Objective: To determine the size of reduction in homocysteine concentrations produced by dietary supplementation with folic acid and with vitamins B-12 or B-6. Design: Meta-analysis of randomised controlled trials that assessed the effects of folic acid based supplements on blood homocysteine concentration. Multivariate regression analysis was used to determine the effects on homocysteine concentrations of different doses of folic acid and of the addition of vitamin B-12 or B-6. Subjects: Individual data on 1114 people included in 12 trials. Findings: The proportional and absolute reductions in blood homocysteine produced by folic acid supplements were greater at higher pretreatment blood homocysteine concentrations (P < 0.001) and at lower pretreatment blood folate concentrations (P < 0.001). After standardisation to pretreatment blood concentrations of homocysteine of 12 μmol/l and of folate of 12 nmol/l (approximate average concentrations for Western populations), dietary folic acid reduced blood homocysteine concentrations by 25% (95% confidence interval 23% to 28%; P < 0.001), with similar effects in the range of 0.5-5 mg folic acid daily. Vitamin B-12 (mean 0.5 mg daily) produced an additional 7% (3% to 10%) reduction in blood homocysteine. Vitamin B-6 (mean 16.5 mg daily) did not have a significant additional effect. Conclusions: Typically in Western populations, daily supplementation with both 0.5-5 mg folic acid and about 0.5 mg vitamin B-12 would be expected to reduce blood homocysteine concentrations by about a quarter to a third (for example, from about 12 μmol/l to 8-9 μmol/l). Large scale randomised trials of such regimens in high risk populations are now needed to determine whether lowering blood homocysteine concentrations reduces the risk of vascular disease. (Less)

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Lowering blood homocysteine with folic acid based supplements: Meta-analysis of randomised trials

A processor-based system for analyzing physiologic data and medical care is provided wherein the patient data is analyzed to construct images that are representative of a patient's condition. The processor provides a self-modulating analysis, which is responsive to the occurrence of additional data items to increase the information contained in the images. Identifications of modes of physiologic failure by the analysis of the generated images provides for earlier recognition and intervention and improved protocolization of testing and treatment.

Patient safety processor

A system and method for organization and analysis of complex and dynamically interactive time series is disclosed. One example comprises a processor based system for relational analysis of physiologic signals for providing early recognition of catastrophic and pathologic events such as pathophysiologic divergence. The processor is programmed to identify pathophysiologic divergence of at least one of first and second physiologic parameters in relationship to the other and to output an indication of the divergence. An object-based method of iterative relational processing waveform fragments in the time domain is described wherein each more complex waveform object inherits the characteristics of the waveform objects from which it is derived. The first physiologic parameter can be the amplitude and frequency of the variation in chest wall impedance or nasal pressure and the second parameter can be a measure or indication of the arterial oxygen saturation.

Microprocessor system for the analysis of physiologic and financial datasets

Obstructive sleep apnea in infants has a distinctive pathophysiology, natural history, and treatment compared with that of older children and adults. Infants have both anatomical and physiological predispositions toward airway obstruction and gas exchange abnormalities; including a superiorly placed larynx, increased chest wall compliance, ventilation-perfusion mismatching, and ventilatory control instability. Congenital abnormalities of the airway, such as laryngomalacia, hemangiomas, pyriform aperture stenosis, choanal atresia, and laryngeal webs, may also have adverse effects on airway patency. Additional exacerbating factors predisposing infants toward airway collapse include neck flexion, airway secretions, gastroesophageal reflux, and sleep deprivation. Obstructive sleep apnea in infants has been associated with failure to thrive, behavioral deficits, and sudden infant death. The proper interpretation of infant polysomnography requires an understanding of normative data related to gestation and postconceptual age for apnea, arousal, and oxygenation. Direct visualization of the upper airway is an important diagnostic modality in infants with obstructive apnea. Treatment options for infant obstructive sleep apnea are predicated on the underlying etiology, including supraglottoplasty for severe laryngomalacia, mandibular distraction for micrognathia, tonsillectomy and/or adenoidectomy, choanal atresia repair, and/or treatment of gastroesophageal reflux.

Obstructive Sleep Apnea in Infants

The disclosed embodiments relate to pulse oximetry. An exemplary pulse oximeter comprises a probe that is adapted to be attached to a body part of a patient to create a signal indicative of an oxygen saturation of blood of the patient, and a processor that is adapted to receive the signal produced by the probe, to calculate an SPO2 value based on the signal, to detect a plurality of pattern types of SPO2 indicative of pathophysiologic events, and to produce an output indicative of a detected one of the plurality of pattern types.

System and method for automatic detection of a plurality of spo2 time series pattern types

Sixteen healthy term infants underwent 12 hour tape recordings of arterial oxygen saturation (SaO2)(Nellcor N100 in beat to beat mode) and breathing movements at around 6 weeks, 3 and 6 months of age. Six of these infants had an additional recording at around their first birthday. Recordings were analysed throughout for pauses in breathing movements of greater than or equal to 4 s (apnoeic pauses), episodes in which SaO2 fell to 80% (desaturations), and (only during regular breathing) baseline SaO2. In the 16 infants studied at 6 weeks, 3 and 6 months, the median frequency of both apnoeic pauses (5.6, 5.7, and 6.1/h, respectively) and desaturations (0.7, 0.4 and 0.5/h, respectively) showed little change. The majority of desaturations followed an apnoeic pause (median 73.2, 86.2 and 93.8% of desaturations). The median proportion of apnoeic pauses followed by a desaturation did not change significantly (9.0, 7.5 and 9.1%), despite an increase in the proportion of apnoeic pauses of greater than or equal to 8 s in duration from 2.0% at 6 weeks to 5.3% at 3 months (P less than 0.01). Baseline SaO2 was 97.3% or higher in all recordings. Median baseline SaO2 increased from 99.6 to 99.9% between 6 weeks and 3 months (P less than 0.02) and remained unchanged thereafter. In the subgroup of infants studied also at one year of age, again no significant differences were found with increasing age in the frequency of either apnoeic pauses or desaturations. The data show that in healthy subjects no major changes occur between 6 weeks and 1 year of life in apnoeic pause frequency or arterial oxygenation.(ABSTRACT TRUNCATED AT 250 WORDS)

Stebbens Va

Papers

Arterial oxygen saturation and breathing movements during the first year of life.