Effect of oral intake of royal jelly on endothelium function in hemodialysis patients: study protocol for multicenter, double-blind, randomized control trial.

BACKGROUND: Hemodialysis (HD) is a common renal replacement therapy for patients with renal failure. Cardiovascular and cerebrovascular diseases are known to shorten survival periods and worsen the quality of life of HD patients. Atherosclerosis is a major cause of vascular diseases, and various factors such as abnormality of lipid metabolism and increased macrophage activity, oxidative stress, and endothelial dysfunction are associated with its pathogenesis and progression. Further, endothelial stem cells (ESCs) have been reported to play important roles in endothelial functions. Royal jelly (RJ) affects atherosclerosis- and endothelial function-related factors. The main aim of this trial is to investigate whether oral intake of RJ can maintain endothelial function in HD patients. In addition, the effects of RJ intake on atherosclerosis, ESC count, inflammation, and oxidative stress will be analyzed. METHODS: This will be a multicenter, prospective, double-blind, randomized controlled trial. We will enroll 270 participants at Nagasaki Jin Hospital, Shinzato Clinic Urakami, and Maeda Clinic, Japan. The participants will be randomized into RJ and placebo groups. The trial will be conducted according to the principles of the Declaration of Helsinki, and all participants will be required to provide written informed consent. The RJ group will be treated with 3600 mg/day of RJ for 24 months, and the placebo group will be treated with starch for 24 months. The primary endpoint will be the change in flow-mediated dilation (FMD), a parameter of endothelium function, from the time before treatment initiation to 24 months after treatment initiation. The secondary and other endpoints will be changes in FMD; ESC count; serum levels of vascular endothelial cell growth factor, macrophage colony-stimulating factor, 8-hydroxydeoxyguanosine, and malondialdehyde; the incidence of cardiovascular diseases, cerebrovascular diseases, and stenosis of blood access; and safety. DISCUSSION: This trial will clarify whether oral intake of RJ can maintain endothelial function and suppress the progression of atherosclerosis in HD patients. In addition, it will clarify the effects of RJ on ESCs, oxidative stress, and angiogenic activity in blood samples. TRIAL REGISTRATION: The Japan Registry of Clinical Trials  jRCTs071200031 .  Registered on 7 December 2020.

Bacterial peritonitis due to duodenal perforation by a fish bone in an elderly peritoneal dialysis patient.

The patient, a 77-year-old-man, began peritoneal dialysis (PD) in August 2005. In January 2009, he developed lower abdominal pain and cloudy PD effluent. A diagnosis of peritonitis was made and Escherichia coli was detected in cultures of the PD effluent. An abdominal computed tomography scan showed a fish bone in the duodenal wall. An upper gastrointestinal endoscopy was performed, and a 3-cm fish bone was removed. We thus recommend careful investigation with the possibility of enteric peritonitis from the intestinal tract when E. coli is detected in effluent cultures during PD.

A case of acute kidney injury with marked hyperuricemia during mizoribine administration.

A 52-year-old woman was diagnosed with Blau syndrome and rheumatoid arthritis and was treated with prednisolone and methotrexate. Joint pain and skin ulcers were poorly controlled; therefore, mizoribine (MZ; 150 mg/day) was administered once daily from March 2011. In early July 2011, the patient was hospitalized because of acute kidney injury (AKI) and acute pancreatitis. We reasoned that AKI resulted from hyperuricemia during MZ administration because serum concentrations of uric acid (31.6 mg/dL) and MZ (trough level, 5.14 µg/mL) were markedly elevated on admission. MZ should be administered with caution because of the risk of marked hyperuricemia leading to AKI.

Serum pro-hepcidin level and iron homeostasis in Japanese dialysis patients with erythropoietin (EPO)-resistant anemia.

BACKGROUND: Resistance to EPO therapy in hemodialysis (HD) patients is ascribed to inflammation and iron deficiency. Hepcidin, an antimicrobial peptide, is a key regulator of iron metabolism and synthesis of hepcidin is regulated by iron status and inflammation. The role of hepcidin in the pathogenesis of EPO-resistant anemia was assessed through measurement of serum pro-hepcidin in HD patients. MATERIAL/METHODS: Serum pro-hepcidin was measured by ELISA in 57 HD patients, who were divided into three groups: Group I (n=19) had EPO-resistance anemia, based on serum ferritin of > or =100 ng/ml and EPO dose (9,000 IU/week maximum dose for 6 months); Group II (n=19) had iron-deficiency anemia, based on serum ferritin of <100 ng/ml and/or <20% transferrin iron saturation (TSAT); and Group III (n=19) had no iron deficiency and anemia. Nineteen age- and sex-matched healthy volunteers were enrolled as controls (Group IV). RESULTS: Serum pro-hepcidin was significantly lower in Group II than in other groups. In Group I, serum pro-hepcidin did not differ significantly from controls. Serum levels of ferritin, hs-CRP and IL-6 were higher in Group I than in other groups, and serum sTfR was higher in Groups I and II than in controls. CONCLUSIONS: In EPO resistant anemia, multiple factors, including iron and inflammation related conditions, are likely to affect the level of hepcidin and this may explain the lack of elevated serum hepcidin in this condition.

Cowfish (Umisuzume, Lactoria diaphana) poisoning with rhabdomyolysis.

A 40-year-old man developed weakness and myalgia of the shoulders and brachia nine hours after eating a cowfish (Umisuzume, Lactoria diaphana). A clinical symptom showed rhabdomyolysis and serum creatine phosphokinase was elevated to 180,000 IU/L on day 3. Cardiopulmonary arrest and acute renal failure developed after 59 hours and hemodiafiltration was performed. Cerebral death was diagnosed on day 9 and the patient died on day 16. The case has the characteristic clinical course of palytoxin poisoning, which has also been reported as blue humphead parrotfish poisoning from other kinds of fish.