Antimicrobial activity of ofloxacin and other agents against mycobacterial isolates from postoperative sternotomy wounds.

In 1987 and 1988, 16 patients in a cardiothoracic hospital developed median sternotomy wound infections from Mycobacterium fortuitum or Mycobacterium chelonei (M fortuitum, 14 patients; M chelonei, two patients). For M fortuitum isolates, the minimum inhibitory concentration (MIC) (by agar dilution) of ofloxacin was 0.32 to 1.25 mg/L; of amikacin, 0.5 to 1 mg/L; of sulfadiazine, 16 to 256 mg/L; of imipenem, less than or equal to 2 to 4 mg/L; of cefoxitin, 4 to 16 mg/L; of ampicillin, 64 to greater than 256 mg/L; of cephapirin, 64 to 128 mg/L; of cefoperazone, greater than 256 mg/L; and of ceftazidime, greater than 256 mg/L. Addition of sulbactam to ampicillin and cefoperazone resulted in at least a four- to eight-fold reduction of their respective MICs. For M chelonei isolates, the MIC of ofloxacin was greater than 20 mg/L; of amikacin, 8 mg/L; of sulfadiazine, 64 mg/L; of imipenem, 8 mg/L; of cefoxitin, 16 mg/L; of ampicillin, 128 mg/L; of cephapirin, 128 mg/L; of cefoperazone, greater than 256 mg/L; and of ceftazidime, greater than 256 mg/L. Addition of sulbactam resulted in much smaller reductions of the MICs of ampicillin and cefoperazone. Synergism was noticed between ofloxacin and amikacin against M chelonei but not against M fortuitum. The results indicate that ofloxacin alone is as effective as the combination of ofloxacin and amikacin in treating M fortuitum, but not M chelonei, infection.

Urinary hydroxyproline excretion in myelofibrosis.

Urinary hydroxyproline measurements were performed in a group of health volunteers as well as patients with cancer and myelofibrosis. Patients in whom there was no metastatic involvement of bone marrow excreted an amount of hydroxyproline not different from that of the control group. Those who had marrow metastasis produced elevated levels of hydroxyproline; the highest excretions were observed when marrow fibrosis was associated with metastasis. These results contrasted with those observed in agnogenic myeloid metaplasia patients whose excretions were equivalent to the control group. The result suggests differences in the pathogenesis of myelofibrosis and a technique potentially useful for distinguishing between patients who may otherwise be diagnostic problems.

Primary hyperparathyroidism and chronic lymphocytic leukemia.

Although hypercalcemia is a frequent event during the course of many malignancies it has only rarely been described with patients with chronic lymphocytic leukemia. Review of the literature revealed only eleven such case reports. The mechanism of the hypercalcemia in these patients was generally unclear although one patient was found to have a parathyroid adenoma and in another patient tested the level of osteoclast activating factor was high. Two additional chronic lymphocytic leukemia patients with hypercalcemia are described in this report and in each a parathyroid adenoma was found. The patient in whom the diagnosis was made ante mortem had an excellent response to parathyroidectomy. Osteoclast activating factor level was measured in one patient and found to be within normal limits. Since three of the thirteen reported cases of chronic lymphocytic leukemia with hypercalcemia have demonstrated parathyroid adenomas, it is suggested that consideration be given to that possibility in such patients so that appropriate surgery may be done.