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Results for “Infiltrative”

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PubMed2006

Capacity of ocular infiltrating T helper type 1 cells of patients with non-infectious uveitis to produce chemokines.

BACKGROUND/AIMS: Chemokines are key molecules that initiate leucocyte infiltration to the inflammatory site. The involvement of chemokines in uveitis is well studied, yet the source of this molecule in the inflamed eye is not clearly identified. The possible sources of chemokines are ocular resident cells or the inflammatory cells infiltrated to the eye. Here the authors examined whether ocular infiltrating T cells of uveitis patients do produce chemokines. METHODS: T cell clones (TCCs) were established from ocular infiltrating cells of patients with non-infectious uveitis. TCCs were characterised using flow cytometry. Spontaneous production of chemokines by TCCs was evaluated by ELISA. RESULTS: TCCs from ocular infiltrating cells were revealed to be memory activated Th1 type CD4 positive cells. Those TCCs produced larger amounts of chemokines than TCCs from peripheral blood mononuclear cells of uveitis or healthy donors. CONCLUSIONS: The present data indicate that ocular infiltrating T cells of patients with non-infectious uveitis produce chemokines and recruit further infiltrating lymphoid cells. Such T cells may have roles in the prolonged/chronic state of non-infectious uveitis.

Acute Disease↗

PubMedDate not supplied

From the archives of the AFIP. Infiltrative renal lesions: radiologic-pathologic correlation. Armed Forces Institute of Pathology.

Most renal masses exhibit an expansile growth pattern characterized by radial tumor enlargement that displaces normal renal parenchyma and forms spherical, often exophytic, lesions. These expansile masses have pushing margins that impress adjacent normal renal parenchyma but do not infiltrate it; this behavior results in a well-defined, encapsulated appearance at both radiologic and gross pathologic examination. In contrast, certain disease processes involve the kidney in an infiltrative fashion by using the normal renal architecture as scaffolding for interstitial growth. These infiltrative renal lesions lack a sharp border of demarcation with the normal parenchyma and therefore demonstrate ill-defined zones of transition between the lesion and normal parenchyma. Although infiltrative lesions frequently enlarge the kidney, its reniform shape is usually maintained. Cross-sectional imaging can often help distinguish infiltrative from expansile growth patterns through analysis of the parenchymal interface between the process and the kidney, the effect of the lesion on the collecting system and renal sinus, and the overall renal morphology. A wide variety of neoplastic and inflammatory conditions characteristically involve the kidney by cellular infiltration. Although considerable overlap of the imaging features exists among the various infiltrative processes, the correct diagnosis may be suspected when the clinical data and associated radiologic findings are considered together.

Diagnosis, Differential↗

PubMed2005

Is infiltrate a useful term in the interpretation of chest radiographs? Physician survey results.

PURPOSE: To determine how physicians interpret the word infiltrate when it is used in a chest radiography report and if the word is helpful in the clinical management of patients. MATERIALS AND METHODS: Informed consent from participants was not required, and the study protocol was granted exempt status. One hundred sixty-five questionnaires were distributed, in conjunction with various physician meetings, at three separate nonaffiliated training hospitals. In the three-question survey, respondents were asked the definition of infiltrate, whether the term is helpful in guiding patient therapy, and whether it implies an etiology. The respondent demographic data obtained included date of graduation from medical school, amount of postgraduate training completed, primary or training specialty, and board or sub-board qualification. RESULTS: There were 151 physician respondents, 94 (62.3%) of whom were house staff members. One hundred fifteen (76%) responders chose bacterial pneumonia as a condition consistent with infiltrate. One hundred thirty (86.1%) respondents replied that infiltrate implied more than one pathophysiologic condition. Eighty-two (54.3%) of those surveyed thought infiltrate could mean any of six or more different pathophysiologic conditions, including nonspecific pneumonia, interstitial pneumonia, viral pneumonia, consolidation, or nonspecific interstitial process. The number of terms selected did not vary according to level of residency training (P = .23); however, there was a significant specialty-related difference in the number of terms selected (P = .018). Internists selected a median of 10 terms, while others selected a median of six. Only 54 (36%) respondents thought that the term infiltrate was helpful in patient care, and only five (3%) thought that the term implied an etiology. CONCLUSION: Infiltrate is a nonspecific and imprecise term when it is used as a radiograph descriptor, and use of this term does not usually enhance patient care.

