Pseudohyperphosphatemia and dysproteinemia.

We report the case of a patient with IgG multiple myeloma and pseudohyperphosphatemia, and the case of another patient in whom unexplained hyperphosphatemia led to the diagnosis of monoclonal gammopathy. The pseudohyperphosphatemia was due to the interference of monoclonal immunoglobulins with the phosphomolybdate colorimetric assay for phosphorus determination widely in use with some automated systems. Ultrafiltration of these patients' serum samples resulted in normalization of the elevated phosphorus values. Knowledge of this phenomenon may obviate confusion, unnecessary testing, and expenditure. It may also provide clinicians with a clue as to the presence of a dysproteinemia.

Diagnostic variability in suspected pulmonary embolism.

Over a 12-month period, we observed adult patients with suspected pulmonary embolism referred for lung scanning to determine variability in the diagnostic process. Among 269 studies, 157 lung scans were judged necessary by predetermined criteria. Ninety-three of these 157 patients had inconclusive results (low probability, intermediate probability, or indeterminate). Of these 93 patients, 42 had pulmonary angiograms, ten of which were positive. Of the 51 patients with necessary but inconclusive scans, five were poor candidates for angiography, 15 had other indications for anticoagulation, seven refused the study, and 24 had physicians who considered further studies unwarranted. Patients with and without pulmonary angiography were demographically and clinically similar. Although confirmatory testing such as pulmonary angiography was used frequently (45%) after an inconclusive lung scan, the question of pulmonary embolism was often left unanswered (55%). Methods for linking clinical judgment to lung scan results are necessary to select proper patients for invasive confirmatory testing.

Complement activation in septic shock patients.

To evaluate the status of the complement system and to determine the effects of corticosteroids on complement component levels in septic shock, C3, C4, and Factor B were measured in 42 patients with severe late septic shock. Serum levels of C4 and Factor B correlated with C3 levels (r = 0.48 and 0.64, respectively; p less than .01) in patients in shock for more than 4 h, but only Factor B correlated with C3 (r = 0.85; p less than .01) in patients in shock for 4 h or less. C3 and Factor B levels were significantly (p less than .05) lower in patients who died (12,174 +/- 1,524 CH50 U/ml and 14 +/- 1 mg/dl, respectively) than in patients who survived (18,418 +/- 2,833 CH50 U/ml and 21 +/- 2 mg/dl, respectively). Corticosteroids did not alter complement component levels. The alternative pathway appears to be activated early in septic shock, whereas the classical pathway is activated later. C3 and Factor B levels may predict survival of patients in septic shock. In this study, corticosteroids did not change the complement component levels of patients in late severe septic shock.

The effects of high-dose corticosteroids in patients with septic shock. A prospective, controlled study.

To determine whether corticosteroids are efficacious in severe septic shock, we conducted a prospective study of 59 patients randomly assigned to a methylprednisolone, dexamethasone, or control group. Patients were treated 17.5 +/- 5.4 hours (mean +/- S.E.M.) after the onset of shock, and 55 patients required vasopressor agents. Early in the hospital course, reversal of shock was more likely in patients who received corticosteroids than in those who did not. Four (19 per cent) of 21 methylprednisolone-treated, 7 (32 per cent) of 22 dexamethasone-treated, and none of 16 control patients had reversal of shock 24 hours after drug administration (corticosteroid groups vs. control group, P less than 0.05). Patients treated with corticosteroids within four hours after the onset of shock had a higher incidence of shock reversal (P less than 0.05). At 133 hours after drug administration, 17 (40 per cent) of 43 corticosteroid-treated patients had died, and 11 (69 per cent) of 16 control patients had died (P less than 0.05). However, these differences in reversal of shock and survival disappeared later in the course. Overall, 16 (76 per cent) of 21 patients receiving methylprednisolone, 17 (77 per cent) of 22 patients receiving dexamethasone, and 11 (69 per cent) of 16 controls in the hospital died. We conclude that corticosteroids do not improve the overall survival of patients with severe, late septic shock but may be helpful early in the course and in certain subgroups of patients.