Familial risk for gastric carcinoma: an updated study from Sweden

Reliable data on familial risks are important for clinical counselling and cancer genetics. However, the estimates of familial risk of gastric cancer vary widely. We examined the risk of familial gastric cancer using the updated Swedish Family-Cancer Database with 5358 patients among offspring and 36 486 patients among parents. There were 133 families with one parent and one offspring diagnosed with gastric cancer, and 20 families with two affected offspring. Familial standardised incidence ratios (SIRs) were 1.63 and 2.93 when parents and siblings presented with gastric cancer, respectively. The high sibling risk was owing to cancer in the corpus (SIR 7.28). The SIR for cardia cancer was 1.54 when parents were diagnosed with any gastric cancer. Cardia cancer associated with oesophageal cancer, particularly with oesophageal adenocarcinoma. Among specific histologies, signet ring cancer showed an increase. A few associations were noted for discordant sites, including the urinary bladder and the endometrium. H. pylori infection, although not measured in the present study, is probably an important risk factor for the high sibling risk of corpus cancer. Familial clustering of cardia cancer is independent of H. pylori infection, and may have a genetic basis. The familial association of cardia cancer with oesophageal adenocarcinoma may provide aetiological clues

Emergency department spirometric volume and base deficit delineate risk for torso injury in stable patients

BACKGROUND: We sought to determine torso injury rates and sensitivities associated with fluid-positive abdominal ultrasound, metabolic acidosis (increased base deficit and lactate), and impaired pulmonary physiology (decreased spirometric volume and PaO(2)/FiO(2)). METHODS: Level I trauma center prospective pilot and post-pilot study (2000–2001) of stable patients. Increased base deficit was < 0.0 in ethanol-negative and ≤ -3.0 in ethanol-positive patients. Increased lactate was > 2.5 mmol/L in ethanol-negative and ≥ 3.0 mmol/L in ethanol-positive patients. Decreased PaO(2)/FiO(2 )was < 350 and decreased spirometric volume was < 1.8 L. RESULTS: Of 215 patients, 66 (30.7%) had a torso injury (abdominal/pelvic injury n = 35 and/or thoracic injury n = 43). Glasgow Coma Scale score was 14.8 ± 0.5 (13–15). Torso injury rates and sensitivities were: abdominal ultrasound negative and normal base deficit, lactate, PaO(2)/FiO(2), and spirometric volume – 0.0% & 0.0%; normal base deficit and normal spirometric volume – 4.2% & 4.5%; chest/abdominal soft tissue injury – 37.8% & 47.0%; increased lactate – 39.7% & 47.0%; increased base deficit – 41.3% & 75.8%; increased base deficit and/or decreased spirometric volume – 43.8% & 95.5%; decreased PaO(2)/FiO(2 )– 48.9% & 33.3%; positive abdominal ultrasound – 62.5% & 7.6%; decreased spirometric volume – 73.4% & 71.2%; increased base deficit and decreased spirometric volume – 82.9% & 51.5%. CONCLUSIONS: Trauma patients with normal base deficit and spirometric volume are unlikely to have a torso injury. Patients with increased base deficit or lactate, decreased spirometric volume, decreased PaO(2)/FiO(2), or positive FAST have substantial risk for torso injury. Increased base deficit and/or decreased spirometric volume are highly sensitive for torso injury. Base deficit and spirometric volume values are readily available and increase or decrease the suspicion for torso injury