Physicians↗

PubMed1998

Correlations among expression of intercellular adhesion molecule 1, cellular infiltration, and coronary arteriosclerosis during chronic rejection using the rat heart transplantation model.

Immunologic mechanisms contribute to the development of coronary arteriosclerosis. In this study the rat heart transplantation model was used to investigate correlations among the expression of intercellular adhesion molecule 1, cellular infiltrate, and coronary arteriosclerosis during chronic rejection. Lewis rats served as heart donors and F-344 rats as recipients. Heart transplantations were performed heterotopically. The recipients were treated with cyclosporin A (5 mg/kg/day) by daily intramuscular injection for 30 days, beginning on the day of transplantation. Rejection grade and the intimal area were measured. The expression of intercellular adhesion molecule 1 and the numbers of infiltrating CD4- and CD8-positive cells and macrophages were examined immunohistochemically. The area of the intima was significantly increased in the allograft group after transplantation. In the allograft group, the level of expression of intercellular adhesion molecule 1 was considerably increased over the same time period. There was increased cellular infiltration in the 60-day group, and many expressed intercellular adhesion molecule 1. The expression of intercellular adhesion molecule 1 in vascular endothelium, infiltrating cells, and the sarcolemmal membrane of myocytes remained constant up to 120 days in the allograft group. In the allograft group, the number of infiltrating CD4- and CD8-positive cells and macrophages increased significantly between 30 and 60 days, and the infiltration of these cells remained constant. Continuous expression of intercellular adhesion molecule 1 induces the infiltration of T cells and macrophages, and the inflammation caused by such cells and their soluble products contributes to the arteriosclerotic process.

Animals↗

PubMed2001

Eosinophil infiltration and degranulation in normal human tissues: evidence for eosinophil degranulation in normal gastrointestinal tract.

Eosinophils play an important role in the pathogenesis of inflammatory diseases such as bronchial asthma and host immunity to parasitic infections. Deposition of eosinophil granule proteins and concomitant tissue damage have been documented in various diseases. Here, we review and summarize results of our immunofluorescence studies of eosinophil infiltration and degranulation in various normal human tissues. Furthermore, because eosinophil infiltration and degranulation are not normally present in healthy tissues, we examine whether eosinophil infiltration and degranulation normally occur in the small intestine and whether tissue procurement methods affect the extent of eosinophil infiltration and degranulation there. Hematopoietic and lymphatic tissues, including the thymus, showed eosinophil infiltration, but the only organ showing remarkable eosinophil infiltration and degranulation was the gastrointestinal (GI) tract. Eosinophil degranulation was significantly increased in specimens obtained by endoscopic forceps compared to those obtained by scalpel. These results suggest that tissue procurement methods affect the degree of eosinophil degranulation in the GI tract and that, among normal human body organs, both eosinophil infiltration and degranulation only occur in the GI tract.

Adult↗

PubMedDate not supplied

Correlation between mononuclear infiltration and changes in VASP phosphorylation patterns after heterotopic cardiac transplantation in the rat.

