[Early diagnosis of lung cancer: impact of autofluorescence bronchoscopy]. / Diagnostic précoce du cancer bronchique : apport de la bronchoscopie en autofluorescence.

INTRODUCTION: Less than 15% of all patients survive five years after a diagnosis of lung cancer. This poor prognosis is attributed to a lack of early detection. Among the methods of early diagnosis of bronchial cancer, autofluorescence bronchoscopy allows for the early identification of preinvasive bronchial lesions. The goal of this prospective study is to evaluate the contribution of the autofluorescence bronchoscopy, on a hospital site, over a period of one year. METHODS: All patients with an indication of autofluorescence bronchoscopy were included in the study. The following parameters were collected: age, sex, smoking status, FEV1, FVC, biopsy sites, histology, duration of examination. RESULTS: Two hundred and seventy-four patients were included. The average age was 63.8 years (+/-12), the smoking status was 35 packs/year (+/-19). A fluorescence abnormality was detected in 131 patients and 165 sites were biopsied. An histological abnormality was found in 76% of the samples, with 34 hyperplasia (28%), 56 squamous metaplasia (46%), three mild dysplasia (3%), two moderate dysplasia (2%), one severe dysplasia (1%), two carcinomas in situ (2%) and 21 invasive carcinomas (18%). CONCLUSION: Autofluorescence bronchoscopy is an effective examination for the detection of the preinvasive neoplasic lesions and may be proposed when lung cancer is suspected.

Response of glutamine metabolism to exogenous glutamine in humans.

To determine whether exogenous glutamine affects whole body glutamine metabolism, preliminary experiments were performed to verify that L-[1-13C]-, L-[U-14C]-, and L-[3,4-3H]glutamine given simultaneously by vein provided similar estimates of glutamine appearance rates [Ra; 355 +/- 24, 373 +/- 19, and 393 +/- 24 (SE) mumol.kg-1.h-1, respectively, P = NS] in six healthy men; glutamine oxidation accounted for 32 +/- 3 and 51 +/- 5% (P < 0.01) of glutamine Ra when it was measured using L-[U-14C]- and L-[1-13C]glutamine, respectively. Five subjects received two 5-h intravenous infusions of L-[3,4-3H]glutamine and a simultaneous nasogastric infusion of L-[1-13C]glutamine on 2 separate days in the postabsorptive state, along with saline on 1 day and natural L-glutamine (856 +/- 45 mumol.kg-1.h-1) on another day in a randomized order. Splanchnic glutamine extraction (determined from [13C]glutamine appearance into systemic blood) reached 74 +/- 4 and 53 +/- 5% during the enteral infusion of tracer alone and in combination with a large load of glutamine, respectively. Glutamine infusion was associated with increased plasma glutamine concentration (from 630 +/- 50 to 1,297 +/- 75 microM), Ra (from 258 +/- 20 to 589 +/- 45 mumol.kg-1.h-1), and oxidation (from 179 +/- 20 to 477 +/- 47 mumol.kg-1.h-1, all P < 0.01), no change in glutamine release from proteolysis, and a decline in glutamine de novo synthesis (from 156 +/- 15 to 93 +/- 13 mumol.kg-1.h-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Determination of glutamine and alpha-ketoglutarate concentration and specific activity in plasma using high-performance liquid chromatography.

A method is described for measuring glutamine (GLN) and alpha-ketoglutarate (KG) concentration and specific activity (SA) using high-performance liquid chromatography (HPLC). Plasma GLN and KG are separated on miniature ion-exchange columns. KG is derivatized with O-phenylene diamine, the derivative is extracted in ethyl acetate, dried, and dissolved in pH 7 phosphate buffer. The isolated GLN is enzymatically converted to KG and analysed as such. Derivatized samples are stable for weeks at -20 degrees C. Samples are injected onto a reversed-phase HPLC column. Absolute standards are injected to determine the nmol content of unknown samples. alpha-Ketoadipate and [3H]-glutamine are used as internal standards to quantitate KG and GLN concentrations, respectively. Collection of the entire peak of interest permits determination of the radioactivity in the GLN and KG peaks; this together with the determination of the nanomoles injected permits the calculation of the SA. Typical precision is 3.5 and 4.6% for GLN and KG concentrations and 5.3 and 3.3% for GLN and KG SA, respectively. Analysis time is ca. 7 min. Using this method, the turnover rate of GLN carbon was determined during a 5-h infusion of L-[U-14C]glutamine in a human subject.

Omeprazole in H2 receptor antagonist-resistant reflux esophagitis.

We conducted a retrospective review of 25 patients with severe reflux esophagitis treated with omeprazole because of failure of H2 receptor antagonists to heal their esophagitis. Prior to beginning omeprazole (40 mg/day), all patients were on H2 antagonists for at least 9 months and still had endoscopic evidence of longitudinal (grade II) or circumferential (grade III) distal esophageal ulceration. Omeprazole therapy brought about complete endoscopic healing in 24 of 25 patients (96%). Twenty-three of 24 healed patients were then restarted on H2 antagonists as maintenance therapy. Repeat endoscopy was performed if symptoms recurred. Fourteen of 24 patients (58%) had recurrence of endoscopic esophagitis documented between 26 and 300 days from the time of starting maintenance therapy. Two of these 14 patients opted for antireflux surgery, whereas the remaining 12 were once again given omeprazole, which again resulted in symptom resolution in all patients. These data suggest that most patients with H2 receptor antagonist-resistant ulcerative esophagitis cannot be successfully maintained on H2 antagonists even after the ulcers have been healed with omeprazole. Further studies are required to determine the role of omeprazole compared to other treatments in the long-term maintenance therapy of these patients.