Helical CT scanning: the primary imaging modality for acute flank pain.

We set out to evaluate the accuracy of nonenhanced helical computed tomography (CT) scanning at stone detection in the patient with acute flank pain, and as a means of detecting noncalculus causes of acute flank pain. Between April 1995 and April 1997, 412 consecutive patients with acute flank pain underwent noncontrast-enhanced helical CT. Two hundred eighty-one patients had confirmation of their CT diagnosis by other radiographic studies, urologic intervention, or spontaneous stone passage of calculi. We determined the presence or absence of urinary calculi, as well as the presence of other noncalculus pathology. CT scanning revealed a stone in 92/281 patients (32.7%) and no stone in 189/281 patients (67.3%). Of the 189 patients, 60/189 patients (32%) had another positive finding as a cause for flank pain. Eighty-one of 92 patients with a stone on CT (88%) had confirmation of stone disease by radiologic or surgical intervention. Eleven of 92 patients (12%) did not have confirmation of their diagnosis because of resolution of symptoms or refusal of further intervention. On helical CT scans 129/189 patients demonstrated no abnormalities. Two of 189 (1.5%) thought to be stone free by CT passed a stone. Helical CT had a sensitivity of 97%, a specificity of 92%, a positive predictive value of 88%, and a negative predictive value of 98% at stone detection. Noncontrast-enhanced helical CT is accurate and rapid in detecting calculus disease in patients with acute flank pain. Perhaps more importantly, it provides the added benefit of detecting noncalculus causes of flank pain in greater than 30% of patients.

B cell maturation and selection at the marrow-periphery interface.

More than 95% of newly formed B cells die in the short interval spanning sIgM acquisition in the bone marrow and entry into the long-lived pool, suggesting that selective events dictating B cell longevity occur at this stage. These likely include both ligand-induced deletion as well as discrete events that mediate recruitment to the long-lived recirculating pool. We are probing these events through the examination of normal B cell differentiation during this critical period: the characterization of a natural mutation that blocks late maturation, an irradiation/autoreconstitution model of marrow-derived B cell differentiation, and the identification of life span regulatory genes whose expression changes within this window.