Chronic cardiac transplant vasculopathy still remains the major cause of late graft failure after the 1st postoperative year, with iNOS playing a central role in the progression of this disease. Since VASP, a recently identified microfilament-associated protein in smooth muscle cells, endothelial cells, and platelets, is phosphorylated by cyclic nucleotide dependent protein kinases, changing amounts of NO-producing mononuclear infiltration cells during cardiac rejection are supposed to change platelet VASP phosphorylation patterns. We investigated whether platelet VASP Ser(157) phosphorylation (VASP shift) after coronary passage of rat cardiac allografts correlates with graft infiltration. The Lew-F344 heterotopic rat cardiac transplantation model was used. Native hearts and grafts were harvested 3-150 days after transplantation and were used for Langendorff perfusion. The platelet VASP shift after native heart and graft perfusion was identified. Additional iNOS stimulation and iNOS inhibition were achieved pharmacologically. Immunohistology revealed graft mononuclear infiltration. Platelet VASP Ser(157) and Ser(239) phosphorylation significantly increased after coronary passage of native hearts and grafts (p < 0.01). Though platelet VASP Ser(157) phosphorylation failed to directly express graft infiltration, we showed a significant correlation between changes of platelet VASP shift and extent of grafts' mononuclear infiltration after competitive iNOS inhibition (p < 0.01). The platelet VASP shift is modified during coronary perfusion, and this modification correlates with mononuclear infiltration in the graft. This emphasizes the influence of mononuclear infiltration cells on microfilamental structures of the cytoskeleton in adjacent cells.

Animals↗

PubMed1989

Immunohistochemical detection of tissue-infiltrating lymphocytes in bladder tumors.

Local immunocompetence in patients with bladder tumors was evaluated immunohistochemically using monoclonal antibodies. As well as investigating the subsets of peripheral blood lymphocytes by flow cytometry, the subpopulations of tissue-infiltrating lymphocytes were investigated in frozen specimens from bladder cancers (n = 25) and from noncancerous tissues (n = 4). Six serial sections were stained with Leu4, Leu7, Leu10, LeuM3, OKT4, and OKT8 antibodies, respectively. Marked lymphocytic infiltration into bladder tumors was a favorable prognostic sign. T cell infiltration was marked in the noninvasive group and was prominent around tumor cells, whereas B cells were rare in the stroma. T cells predominated over B cells in 19 of 25 bladder tumors. In patients with low-stage tumors, OKT8 cells were more prominent than OKT4 cells. NK cells accumulated around the cancer cells and infiltrated within cancer nests; NK cell infiltration was scanty in high-stage cases. There was a slight scattering of macrophages in 13 cases. In contrast to the findings in subsets of tissue-infiltrating lymphocytes, subsets of peripheral blood lymphocytes did not correlate with stage of disease. These findings suggest the presence of local immunosurveillance against bladder tumors. To elucidate host immune response against tumor, it may be important to characterize tissue-infiltrating lymphocytes.

Antibodies, Monoclonal↗

PubMed1991

Expression of perforin in infiltrating cells in murine hearts with acute myocarditis caused by coxsackievirus B3.

BACKGROUND: Cell-mediated autoimmunity has been strongly implicated in the pathogenesis of viral myocarditis. METHODS AND RESULTS: Using a murine model of acute myocarditis caused by coxsackievirus B3, we analyzed the phenotypes and morphology of the infiltrating cells in the hearts by immunofluorescence and electron microscopy. We also examined the expression of a cytolytic factor, perforin, in the infiltrating cells by immunoperoxidase and in situ hybridization. We found that the dominant population of the infiltrating cells were asialo GM1 positive, were negative for T-cell markers, and had electron-dense cytoplasmic granules, which is consistent with a morphology of large granular lymphocytes. Perforin was found in the cytoplasmic granules of the infiltrating cells expressing perforin messenger RNA. These findings provide for the first time the direct evidence that the first wave of cell infiltration in hearts mainly consists of killer cells and strongly suggests that perforin plays, in part, an important role in myocardial cell damage involved in acute viral myocarditis. T-helper cells and cytotoxic T lymphocytes made up the second wave of cell infiltration. CONCLUSIONS: As we previously reported, the expression of major histocompatibility complex class I antigen on cardiac myocytes induced by the infiltrating cells, such as killer cells, may facilitate the interaction between cardiac myocytes and cytotoxic T lymphocytes, and may lead to further myocardial cell damage in a later phase.

