Search

Glomerular filtration rate (GFR) is an important factor when considering carboplatin dosage adjustment. The Japanese equation for estimating GFR (eGFR) was recommended as a guideline for evaluating GFR in 2009 by The Japanese Society of Nephrology. However, benefits in the field of cancer chemotherapy with the use of eGFR have not yet been shown. To clarify the clinical benefits of eGFR, we investigated the renal function of 100 patients with gynecologic cancer who were treated with carboplatin from 2003 through 2009, and the carboplatin dosage was calculated by the Calvert formula in which eGFR was substituted for GFR. To predict the clinical benefit on the basis of carboplatin dosage using eGFR, we retrospectively divided the patients into two groups so that carboplatin dosage was within dosage in using eGFR and one was not. We compared response rates and adverse effects of the two groups. Renal function using eGFR was lower than renal function calculated by using the other formulae. Carboplatin dosage using eGFR was significantly lower than the dosage calculated with the other formulae (p<0.01). Moreover, the patients group actually, administered the dosage calculated by eGFR showed less side effects than the group of patients not treated this way, but the efficacy did not change. Thus, using eGFR in planning carboplatin dosage suggested clinical application to patients with Japanese gynecologic cancer.

We report the case of an 86-year-old female with licorice-induced hypokalemic myopathy. For four years, she had been taking two kinds of Chinese medicines containing licorice. The patient presented with difficulty in holding her head up and proximal-dominant tetraparesis with significant laterality. In manual muscle tests, the right extremities showed grade 2/5 and the left extremities, grade 4/5. The general reflexes were decreased, and the bilateral Chaddock's reflexes were repeatedly positive. The sensory, cerebellar and autonomic systems were normal and discrete movements of all extremities were well preserved. Laboratory tests showed elevated levels of CK (559 IU/1), hypokalemia (1.6 mEq/1), and metabolic alkalosis (pH 7.51, base excess 10.9 mmol/1). Magnetic resonance imaging showed mild compression of the spinal cord due to cervical spondylosis. Electromyography revealed myopathic patterns in the deltoid muscle. Steady clinical recovery was noted following treatment including cessation of licorice intake and administration of potassium supplementation. Neck weakness, tetraparesis with laterality and Chaddock's reflexes were diminished. We conclude that the pathologic reflex was caused by the aggravation of cervical spondylotic myelopathy due to neck weakness and that tetraparesis with laterality was caused by hypokalemic myopathy.

In post-menopausal osteoporosis, lack of estrogen will affect the remodeling of the bone tissue in such a way that, in most patients with periodontitis, the amount of bone resorbed exceeds that being formed, resulting in net bone loss. Osteoporosis can be treated by a variety of methods, the hormone replacement therapy (HRT), the selective estrogen receptor modulators (SERM) and the bisphosphonates. The HRT or bisphosphonates treatments improve the clinical outcome of periodontal disease and may be an adjunctive treatment to preserve periodontal bone mass. This paper reviews the current evidence on the mechanism of periodontal breakdown after menopause and the benefit to oral health by treatments for osteoporosis.

Many studies have attempted to define the relationship between postmenopausal osteoporosis and periodontal disease. Most studies support a positive association between these common diseases; however, many are cross-sectional in nature, include relatively small sample sizes, and have inadequate control of potential confounding factors, such as age, gender, hormone intake, race, and smoking, limiting our understanding of the nature of the relationship between these diseases. Clinical conditions causing low estrogen environments in postmenopausal women allow T- and B-cell abnormalities, increased local production of the bone-active cytokines (i.e., Interleukin-1, -6 and -8, tumor necrosis factor [TNF]-alpha) and a rise in prostaglandin E(2), resulting in the progression of periodontitis.