Validation of the blood pressure measurement device Beurer BM 28 according to the European Society of Hypertension International Protocol revision 2010.

OBJECTIVE: The aim of the present study was to validate the blood pressure (BP) monitor Beurer BM 28 according to the International Protocol of the European Society of Hypertension (ESH-IP) revision 2010. METHODS: In 33 subjects of age 27-81 years, BP measurements were performed according to the ESH-IP protocol, which alternates reference mercury sphygmomanometer and device-under-test (Beurer BM 28) measurements, resulting in a total of 99 comparisons. RESULTS: As to part 1 of the protocol, an absolute difference within 5 mmHg between the Beurer BM 28 and the test device was found in 83 out of 99 comparisons for the SBP and 82 out of 99 comparisons for the DBP. In 95 out of 99 SBP comparisons and 96 out of 99 DBP comparisons, the difference was found to be within 10 mmHg, whereas only one outlier was noted with an SBP difference higher than 15 mmHg. Mean difference between the test device and the reference was 0.4 ± 4.4 mmHg for SBP, and 0.5 ± 4.3 mmHg for DBP. According to part 2 of the protocol, 30 out of 33 subjects for SBP, and 28 out of 33 for DBP had a minimum of two out of three comparisons staying within the range of 5 mmHg. In none of the subjects, all three comparisons stayed outside the 5 mmHg absolute difference, while in three subjects this was the case for the DBP. CONCLUSION: The Beurer BM 28 met all requirements of the ESH-IP revision 2010 and can be recommended for BP measurements in the study population under investigation.

Validation of the Beurer BM 44 upper arm blood pressure monitor for home measurement, according to the European Society of Hypertension International Protocol 2002.

OBJECTIVE: The present study aimed to validate the automated upper arm blood pressure (BP) measuring device BM 44 for home BP monitoring according to the 2002 Protocol of the European Society of Hypertension. The most important new feature of the new device was an integrated 'WHO indicator', which categorizes the patient's individual result within the WHO recommendations for target BP by a coloured scale. METHODS: Systolic and diastolic BPs were measured sequentially in 35 adult participants (16 men, 19 women) using a standard mercury y-tubed reference sphygmomanometer (two observers) and the BM 44 device (one supervisor). Ninety-nine pairs of comparisons were obtained from 15 participants in phase 1 and a further 18 participants in phase 2 of the validation study. RESULTS: The BM 44 device passed phase 1 of the validation study successfully with a number of absolute differences between device and observers of 5, 10 and 15 mmHg for at least 28 out of 25, 35 out of 35 and 40 out of 40 measurements, respectively. The device also achieved the targets for phases 2.1 and 2.2, with 23 and 26 participants having had at least two of three device-observers differences within 5 mmHg for systolic and diastolic BP, respectively. CONCLUSION: The Beurer BM 44 upper arm BP monitor has passed the International Protocol requirements, and hence can be recommended for home use in adults.

Impact of dehydroepiandrosterone on hepatocarcinogenesis in the rat (Review).

The role of dehydroepiandrosterone (DHEA) in liver carcinogenesis remains a topic of widespread research. Studies in rats suggest a hepatocarcinogenetic effect of DHEA. The incidence of DHEA-induced hepatocellular neoplasms depends on the rat strain, the gender, and the dose and duration of the treatment. Gender specific differences observed regarding the incidence of DHEA-induced hepatocellular neoplasms suggest a hormonal impact of the treatment. Studies in rats, which initially had been treated with chemical carcinogens and subsequently underwent a DHEA administration with various doses, disclose both, DHEA associated hepatic tumour promotion and hepatic tumour inhibition. These findings depend on the type, dose and duration of the initial intoxication and of the DHEA treatment. DHEA administration to rats also induces multiple profound alterations of the liver metabolism. Metabolism during DHEA treatment is characterized by an overall increase in energy expenditure. Lipid and glucose metabolism of the liver is changed profoundly switching from an anabolic to a catabolic state. This energy waste may be related to the inhibitory action of DHEA on tumour growth. Tumour enhancement is due to promotion of a specific type of preneoplastic liver lesions with a basophilic phenotype. This review summarizes the current knowledge on DHEA effects on the liver and discusses molecular and functional aspects that may explain the paradoxical effects of DHEA regarding hepatocarcinogenesis.

Induction and modulation of hepatic preneoplasia and neoplasia in the rat by dehydroepiandrosterone.

Dehydroepiandrosterone (DHEA), the main adrenal steroid in humans and a precursor in androgen and estrogen biosynthesis, acts as a peroxisome proliferator and as a hepatocarcinogen in rats. Neoplasms emerge from a glycogenotic/amphophilic/basophilic preneoplastic cell lineage. A higher female tumor incidence suggests a relevant influence of sex hormones. DHEA enhances hepatocarcinogenesis induced by N-nitrosomorpholine (NNM), which is characterized by the glycogenotic/basophilic cell lineage. The tumor promoting effect is related to an additional amphophilic/basophilic preneoplastic lesion sequence and to faster proliferation of the basophilic preneoplastic lesions. Nevertheless, hepatocellular carcinomas provided under DHEA treatment seem to have a less malignant phenotype compared to tumors induced by NNM only. Further, DHEA treatment reduces growth and generation of glycogen storage foci (GSF) in initial NNM-treated rats. Thus, DHEA treatment results in both, a growth stimulation of the late basophilic lesion type with an additional amphophilic lesion sequence, and in a growth inhibition of early preneoplastic lesions, addressing especially GSF. DHEA also inhibits the growth of physiologically proliferating liver tissue. This might be explained by a DHEA related cellular metabolism, which results in significant energy consumption. Additionally, a DHEA-induced alteration of cytokine levels might contribute to this growth inhibition as well.