Tolvaptan corrects hyponatremia and relieves the burden of fluid/dietary restriction and hospitalization in hyponatremic patients with terminal lung cancer: a report of two cases.

Case 1: A 45-year-old man, admitted for symptomatic hyponatremia, was diagnosed with advanced small-cell lung cancer and severe hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone. In addition to chemotherapy, the patient was treated with increased dietary salt intake (15 g/day), fluid restriction of 500 mL/day, and amino acid supplementation to maintain a urea load of 31 g/day. Due to the difficulty in changing his habit of drinking 2-3 L/day after discharge, tolvaptan was started. This resulted in correction of hyponatremia, which facilitated earlier discharge and improved his quality of life by eliminating the need for dietary restriction.Case 2: An 88-year-old man with asymptomatic hyponatremia was admitted for assessment of pleural effusion. He was diagnosed with small-cell lung cancer with mild hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone. He was treated with best supportive care and dietary modification (salt intake of 15 g/day and fluid restriction of 400 mL/day). He found it difficult to comply with the dietary changes, and prolonged hospitalization was required for hyponatremia correction. Therefore, tolvaptan was initiated, which corrected his hyponatremia, and the patient was discharged.In summary, tolvaptan results in stable correction of hyponatremia in patients with terminal small-cell lung cancer complicated by the syndrome of inappropriate secretion of antidiuretic hormone. Furthermore, it improves the quality of life of these patients by relieving the burden of strict dietary modifications and prolonged hospitalization.

Aldosterone Response in Severe Hypokalemia and Volume Depletion: A Case Report and Review of the Recent Research.

We report a case of severe hypokalemia and volume depletion complicated by chronic watery diarrhea resulting from chronic alcoholism in a 57-year-old man. Prompt replacement of normal saline with potassium chloride and cessation of alcohol intake resulted in a favorable outcome. We discuss the pathophysiology of the case, emphasizing the response of aldosterone in both hypokalemia and volume depletion, and provide a review of recent research.

Single low-dose rituximab for the treatment of steroid-resistant nephrotic syndrome with acute kidney injury.

The efficacy of rituximab for kidney disease, such as frequent relapsing nephrotic syndrome, has been reported recently. Herein, we report a case of a patient with acute kidney injury that was steroid-resistant nephrotic syndrome who responded to a single administration of low-dose rituximab. An 86-year-old Japanese woman with hypertension presented with severe peripheral edema within several days after onset. Due to the patient's age, renal biopsy was not performed, nephrotic syndrome was diagnosed and prednisolone was administered at 40 mg/day on the day after admission. However, anuria developed and hemodialysis was inevitably initiated on the 5th hospital day. The renal function did not recover, and the general condition gradually became aggravated. On the 50th hospital day, 100 mg rituximab was administered, which led to immediate depletion of CD20-positive cells. The urine volume gradually increased from 2-3 weeks after the rituximab administration, and the renal function recovered slightly. After 5 weeks, it became possible to wean the patient from dialysis, which had been applied for 3 months. Rituximab might be an option for the treatment of acute kidney injury due to steroid-resistant nephrotic syndrome.

Anthocyanidins inhibit activator protein 1 activity and cell transformation: structure-activity relationship and molecular mechanisms.

Anthocyanins are the chemical components that give the intense color to many fruits and vegetables, such as blueberries, red cabbages and purple sweet potatoes. Extensive studies have indicated that anthocyanins have strong antioxidant activities. To investigate the mechanism of anthocyanidins as an anticancer food source, six kinds of anthocyanidins representing the aglycons of most anthocyanins, were used to examine their effects on tumor promotion in mouse JB6 cells, a validated model for screening cancer chemopreventive agents and elucidating the molecular mechanisms. Of the six anthocyanins tested, only those with an ortho-dihydroxyphenyl structure on the B-ring suppressed 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced cell transformation and activator protein-1 transactivation, suggesting that the ortho-dihydroxyphenyl may contribute to the inhibitory action. Delphinidin, but not peonidin, blocked the phosphorylation of protein kinases in the extracellular signal-regulated protein kinase (ERK) pathway at early times and the c-Jun N-terminal kinase (JNK) signaling pathway at later times. p38 kinase was not inhibited by delphinidin. Furthermore, two mitogen-activated protein kinase (MAPK) specific inhibitors (SP600125 for JNK and UO126 for ERK) could specifically block the activation of JNK and ERK and cell transformation. Those results demonstrate that anthocyanidins contribute to the inhibition of tumorigenesis by blocking activation of the MAPK pathway. These findings provide the first molecular basis for the anticarcinogenic action of anthocyanidins.