Massive hyperphosphatemia in a patient with neuronal intestinal dysplasia after bowel preparation with oral sodium phosphate.

Oral sodium phosphate-based laxatives are frequently used for bowel preparation or relief of constipation in some countries. However, these agents are not without risk. Small and clinical insignificant increments on serum phosphorus levels are observed in almost all individuals after use of oral sodium phosphate. Some patients are prone to severe hyperphosphatemia such as elders, those with chronic or acute renal disease and those with poor bowel motility. Severe hyperphosphatemia accompanied with hypocalcemia may be life-threatening in these patients. We present an 18-year-old woman with neuronal intestinal dysplasia who developed symptomatic and severe hyperphosphatemia after bowel preparation with oral sodium phosphate enema. Urgent hemodialysis was performed two times for severe hyperphosphatemia.

Preoperative serum leptin levels in patients with breast cancer.

Leptin is an adipocyte-derived protein and plays an important role in the control of body weight by acting as a neurohormone regulating energy balance and food intake in the hypothalamus. The high serum leptin levels and the overexpression of leptin receptors have been documented in breast cancer patients, but the levels never checked preoperatively. In the present study, the relationship between preoperative serum leptin levels of the breast cancer patients and the healthy controls were evaluated. The serum leptin levels in 30 breast cancer patients were compared to 30 healthy female volunteers. In addition, the association of serum leptin levels and the various well-known risk factors were studied. Serum leptin levels of patients with breast cancer (28.55 + 19.7 ng/ml) were tended to be higher than those of controls (26.43 + 19.4 ng/ml), but it did not reach statistical difference (P = 0.712). There was significant correlation between the expression of ER, PR, and serum leptin levels (P = 0.018 and 0.037, respectively), but not with the HER-2/neu receptor expression (P = 0.067). Also association was not found between the tumor size, lymph node involvement, and the levels of serum leptin (P = 0.235, 0.34, and 0.86, respectively). The serum leptin level was also found to be similar in premenopausal (24.85 +/- 18.14 ng/ml) and postmenopausal (30.49 +/- 17.19 ng/ml) patients (P = 0.235). The preoperative serum leptin levels in breast cancer patients were similar to healthy controls. In subset analysis, the significant correlation between the leptin level and hormonal status was noted, but association with HER-2/neu was not detected. These findings should be confirmed with larger studies.

5-Fluorouracil induces arterial vasoconstrictions but does not increase angiotensin II levels.

Because the mechanisms of 5-Fluorouracil (5-FU) cardiotoxicity have not yet been completely identified, prophylactic options are not available. To our knowledge, there are no published data investigating the use of angiotensin converting enzyme (ACE) inhibitors for 5-Fluorouracil-associated cardiotoxicity. In this study, we aimed to evaluate the influence of 5-FU administration on the diameter of the brachial artery and the levels of angiotensin II. The patients were administered bolus 5-FU/leucovorin in the study group. Angiotensin II and troponin T assays, complete blood cell counts, hepatic and renal function tests were analyzed in five consecutive blood samples in the initiation, just after termination, and on 24, 48, and 72 h after termination of the regimen. Pre- and post-treatment angiotensin II and troponin T assays, complete blood cell counts, hepatic and renal function tests were also analyzed in the control group. Brachial arterial diameters were measured and recorded in all patients before and after the treatment. A total of 59 patients were included in this study. Thirty one out of 59 patients (52.5%) were in the 5-FU study group and the remaining 28 patients (47.5%) were in the control group. Basal and post-treatment brachial artery diameters in the 5-FU study group were 0.436 +/- 0.51 and 0.423 +/- 0.50 cm, respectively (P = 0.001). The corresponding values in the controls were 0.3954 +/- 0.50 and 0.3957 +/- 0.49 cm, basal and post-treatment, respectively (P = 0.979). Angiotensin II levels were not changed significantly at serial measurements (P = 0.496). Moreover, the corresponding measurements were not statistically different in both two groups treated with and without 5-FU (P = 0.372). The pathophysiology of 5-FU-induced cardiac toxicity has not yet been elucidated. In the present study, 5-FU-associated vasoconstriction was not dependent on angiotensin II levels, thus we suggest that the prophylactic administration of ACE inhibitors cannot prevent cardiotoxicity in these patients. The underlying mechanisms of cardiotoxicity related to 5-FU might be multifactorial; nevertheless, further prospective investigation for the toxic effects of fluoropyrimidines on the coronary endothelium and myocardium are needed.