[A case of lacrimal duct obstruction caused by capecitabine].

In recent years, the incidence of adverse ocular reactions, including corneal problems and lacrimal duct obstruction, due to antineoplastic agents such as S-1 has increased. Very few reports of adverse ocular reactions caused by capecitabine, a fluorinated pyrimidine antineoplastic agent like S-1, exist, and consequently, the mechanism underlying these reactions is not well understood. This report describes our recent experience with a case of lacrimal duct obstruction caused by capecitabine. The patient was a 71-year-old woman who was being administered trastuzumab plus capecitabine combination chemotherapy for breast cancer-related bone metastasis. She complained of epiphora 7 days after capecitabine was initiated. Thereafter, her capecitabine dose was reduced owing to exacerbation of hand-foot syndrome, but the epiphora persisted. Capecitabine was discontinued 287 days after initiation owing to exacerbation of the hand-foot syndrome. However, because the epiphora persisted, the patient visited the ophthalmology department. The ophthalmologist diagnosed the patient with binocular nasolacrimal duct obstruction and cataract, and prescribed a 0.3% gatifloxacin ophthalmic solution and 0.1% fluorometholone ophthalmic suspension. Thereafter, the epiphora reduced. When the patient returned to the ophthalmology department, symptom improvement was confirmed. In this case, lacrimal duct obstruction likely developed due to capecitabine. The symptoms were reversible with discontinuation of capecitabine and ophthalmic treatment. We believe that reporting this case could be valuable in discussing capecitabine-induced lacrimal duct obstruction.

[Survey of the current status of capecitabine-induced hypertriglyceridemia].

We encountered cases of capecitabine-induced increase in blood triglyceride (TG) levels, which is relatively rare in routine medical practice. Although capecitabine-induced hypertriglyceridemia (CI-HTG) has been occasionally reported in other countries, such cases have not been reported in Japan. Therefore, the details of this condition remain to be clarified. To obtain evidence that would be useful in routine medical practice, we conducted a retrospective study of patients with CI-HTG. The study included 56 patients, of whom, 14 (25.0%) had TG levels < 150 mg/dL before capecitabine treatment that increased to ≥ 150 mg/dL after treatment. Adverse events were graded according to the Common Terminology Criteria for Adverse Events, v4.0, Japanese edition, Japan Clinical Oncology Group version (CTCAE v4.0-JCOG). We found that TG levels were markedly elevated (≥ Grade 3) in 2 patients (3.6%). Thus, CI-HTG also affects Japanese patients, although its frequency is relatively low. Detailed studies including a larger number of facilities should be conducted in future.

Muscle force estimation during gait using Angle-EMG-Force relationship.

Measuring the muscle force during gait can provide crucial knowledge for clarifying the walking mechanism and preventing injuries. However, non-invasive muscle force measurement is a major challenge in biomechanics. Previous research has investigated the relationship between the amplitude of electromyography (EMG) and muscle force. By examining the EMG-force relationship of each muscle, the generated muscle force can be measured on the basis of the EMG amplitude during gait. This study aimed to investigate the angle-EMG-force relationship of lower limb muscles and estimate the muscle force during gait. The EMG and muscle force were measured in a static muscle force measurement task, and the angle-EMG-force relationship was analyzed based on these data. The results indicate that the muscle force can be estimated using the angle-EMG-force relationship during gait.Clinical Relevance-This study contributes to a more correct analysis of the muscle force during gait.

Inhibition of the renal renin-angiotensin system and renoprotection by pitavastatin in type1 diabetes.

1. The aim of the present study was to investigate whether or not pitavastatin ameliorates diabetic nephropathy and if inhibition of the rennin-angiotensin-aldosterone system (RAAS) is associated with any renoprotective effects. Pitavastatin (10mg/ kg/day) and/or spironolactone (100mg/kg/day) were given by gavage for 3weeks to uninephrectomized rats with streptozotocin-induced diabetes. 2. Pitavastatin or spironolactone significantly reduced proteinuria and collagen deposition, and normalized creatinine clearance, serum creatinine levels and blood urea nitrogen concentrations. 3. Reverse transcription polymerase chain reaction analysis showed that the renal expression of collagenI, transforming growth factor-ß and monocyte chemoattractant-1 were increased in diabetic rats and reduced by the pitavastatin and/or spironolactone treatment. 4. These agents also decreased angiotensin converting enzyme expression and aldosterone concentrations in the renal homogenate, but had no effect on blood glucose, haemoglobinA(1c) , and plasma total cholesterol, Na(+) , K(+) , aldosterone and NOx levels, or on systolic blood pressure measured by the tail-cuff method. Interestingly, cotreatment with pitavastatin and spironolactone did not result in additional normalization. 5. These results suggest that pitavastatin shows renoprotective effects against diabetic nephropathy mediated in part by inhibition of the renal RAAS, including the suppression of angiotensin-converting enzyme expression and aldosterone production.