Acute Disease↗

PubMed1992

CD4+ T-lymphocytes and interleukin-5 mediate antigen-induced eosinophil infiltration into the mouse trachea.

In order to determine the role of CD4+ and CD8+ T-cells and of interleukin-5 (IL-5) in causing antigen-induced eosinophil infiltration into the site of airway late-phase reaction, we examined the effect of the in vivo depletion of CD4+ and CD8+ T-cells on the eosinophil infiltration of the trachea induced by antigen inhalation in mice. We also studied the effect of anti-murine IL-5 monoclonal antibody (mAb) on the antigen-induced eosinophil infiltration in the trachea. The eosinophil infiltration into the trachea of ovalbumin (OVA)-sensitized BALB/c mice began to increase 9 h after OVA inhalation and persisted for more than 48 h. The in vivo depletion of CD4+ T-cells by pretreatment with anti-L3T4 mAb significantly decreased the eosinophil infiltration induced by OVA inhalation in the trachea of sensitized mice. However, the in vivo depletion of CD8+ T-cells by pretreatment with anti-Lyt-2 mAb had no significant effect on OVA-induced eosinophil infiltration in the trachea. Pretreatment with anti-murine IL-5 mAb also decreased OVA-induced eosinophil infiltration in the trachea. In contrast, neither disodium cromoglycate nor a selective antagonist for platelet-activating factor CV-6209 decreased OVA-induced airway eosinophilia in the mouse. Our results provide direct evidence that CD4+ but not CD8+ T-cells mediate antigen-induced eosinophil recruitment in the airways and that IL-5 mediates this eosinophil recruitment.

Administration, Inhalation↗

PubMedDate not supplied

Effect of the continuous administration of fat emulsion on the infiltration of intravenous lines in infants receiving peripheral parenteral nutrition solutions.

Animal data and anecdotal human experience suggest that vascular damage induced by the infusion of dextrose/amino acid solutions may be ameliorated by the concomitant administration of fat emulsion. We prospectively evaluated the effect of the continuous infusion of peripheral nutrition solutions with and without fat emulsion on the incidence of, probability of, and time to infiltration of peripheral venous lines in infants (median age: 1.0 month; range 1 day-11.9 months). Ninety-seven peripheral venous lines were studied in 53 infants who received 10% dextrose (n = 34), 10% dextrose/2% amino acids (n = 30), or 10% dextrose/2% amino acids/fat emulsion (n = 33). Solutions were administered by positive pressure infusion devices through Teflon catheters with similar gauge. Dextrose, amino acid, electrolyte, and mineral content was standardized for the dextrose/amino acid and dextrose/amino acid/fat emulsion groups. The three groups were similar with respect to age, race, gender, weight, administration of intravenous medications, and catheter site (p greater than 0.05). Patients receiving dextrose/amino acid or dextrose/amino acid/fat emulsion had greater rates of solution administration than those receiving dextrose alone (p less than 0.002). Infiltration occurred in 71% of dextrose, 66% of dextrose/amino acid, and 67% of dextrose/amino acid/fat emulsion solutions (p greater than 0.05). The probability of infiltration was greater for infants receiving dextrose/amino acid than for those receiving either dextrose or dextrose/amino acid/fat emulsion (p = 0.01). The mean +/- SEM length of time the intravenous sites were viable was significantly shorter for the dextrose/amino acid solutions (26.3 +/- 3.3 hr) compared to the dextrose (54.9 +/- 7.8 hr) and dextrose/amino acid/fat emulsion (43.6 +/- 4.2 hr) groups. No site complications were associated with the infiltration of any solution. We conclude that the incidence of infiltration among the three solution groups studied is not different. However, the time to infiltration is prolonged and the probability of infiltration is decreased following the infusion of either dextrose alone or dextrose/amino acid/fat emulsion solutions when compared to the administration of dextrose/amino acid solutions without concomitant fat emulsion infusion.

