Ginseng for Treating Hypertension: A Systematic Review and Meta-Analysis of Double Blind, Randomized, Placebo-Controlled Trials.

BACKGROUND: Evidence of ginseng for reducing blood pressure (BP) in hypertensive patients is controversial. This systematic review updated the previous reviews and evidence for it. METHODS: Ten databases were searched from their inception through October 2016, without language restriction. Randomized clinical trials (RCTs) were included if any types of ginseng were tested as the sole treatment or as an adjunct to other treatments for pre-hypertension or hypertension. The risk of bias (ROB) was assessed with Cochrane ROB tools by two independent reviewers. RESULTS: We found 528 potentially relevant articles, of which 9 RCTs met our inclusion criteria. Two studies reported positive effects of Korean red ginseng (KRG) on acute reduction of systolic BP (SBP: n=54, mean differences (MD), -6.52; P=0.0002; I2=0%) and diastolic BP DBP: MD, -5.21; P=0.0001; I2=0%), while two other trials failed to do so with north American ginseng (NAG) in both SBP and DBP. Five RCTs assessed the long-term effects of ginseng (KRG or NAG) on SBP and DBP. Two studies showed positive effects of KRG on reducing SBP and DBP compared with placebo (SBP: n = 183, MD, -2.92, P=0.04; I2 = 0%; DBP: MD, -3.19, P=0.008; I2 = 0%). CONCLUSION: This systematic review provides positive evidence for the efficacy of KRG on reducing blood pressure in patients with pre-hypertension and hypertension in acute and long-term. Future RCTs appear to be warranted.

Psychiatric presentations/manifestations of medical illnesses.

Psychiatry is clearly an integral part of medicine. With a history and physical exam (called the mental status exam in psychiatry), appropriate laboratory or imaging studies, a differential diagnosis is made. If a specific DSM-IV-TR diagnosis is made, then the treatment will naturally follow. The diagnoses are scientifically established with good validity, specificity, sensitivity and inter-rater reliability. Similarly the treatments are established through scientific research. However, sometimes medical illnesses may present with symptoms seemingly pointing to a psychiatric origin. Making a misdiagnosis can be quite problematic and dangerous for the patient. The opposite is also true, that psychiatric illnesses may present with symptoms implying a medical diagnostic origin. Finally, psychiatric patients may have more than one psychiatric diagnosis and in addition, a medical diagnosis too. A high degree of suspicion should always be entertained by the diagnosing physician, psychiatric or non-psychiatric. This paper reviews the literature regarding these situations and then presents several clinical cases where this conundrum was present. Making the correct diagnosis was critical in the successful treatment outcome of each of the clinical cases. When asked to consult on a patient by non-psychiatric physicians, the psychiatrist must be careful to also look for non-psychiatric origins for the referring symptoms. It is important for psychiatrists to build on their medical knowledge from medical school and internship and continue to be kept abreast of confounding symptomatology.

To autoregulate or not to autoregulate--that is no longer the question.

In the late 1970s, high cerebral blood flow was perceived as a cause of intracranial hemorrhage in the preterm infant. Intracranial hemorrhage was diagnosed by computed tomography and ultrasound found to be frequent not only in babies who died. Hemorrhage was soon linked to cerebral palsy in survivors. The analogy was hypertensive hemorrhagic stroke in the adult. Cerebral hemorrhage was perceived as the major (preventable) cause of brain injury in the preterm baby. An immature cerebral autoregulation or a vulnerability of the autoregulation exposed by preceding hypoxia or ischemia therefore became a focus of neonatal brain research in the 1980s. Over the years the focus has changed, first to the pathogenesis of hypoxic-ischemic brain injury, then to the effects of pCO(2), and now 30 years later to a more comprehensive, less clearly hypothesis-driven exploration of the multitude of factors involved in cerebral blood flow and oxygenation. Meanwhile, some basic questions regarding autoregulation remain unanswered, and some concepts from the 1970s still direct clinical practice.

A comparison of renal-related adverse drug reactions between rofecoxib and celecoxib, based on the World Health Organization/Uppsala Monitoring Centre safety database.

BACKGROUND: Two isoforms of cyclooxygenase (COX) have been identified, both of them inhibited by traditional nonsteroidal anti-inflammatory drugs (NSAIDs). Inhibition of COX-2 has been associated with the therapeutic effects of NSAIDs, whereas inhibition of COX-1 is believed to be the cause of the adverse gastrointestinal effects associated with NSAID therapy. When administered at therapeutic doses, new COX-2-specific inhibitors inhibit only the COX-2 isoform. OBJECTIVE: This study sought to compare renal safety signals between the COX-2-specific inhibitors rofecoxib and celecoxib, based on spontaneous reports of adverse drug reactions (ADRs) in the World Health Organization/Uppsala Monitoring Centre (WHO/UMC) safety database through the end of the second quarter 2000. METHODS: Disproportionality in the association between a particular drug and renal-related ADR was evaluated using a bayesian confidence propagation neural network method in which a statistical parameter, the information component (IC) value, was calculated for each drug-ADR combination. In this method, an IC value significantly greater than 0 implies that the association of a drug-ADR pair is stronger than background; the higher the IC value, the more the combination stands out from the background. The ratio of actual to expected numbers of ADRs was also used to assess disproportionality. RESULTS: As with traditional NSAIDs, both COX-2-specific inhibitors were associated with renal-related ADRs. However, the adverse renal impact of rofecoxib was significantly greater than that of celecoxib. IC values were significantly different for the following comparisons: water retention (1.97 rofecoxib vs 1.18 celecoxib; P < 0.01); abnormal renal function (2.38 vs 0.70; P < 0.01); renal failure (2.22 vs 1.09; P < 0.01); cardiac failure (2.39 vs 0.48; P < 0.01); and hypertension (2.15 vs 1.33; P < 0.01). In an additional analysis, celecoxib was shown to have a similar renal safety profile to that of diclofenac and ibuprofen. CONCLUSIONS: Based on spontaneous ADR reports in the WHO/UMC safety database at the end of the second quarter 2000, this analysis indicates that rofecoxib has significantly greater renal toxicity than celecoxib or traditional NSAIDs. This negative renal impact may have the potential to increase the risk for serious cardiac and/or cerebrovascular events.