Mammographic appearance of ductal carcinoma in situ does not reliably predict histologic subtype

Histologic subtypes of ductal carcinoma in situ (DCIS) have been correlated with disease prognosis. There are conflicting reports on whether the grade of DCIS can be predicted by the morphology of calcifications seen on mammography. We undertook this study to determine whether the grade of DCIS can be reliably and accurately determined by mammography prior to excisional biopsy. Ninety consecutive cases of DCIS from 1993 to 1996 were identified, of which 75 cases had mammograms available for review. Any lesion with invasion was excluded. The mammogram showed only a mass in 10 of 75 cases, a mass and calcifications in 3 of 75 cases, and calcifications alone in 62 of 75 cases. Three board-certified radiologists with special expertise in mammography reviewed and categorized the mammographic findings as well, intermediate or poorly differentiated DCIS without knowledge of the histologic diagnosis. Histologic grading was performed without knowledge of the mammographic finding. Receiver operating curves (ROCs) were computed for each of the radiologists. For microcalcifications, the ROC comparisons of the radiologists' opinions of tumor grade and random chance were not significantly different. In those cases with available magnification views, the grade assessment did not change significantly. If only a mass was present on mammography, well-differentiated DCIS was the predominant histologic subtype. A histologic grade of DCIS cannot accurately be determined prospectively based on the mammographic appearance of microcalcifications. However, if only a mass is present, this is more likely to represent well-differentiated DCIS.     

Gamma-knife radiosurgery for trigeminal neuralgia

Gamma knife was installed at the PD Hinduja National Hospital and Medical Research Centre, Mumbai, India, in January 1997. In the first year of gamma-knife radiosurgery to January 1998, we treated 110 patients, of whom six had medically refractory trigeminal neuralgia. Seven treatments were administered to this group of six patients (one had bilateral neuralgia). This report evaluates the effectiveness of radiosurgery treatment in these patients. The median age of the patients was 56 years and there were five males and one female. Following Leksell stereotactic frame fixation, a magnetic resonance imaging scan was done in all. The Leksell gamma plan was used for planning. A radiosurgery dose of 70–80 Gy was delivered to the trigeminal root entry zone, 2–4 mm anterior to the junction of the pons and trigeminal nerve with a single 4 mm collimator helmet. Complete pain relief was achieved in four patients. Two had partial relief. No patient developed any radiosurgery related morbidity during the follow-up period of 5–16 months. Radiosurgery seems to be an effective approach for medically or surgically refractory trigeminal neuralgia.     

Hypoaldosteronism in three sibs due to 18-dehydrogenase deficiency

Three sibs all presented in the early neonatal period with a salt-losing syndrome. The salt-losing form of congenital adrenal hyperplasia was diagnosed and appropriate treatment with glucocorticosteroids, mineralocorticosteroids, and additional dietary salt started. Although early life was maintained with difficulty, with age all 3 children required decreasing amounts of replacement steroids to maintain normal plasma electrolyte balance. They were reinvestigated at the ages of 15 years and 8 years (twins), when cortisol synthesis and metabolism proved normal, but aldosterone synthesis was blocked by deficiency of 18-dehydrogenase. Rational treatment of these cases of a salt-losing syndrome in which aldosterone synthesis alone is blocked due to lack of the enzyme 18-dehydrogenase requires the administration of a mineralocorticosteroid drug only. Since deoxycorticosterone (acetate or pivalate) requires intramuscular administration, as life-long therapy oral fludrocortisone is preferable. Although fludrocortisone has glucocorticoid activity, the "hydrocortisone equivalent" effect of the small dosage used was unlikely to inhibit either pituitary corticotrophin or growth hormone production.     

Systematic review: Helicobacter pylori and the risk of upper gastrointestinal bleeding risk in patients taking aspirin

Aliment Pharmacol Ther 2010; 32: 831–839

Summary

Background Aspirin is widely used to modify the risk of recurrent vascular events. It is, however, associated with increased upper gastrointestinal bleeding risk. The influence of Helicobacter pylori on this risk is uncertain. Aim To determine the influence of H. pylori on upper gastrointestinal bleeding risk in patients taking aspirin. Methods MEDLINE and EMBASE databases were searched. All studies providing data regarding H. pylori infection in adults taking aspirin and presenting with upper gastrointestinal bleeding were included. Results A total of 13 studies that included 1 case–control, 10 cohort studies and 2 randomized‐controlled trials (RCTs) were analysed. The case–control study (n = 245) determined H. pylori to be a significant independent risk factor for upper gastrointestinal bleeding. The cohort studies were heterogeneous, varying in inclusion criteria, doses and duration of aspirin used, mode of H. pylori testing and causative GI pathology considered. Comprising 5465 patients, H. pylori infection was tested for in 163 (0.03%) aspirin users with upper gastrointestinal bleeding. The RCTs yielded no significant results. Conclusions The current data are not sufficient to allow meta‐analyses. The widely held belief that H. pylori is a risk factor for upper gastrointestinal bleeding in regular aspirin users is not supported by the very limited evidence available.     

Centrilobular emphysema: CT-pathologic correlation

Over a 5-year period, 25 patients who had undergone chest computed tomography (CT) died and were autopsied. Their lungs were fixed in the inflated state and were assessed for the presence and severity of centrilobular emphysema (CLE). Three radiologists independently evaluated the CT scans for nonperipheral low-attenuation areas, peripheral low-attenuation areas, pulmonary vascular pruning, pulmonary vascular distortion, and pulmonary density gradient. The CT criterion that best correlated with the presence and severity of CLE was the nonperipheral low-attenuation area. With this CT criterion, lung destruction was correctly identified in 13 of 15 cases. The absence of this criterion resulted in correct identification of eight of ten normal lungs. These preliminary data suggest that CLE can be reliably identified and quantified with current CT scanners.     

The effect of storage on the ganglioside content of human platelets

Gangliosides are glycolipids which contain sialic acid and are found in the membranes of mammalian cells. By analogy with recent studies of other cells, it is possible that gangliosides play a role in the membrane functions and in vivo survival of platelets. In order to determine if ganglioside destruction plays a role in the storage-induced loss of platelet viability and function (storage lesion), the ganglioside content of platelets was measured after 24 and 96 hours of storage. Samples were taken from platelet concentrates that were stored either on a flat-bed shaker (n = 6) or on a circular rotator (n = 6). Total ganglioside content was determined colorimetrically from the total lipid extracts of purified platelet pellets using the Svennerholm resorcinol method. Ganglioside GM3 content was determined by Folch partitioning, high performance thin-layer chromatography, and densitometric scanning. Ganglioside content, measured as microgram of lipid-bound sialic acid per 10(10) platelets, was significantly decreased (p less than 0.005) between 24 and 96 hours of storage, whether measured as total or GM3 ganglioside. The mean values +/- SEM at 24 and 96 hours of storage were 9.4 +/- 0.6 and 6.7 +/- 0.6, respectively (n = 12 for each). These data indicate that storage causes irreversible loss of membrane ganglioside, which may be detrimental to the function and in vivo survival of platelets.