Amino Acids↗

PubMed1986

Lymphocyte subpopulations infiltrating squamous carcinomas of the head and neck: correlations with extent of tumor and prognosis.

Because little is known about the mechanisms involved in local tumor-host immune reactions in squamous carcinoma of the head and neck, a study was undertaken to better characterize the types of immune cells present at the local tumor site and determine their relationship to tumor extent, systemic cellular immune parameters, and clinical outcome. In 40 untreated patients, lymphocyte subsets (LS) at the tumor-host interface were quantitated immunohistologically from serial sections of frozen tumor specimens and correlated with concurrently measured peripheral LS levels and in vitro lymphocyte reactivity to phytohemagglutinin (PHA). The majority of infiltrating lymphocytes were T cells with rare B or Leu 7 cells. Proportions of T4 and T8 were similar in peritumor stroma; however, T8 cells predominated tumor parenchyma. Stromal and parenchymal infiltration by LS were not related to peripheral blood LS levels, lymphocyte reactivity, or tumor site. However, parenchymal T11 and T4 cell infiltration was less in advanced primary tumors (T3, T4) than in early tumors (T1, T2) (P = 0.01, P = 0.067, respectively), as was peripheral lymphocyte reactivity to PHA (P = 0.013). Short-term disease-free interval and actuarial survival differed significantly--according to parenchymal T11 and T4 cell infiltration--and were not related to T8, Leu 7, and B-cell infiltration. The findings extend prior studies of lymphocytic infiltration in head and neck cancer and demonstrate the potential importance of differences in tumor stromal and parenchymal infiltration. Together with recent evidence that T4 cells are critical for lymphokine production and for the proliferation of cytotoxic effector cells, the current results suggest that T4 cells play a critical role in the local immune response in squamous carcinoma of the head and neck.

B-Lymphocytes↗

PubMed2006

Enumeration of leukocyte infiltration in solid tumors by confocal laser scanning microscopy.

BACKGROUND: Leukocytes commonly infiltrate solid tumors, and have been implicated in the mechanism of spontaneous regression in some cancers. Conventional techniques for the quantitative estimation of leukocyte infiltrates in tumors rely on light microscopy of immunostained thin tissue sections, in which an arbitrary assessment (based on low, medium or high levels of infiltration) of antigen density is made by the pathologist. These estimates are relatively subjective and often require the opinion of a second pathologist. In addition, since thin tissue sections are cut, no data regarding the three-dimensional distribution of antigen can be obtained. RESULTS: To overcome these problems, we have designed a method to enumerate leukocyte infiltration into tumors, using confocal laser scanning microscopy of fluorescently immunostained leukocytes in thick tissue sections. Using image analysis software, a threshold was applied to eliminate unstained tissue and residual noise. The total antigen volume in the scanned tissue was calculated and divided by the mean cell volume (calculated by "seeding" ten individual cells) to obtain the cell count. Using this method, we compared the calculated leukocyte counts with those obtained manually by ten laboratory personnel. There was no significant difference (P > 0.05) between the cell counts obtained by either method. We then compared leukocyte infiltration into seven tumors and matched non-malignant tissue obtained from the periphery of the resected tissue. There was a significant increase in the infiltration of all leukocyte subsets into the tumors compared to minimal numbers in the non-malignant tissue. CONCLUSION: From these results we conclude that this method may be of considerable use for the enumeration of cells in tissues. Furthermore, since it can be performed by laboratory technical staff, less time input is required by the pathologist in assessing the degree of leukocyte infiltration into tumors.

Antigens, CD↗

PubMed2006

Extensive myocardial infiltration by hemopoietic precursors in a patient with myelodysplastic syndrome.

