Immunoreactivity for CEA can be of help in the detection of the glandular component of this tumor.

Primary graft failure after heart transplantation. Successful recovery with pneumatic biventricular assistance.

A 41-year-old male underwent orthotopic heart transplantation complicated by intraoperative acute allograft failure. The patient required immediate placement of a pneumatic biventricular assist device which was kept for 49 days until graft recovery resulted in successful explantation of the device. The patient was discharged from hospital on postoperative day 112. Management of primary cardiac allograft failure with mechanical ventricular assistance is discussed.

[Bladder leiomyoma: report of a new case]. / Leiomioma vesical: aportación de un nuevo caso.

We present one case of vesical intramural leiomyoma in one adult woman in which an echographic fortuitous diagnostic was made. We have reviewed the bibliography and the diagnostic and therapy considerations.

[The application of the Minimum Data Set (MDS) in the surveillance of nosocomial infections]. / Utilidad del conjunto mínimo básico de datos (CMBD) en la vigilancia de las infecciones nosocomiales.

BASIS: Analysis of the application of the Minimum Data Set in the vigilance of nosocomial infection. Study of the risk of nosocomial infection according to the Deyo-Charlson Comorbidity Index. METHODS: The database of the Minimum Data Set of the hospital was related with the database containing the infections collected by the Infectious Diseases Surveillance Unit of the Preventive Medicine Service for the year 1997. Surgical procedures were classified by the North American system of vigilance of nosocomial infections. The diagnoses appearing in the Deyo-Charlson Index were localised. The rates of nosocomial infection were calculated in relation to the presence of comorbidities and procedures. RESULTS: Not all discharges were codified (6.2%). Mortality and the rate of nosocomial infection were lower in codified discharges than in non-codified (4 and 1.5 respectively, p<0.01). Amongst the codified discharges, the rates of nosocomial infection and the surgical site are higher amongst surgery patients than in non-surgery cases according to the North American vigilance system of nosocomial infections. Nosocomial infection is associated with a higher hospital mortality. As scoring increases on the Deyo-Charlson Index, there is a rise in the rate of nosocomial infection (1.8% to 9.9%), average stay (average 14-22 days) and hospital mortality (0.2% to 17.8%). CONCLUSIONS: The validity of these results depends on the validity of the data gathered in the Minimum Data Set, which is in its turn determined, amongst other factors, by the quality of the Discharge Report with respect to its inclusion of diagnoses and principal and secondary procedures, and by exhaustiveness in the codification of hospital discharges.