Staging of lymph nodes with FDG dual-headed PET in patients with non-small-cell lung cancer

Accurate assessment of mediastinal lymph node involvement in patients with non-small-cell lung cancer (NSCLC) is necessary to select patients for direct surgical treatment. The aims of the present study were to assess the feasibility of staging NSCLC with FDG using a dual-headed positron emission tomographic (PET) camera and to compare this non-invasive technique with computed tomography (CT) and lymph node sampling, since both modalities are currently used for staging NSCLC. Thirty-three patients (29 men and 4 women, mean age 60 years) with newly diagnosed NSCLC were studied. In all patients, CT, FDG dual-headed PET and mediastinoscopy were performed within 4 weeks. The results of mediastinoscopy were used to select patients for thoracotomy. For both the assessment of individual lymph node involvement and the patient-based classification, the results of FDG dual-headed PET and CT were compared using the McNemar test. Thirty-one of 187 lymph nodes studied contained tumour metastases. FDG dual-headed PET showed a significantly higher sensitivity (P < 0.001) and specificity (P < 0.001) than CT. FDG dual-headed PET and CT correctly staged 27 and 20 patients, respectively. Due to the significantly higher negative predictive value of FDG dual-headed PET versus CT (P = 0.012), it was a better non-invasive diagnostic tool for selecting patients for surgery. In seven of eight patients, additional intrapulmonary sites of increased uptake were found, which revealed malignancy on histological examination. CT was false-negative in three of these patients. In one patients, increased FDG uptake was caused by an infection. In conclusion, it is possible to stage mediastinal lymph nodes in patients with NSCLC using a dual-headed PET camera. The high negative predictive value of FDG dual-headed PET suggests that mediastinoscopy may be omitted in patients with NSCLC.     

Diphenylhydantoin-induced pure red cell aplasia

The pathogenesis of diphenylhydantoin-induced pure red cell aplasia was investigated in the case of a 32-year-old man who developed pure red cell aplasia while he was under treatment with diphenylhydantoin. The patient's serum IgG purified from serum drawn at the time of diagnosis suppressed normal allogeneic marrow colony-forming (CFU-E) and burst- forming (BFU-E) and autologous blood BFU-E growth in vitro only in the presence of diphenylhydantoin. This IgG-diphenylhydantoin complex had no effect on CFU-GM growth in vitro. Normal IgG or patient's IgG purified from serum drawn after the remission of red cell aplasia had no effect on erythroid colony formation in vitro in the presence of diphenylhydantoin. The IgG-diphenylhydantoin complex exerted no direct cytotoxic effect on normal marrow erythroblasts, CFU-E, and BFU-E, nor did it interfere with the action of erythropoietin on marrow erythroblasts. These studies suggest that diphenylhydantoin-induced red cell aplasia is immunologically mediated through an IgG inhibitor, which requires the presence of the drug to suppress erythroid colony formation in vitro. This inhibitor seems to exert its effect on erythroid progenitors at or beyond the stage of differentiation of CFU- E, but not on erythroblasts.     

Heterogeneity of B cell involvement in acute nonlymphocytic leukemia

In order to study the pattern of B cell involvement in acute nonlymphocytic leukemia (ANLL), multiple B lymphoid cell lines were established by Epstein-Barr virus transformation of peripheral blood mononuclear cells from two patients with the disease who were heterozygous for the X chromosome-linked glucose-6-phosphate dehydrogenase (G6PD). In one patient, the progenitor cells involved by the leukemia exhibited multipotent differentiative expression, whereas in the other patient the cells showed differentiative expression restricted to the granulocytic pathway. In the patient whose abnormal clone showed multipotent expression, the ratio of B-A G6PD in B lymphoid cell lines was skewed in the direction of type B (the enzyme characteristic of the leukemia clone) and significantly different from the 1:1 ratio expected. It is, therefore, likely that the neoplastic event occurred in a stem cell common to the lymphoid series as well as to the myeloid series. In contrast, evidence for B cell involvement was not detected in the patient whose ANLL progenitor cells exhibited restricted differentiative expression. These findings underscore the heterogeneity of ANLL. Clinically and morphologically similar malignancies in these two patients originated in progenitors with different patterns of stem cell differentiative expression. This difference may reflect differences in cause and pathogenesis.     