BACKGROUND: Although myocardial infiltration with leukemic blasts is a known finding in patients with acute leukemia, this phenomenon in myelodysplasia is not reported in the literature. Cardiac symptoms in patients with myelodysplasia are often due to anemia and may be due to iron overload and side effects of therapy. CASE PRESENTATION: Herein we report the first case of neoplastic infiltration of the heart with associated myocardial necrosis in a patient with myelodysplasia. It was associated with unicellular and multifocal geographic areas of necrosis in the left ventricle and the interventricular septum. It is likely that cardiac compromise in our patient was due to a combination of restrictive cardiomyopathy due to leukemic infiltration, concomitant anemia, cardiac dilatation, conduction blocks and myocardial necrosis. Myocardial necrosis was most likely due to a combination of ischemic damage secondary to anemia and prolonged hypotension and extensive leukemic infiltration. Markedly rapid decrease in ejection fraction from 66% to 33% also suggests the role of ischemia, since leukemic infiltration is not expected to cause this degree of systolic dysfunction over a 24-hour period. The diagnosis was not suspected during life due to concomitant signs and symptoms of anemia, pulmonary infections, and pericardial and pleural effusions. The patient succumbed to cardiac failure. CONCLUSION: Hemopoietic cell infiltration was not considered in the differential diagnosis and contributed to this patient's morbidity and mortality. This case highlights the clinical importance of considering myocardial infiltration in patients with myelodysplasia and cardiac symptoms.

Journal Article↗

PubMed2004

Type-selective muscular degeneration promotes infiltrative growth of intramuscular lipoma.

BACKGROUND: Intramuscular lipoma is a relatively common benign neoplasm that is occasionally described as an infiltrating lipoma. Typical benign tumors show a clear margin, however, the infiltrative growth pattern of this lipoma mimics that of a malignant tumor. Although its growth has an effect on muscle bundles and it is known to never metastasize, the mechanism of infiltrative growth is not well understood. Previously, little attention has been paid to pathogenic features of muscle fibers around an intramuscular lipoma. METHODS: In the present study, we focused on pathologic changes of the surrounding skeletal muscles especially to the degenerative features of involving muscular types, and evaluate the role of type-selective muscular degeneration for the infiltrative growth of intramuscular lipomas. Following a review of the medical records in our institute, 17 lesions containing muscle tissues in their specimens (15 infiltrating lipomas, 2 well-circumscribed lipomas) were analyzed immunohistochemically. The tumor from the most recent case was also subjected to ultrastructural analysis. Two cases of the traumatic muscle damage were also evaluated as the control experiments. RESULTS: These analyses revealed type-selective muscle involution in 11 of 17 intramuscular lipomas and in 10 of 11 of the infiltrative type, with an involving pattern that resembled that of a neurogenic or myogenic disorder. Immunoreactivity to cathepsin-D, a lysosomal catabolic enzyme, was increased in the involved muscle fibers. Subsarcolemmal vacuoles in the muscle fibers of the peripheral areas were also positive for cathepsin-D, while degenerative findings were not visually apparent in these areas. Ultrastructural analysis revealed degenerative changes in those fibers. Neither positive staining for cathepsin-D nor type-selective atrophy was detected in the sections of traumatic muscle damage. CONCLUSIONS: Our findings suggest that type-selective muscular degeneration and endomysial fatty growth as a result of atrophy may modulate the infiltrating growth characteristic of intramuscular lipoma.

Adipocytes↗

PubMed2004

Gene deletion of P-Selectin and ICAM-1 does not inhibit neutrophil infiltration into peritoneal cavity following cecal ligation-puncture.

