Clinical Search for Undiagnosed Mesenteric Phlebosclerosis at Outpatient Departments Specializing in Herbal (Kampo) Medicine.

OBJECTIVE: Mesenteric phlebosclerosis (MP) is a disease characterized by calcification of the mesenteric vein, which causes chronic mesenteric ischemia. Recently, the long-term intake of gardenia fruit ('Sanshishi' in Japanese) has been attracting attention as a possible cause. Usually, only advanced, severe MP cases get reported. However, we suspected that some latent cases of this disease may exist. We performed this study in order to determine the prediagnostic cases at our outpatient departments of herbal (Kampo) medicine, with particular attention paid to the initial changes, such as any slight color change of the colon, as shown in colonoscopy. METHODS: We recommend colonoscopy and computed tomography (CT) scans for patients with a long-term history of taking herbal medicines containing gardenia fruit. Clinical examinations were performed upon receiving patients' consent from December 2013 to November 2014. RESULTS: Of the 103 patients who took gardenia fruit long-term, 29 agreed to be checked for MP. 14 patients underwent colonoscopy. Four patients were confirmed to have MP due to the presence of fibrotic deposition of the colonic membrane on histological inspection. Twenty-one patients underwent abdominal CT screening. Characteristic calcification of the mesenteric vein was observed on CT scans in 2 patients. All 4 MP patients took Kampo formulas containing gardenia fruit for more than 6.8 years. The other patients did not develop MP, despite long-term gardenia fruit intake. CONCLUSION: We detected the latent and undiagnosed MP cases. All diagnoses were made while paying careful attention to any slight changes in colonoscopy and CT scans.

[A Case of Wernicke's Encephalopathy Presenting with Acute Deterioration of Consciousness Caused by Peripheral Parenteral Nutrition].

We report the case of a 67-year-old woman with Wernicke's encephalopathy(WE), who had been suffering from repeated vomiting and poor oral intake due to both reflux esophagitis and atrophic gastritis. She presented with altered of consciousness, horizontal nystagmus, and gait disturbance, and acute deterioration of consciousness was observed after starting peripheral parenteral nutrition (PPN). Brain MRI showed bilateral high intensity lesions in the medial thalamus and the dorsal midbrain on FLAIR and T2-weighted images. Although brain MRI characteristics are useful for diagnosing WE, it is possible that there are no abnormal MRI findings in its early stages. In addition, only 10-20% of WE cases present with the classical clinical triad of confusion, ophthalmoplegia, and ataxia. Therefore, confirming the diagnosis can be challenging. In general, rapid improvement of symptoms is observed with prompt vitamin B1 supplementation. However, delays in treatment can result in irreversible amnesia and ataxia. Furthermore, in the state of vitamin B1 deficiency, even PPN, not just total parenteral nutrition, can worsen symptoms, and this deterioration is attributed to the glucose load.

[Gymnema sylvestre leaf extract: a 52-week dietary toxicity study in Wistar rats].

A 52-week study of oral-repeated-dose toxicity for the extraction powder of Gymnema sylvestre (GS), Indian-native genus, Metaplexis japonica, was conducted in both genders of Wistar rats. The rats were administered a graded dose of GS at 0.01, 0.10 and 1.00% of basal powder diet, along with a group fed solely with the basal powder diet without GS, for 52 weeks. General conditions were recorded daily. Body weights and food consumptions were recorded weekly up to 12 weeks, and thereafter at longer intervals. At 26 weeks, for an intermediate examination, and 52 weeks, for the final examination, animals were subjected to hematology, serum chemistry, and pathological examination. None of the animals died in the period up to 52 weeks. No exposure-related changes in body-weight, in the food consumption, in the hematological examinations, or in the serum biochemical examinations were recognized. No histopathological alterations were seen. Thus, it was concluded that there was no toxic effect in rats treated with GS at up to 1.00% in the diet for 52 weeks. The no-observable-effect level from this study is 1.00% GS, i.e., 504 mg/kg/day for male and 563 mg/kg/day for female as mean daily intake, for 52 weeks.

[Kooroo color: 90-day dietary toxicity study in F344 rats].

A subchronic toxicity study on kooroo color was conducted using F344 rats of both genders. Kooroo color is an extract of yam root, Dioscorea matudai Hayata, of which the major components are known to be flavonoid pigments. Use of kooroo as a food color is permitted by the Food Sanitation Law in Japan, but the chronic toxicity has not been evaluated in the literature. Rats were fed the product of kooroo color (PKC) at doses of 0.5%, 1.50%, and 5.0% in basal powder diet, while control groups received PKC-free basal diet, for ninety days. A vehicle control given propylene glycol (PG) alone, at the same dosage that the 5.0% group received, was included, because PKC used in this study contained ca. 80 percent PG, used as an extractant during the manufacturing processes. Daily observation of general behavior, and weekly measurement of body weight as well as food consumption were performed. Hematological, serum biochemical and anatomopathological examinations were conducted at the end of administration. No abnormalities ascribable to the treatment with PKC or PG were noted in any examination in this study. Hence, dietary intake of 5.0% of PKC, i.e., 2,993 mg/kg/day for males, and 3,376 mg/kg/day for females, as a mean daily intake for 90 days, had no observable adverse effect in F344 rats. Therefore, kooroo color has no significant general toxicity, and its toxicity, if any, is of a very low order.