CGA-7 and HHF, two monoclonal antibodies that recognize muscle actin and react with adherent cells in human long-term bone marrow cultures

The CGA-7, a monoclonal antibody that reacts with smooth muscle cell actin but not with endothelial cell or fibroblast actin, and HHF, a monoclonal antibody that reacts with smooth muscle, skeletal muscle, and cardiac muscle actin, both recognize microfilaments present within adherent cells from actively hematopoietic human long-term marrow cultures. Macrophages, monocytes, and cultured marrow fibroblasts do not react with either antibody. These data suggest that the anti-actin antibodies may serve as useful markers for in vitro microenvironmental cells and lend support to the hypothesis that stromal cells from long- term marrow cultures are different from marrow fibroblasts and may constitute a unique cell lineage.     

Need for closure of secundum atrial septal defect in infancy

OBJECTIVES: Closure of isolated secundum atrial septal defect is generally recommended at the age of 4 to 5 years. However, there are children with isolated secundum atrial septal defect in whom early closure should be performed. We aimed to assess the underlying conditions that led to earlier closure in this special patient group and to analyze the outcome. METHODS AND RESULTS: From January 1990 through August 2002, 24 infants with isolated secundum atrial septal defect underwent surgical closure within the first year of life. All children were symptomatic. Signs of pulmonary hyperperfusion, such as tachydyspnea, failure to thrive, recurrent respiratory infections, or heart failure, were present. Four infants required artificial ventilation. Ten patients had additional problems, such as prematurity with chronic lung disease, hepato-omphalocele and congenital diaphragmatic hernia, which were present in 1 patient each. Eleven patients had defined dysmorphic syndromes. All but 1 infant underwent preoperative invasive hemodynamic evaluation. Thirteen patients had pulmonary hypertension preoperatively. The follow-up time was 46 +/- 33 months (range, 4-125 months). At follow-up, pulmonary artery pressure proved to be normal in 11 of the 13 children who had pulmonary hypertension previously. One patient died of persistent pulmonary hypertension. Clinical performance, growth, and development improved in nearly all patients. All ventilator-dependent children could be weaned shortly after atrial septal defect closure. CONCLUSIONS: If lungs are compromised, even a minor left-to-right shunt might be poorly tolerated in infancy. In these children early surgical closure of an isolated secundum atrial septal defect should be performed to support thrive and growth and to prevent the onset of irreversible changes of the pulmonary vasculature.     

Solitary rectal ulcer syndrome: findings at barium enema study and defecography

Sixteen cases of histopathologically proved solitary rectal ulcer syndrome were encountered. Fifteen patients underwent barium enema study; in nine cases the findings--including rectal stricture, granularity of the mucosa, and thickened rectal folds-were nonspecific. In six cases the study was normal. All patients had a long history of defecation disorders, and defecography was performed in all. In seven cases, intussusception of the rectal wall was seen; in another case the intussusception was accompanied by a rectocele. One case showed rectal prolapse. In four cases, failed relaxation of the puborectalis occurred and prevented the passage of the bolus; in another case there was abnormal perineal descent. In two patients studies were normal. In patients with defecation disorders, the possibility of this syndrome should be considered. Defecography is the method of choice for establishing the diagnosis.     

Inhibition of endotoxin-induced activation of the coagulation and fibrinolytic pathways using a recombinant endotoxin-binding protein (rBPI23)

A recombinant endotoxin-neutralizing protein, rBPI23, was shown to partially prevent endotoxin-induced activation of the fibrinolytic and coagulation systems in experimental endotoxemia in humans. In a placebo- controlled, blinded crossover study, eight volunteers were challenged twice with an intravenous bolus injection of endotoxin (40 EU/kg of body weight) and concurrently received either rBPI23 (1 mg/kg) or placebo (human serum albumin, 0.2 mg/kg). rBPI23 treatment significantly lowered the endotoxin-induced fibrinolytic response, ie, reduced the release of tissue-type plasminogen activator, urokinase- type plasminogen activator, plasminogen activator inhibitor antigen, and complex formation of plasmin alpha 2-antiplasmin (P = .0078 for each). Plasminogen activator inhibitor activity was also reduced, but not significantly according to the Hochberg method (P = .0304). The endotoxin-induced activation of the procoagulant state as reflected by increase in F1 + 2 fragments and TAT complexes was blunted by rBPI23 infusion (P = .0391 [not significant according to the Hochberg method] and .0078, respectively). These results indicate that rBPI23 is capable of reducing both the activation of the fibrinolytic and the coagulation systems after low-dose endotoxin infusion in humans.