BACKGROUND: Neutrophil infiltration is one of the critical cellular components of an inflammatory response during peritonitis. The adhesion molecules, P-selectin and intercellular adhesion molecule (ICAM)-1, mediate neutrophil-endothelial cell interactions and the subsequent neutrophil transendothelial migration during the inflammatory response. Despite very strong preclinical data, recent clinical trials failed to show a protective effect of anti-adhesion therapy, suggesting that the length of injury might be a critical factor in neutrophil infiltration. Therefore, the objective of this study was to determine the role of P-selectin and ICAM-1 in neutrophil infiltration into the peritoneal cavity during early and late phases of peritonitis. METHODS: Peritonitis was induced in both male wild-type and P-selectin/ICAM-1 double deficient (P/I null) mice by cecal ligation-puncture (CLP). Peripheral blood and peritoneal lavage were collected at 6 and 24 hours after CLP. The total leukocyte and neutrophil contents were determined, and neutrophils were identified with the aid of in situ immunohistochemical staining. Comparisons between groups were made by applying ANOVA and student t-test analysis. RESULTS: CLP induced a severe inflammatory response associated with a significant leukopenia in both wild-type and P/I null mice. Additionally, CLP caused a significant neutrophil infiltration into the peritoneal cavity that was detected in both groups of mice. However, neutrophil infiltration in the P/I null mice at 6 hours of CLP was significantly lower than the corresponding wild-type mice, which reached a similar magnitude at 24 hours of CLP. In contrast, in peritonitis induced by intraperitoneal inoculation of 2% glycogen, no significant difference in neutrophil infiltration was observed between the P/I null and wild-type mice at 6 hours of peritonitis. CONCLUSIONS: The data suggest that alternative adhesion pathway(s) independent of P-selectin and ICAM-1 can participate in neutrophil migration during peritonitis and that the mode of stimuli and duration of the injury modulate the neutrophil infiltration.

Journal Article↗

PubMed1995

The correlation between papillary thyroid carcinoma and lymphocytic infiltration in the thyroid gland.

Ninety-five patients with papillary thyroid carcinoma (PTC) who received primary surgical treatment in 1983 at Kuma Hospital and were followed until 1992 were the subjects of this study. Initial therapy was tumor resection for 5 patients, lobectomy for 23 patients, total thyroidectomy with unilateral modified neck dissection for 60 patients, and total thyroidectomy with bilateral modified neck dissection for 7 patients. Clinical stage at diagnosis was as follows. Class I included 28 patients with intrathyroidal disease, class II included 60 patients with positive cervical lymph nodes, and class II included 7 patients with tumor invasion into tissue outside of the thyroid gland. Recurrence of the tumor was evaluated according to lymphocytic infiltration in the thyroid gland. Group A consisted of 36 patients with PTC associated with lymphocytic infiltration, 26 with infiltration surrounding the tumor, 3 with infiltration inside of the tumor, and 7 with both. Group B consisted of the remaining 59 patients with PTC with no lymphocytic infiltration. There were no differences in age, sex, initial tumor size, or initial treatment between groups A and B. Antithyroglobulin antibody and/or antimicrosomal antibody were positive in 16 patients from group A and 4 patients from group B (P < 0.001). Class I included 14 patients from each group, class II included 22 patients from group A and 38 patients from group B, and class III included 7 patients, all from group B. Recurrence of the tumor was found in only 1 group A patient (2.8%), but in 11 patients of group B (18.6%). The percentage of patients free from recurrence over the 10 yr of follow-up in group A was significantly higher than that in group B (by Cox-Mantel test, P < 0.01). The time between initial treatment and recurrence was 2-10 yr. In comparing the clinical stage at the time of initial treatment, recurrence was found in 1 class II patient from group A (4.5%) and in 1 class I (7.1%), 6 class II (15.8%), and 4 class III (57.1%) patients from group B. No patients died during the 10 yr of follow-up. In conclusion, 1) lymphocytic infiltration surrounding the tumor or inside the tumor in PTC might be of use as a means for predicting a favorable prognosis; and 2) class II or class III patients with no lymphocytic infiltration had a high rate of recurrence.

Adult↗

PubMed2003

Continuous wound infiltration with ropivacaine reduces pain and analgesic requirement after shoulder surgery.

UNLABELLED: After achieving a reduction of pain scores for 10 h with a single dose wound infiltration after shoulder surgery, we examined in a prospective, placebo-controlled and double-blinded study the analgesic effects of continuous wound infiltration with different concentrations of ropivacaine. Forty-five patients undergoing shoulder surgery were randomly assigned into three groups to receive single dose wound infiltration with 30 mL saline (group S) or ropivacaine 7.5 mg/mL (groups R2 and R3.75) after skin closure. Postoperatively, patients received a continuous wound infiltration with saline (group S), ropivacaine 2 mg/mL (group R2) or ropivacaine 3.75 mg/mL (group R3.75) for 48 h. Supplemental pain relief was provided by IV patient-controlled analgesia with the opioid piritramide. At 1, 2, 3, 4, 24, and 48 h postoperatively visual analogue scale (VAS) values (0-100 mm), piritramide requirements and side effects were registered. Plasma levels of ropivacaine were measured preoperatively and at 24 h and 48 h after surgery. Until 48 h VAS values were smaller in group R3.75 compared with group S (group R3.75, 8 +/- 9 mm; group S, 31 +/- 14 mm; P < 0.005), whereas 4 h and 48 h postoperatively VAS values were even smaller in group R3.75 compared with group R2 (P < 0.05). Cumulative piritramide consumption was always smaller in groups R2 and R3.75 compared with group S (1-24 h, P < 0.005; 48 h, P < 0.05). Plasma ropivacaine levels remained less than the toxic threshold. We conclude that continuous postoperative wound infiltration with ropivacaine, especially using 3.75 mg/mL, provides smaller VAS values and opioid requirement in comparison with saline after shoulder surgery. IMPLICATIONS: The continuous postoperative wound infiltration after shoulder surgery with different concentrations of ropivacaine, 2 mg/mL and 3.75 mg/mL, results in lower pain scores and opioid requirement compared with infiltration with placebo. Plasma levels of ropivacaine remained less than the toxic threshold.

Adult↗

PubMed1998

Pulmonary infiltrates in neutropenic patients with acute leukemia during chemotherapy: outcome and prognostic factors.

STUDY OBJECTIVE: To determine predictors of mortality from pulmonary infiltrates in neutropenic patients with acute leukemia during chemotherapy, and the significance of those factors related to the underlying malignancy and its therapy as well as of those related to the severity of the illness associated with pulmonary infiltrates. DESIGN: A historical cohort study. SETTING: A university teaching hospital and tertiary referral center. PATIENTS AND METHODS: Overall, 53 patients with neutropenia during chemotherapy and with first episodes of pulmonary infiltrates during a 4-year period were studied. Prognostic analysis included 38 variables. Multivariate analyses were performed by logistic regression. RESULTS: The survival rate from pneumonia was 57% (30/53). The following eight parameters were significantly associated with death in univariate analysis: comorbidity present; development of "late" pulmonary infiltrates (> or = 14 days after hospital admission); heart rate > or = 100 beats/min; a ratio heart rate/systolic blood pressure (HR/SBP) > or = 1.2; urea nitrogen > 7 mmol/L; radiographic score > or = 3; neutropenia < 1.0x10(9)/L at the treatment end point; and failed complete remission. In a multivariate model including only parameters available at diagnosis of pulmonary infiltrates, the presence of a ratio HR/SBP > or = 1.2 and of a radiographic score > or = 3 remained independently associated with death. In a second model also including the evolutionary parameter neutropenia < or = 1.0x10(9)/L at the treatment end point, both parameters remained significant together with neutropenia <1.0x 10(9)/L at the treatment end point. The presence of a ratio HR/SBP > or = 1.2 was a strong marker of early death. CONCLUSION: Both therapy- and malignancy-associated neutropenia as well as the severity of illness associated with pulmonary infiltrates are independent prognostic factors. Patients with a ratio HR/SBP > or = 1.2 at diagnosis of pulmonary infiltrates suffer from potentially reversible acute illness, are at risk for early death and, therefore, may be appropriate candidates for treatment in an ICU.

Adult↗