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A couple of cases with HPgV seroconversion have been associated with a particularly worse prognosis (Williams 2004 kamagra oral jelly 100mg lowest price what causes erectile dysfunction treatment, Bjorkman 2004 order kamagra oral jelly discount impotence pumps, van der Bij 2005) cheap kamagra oral jelly master card encore vacuum pump erectile dysfunction. This raised concerns about interferon-based HCV-therapies, which are able to terminate HPgV replication and to induce anti-E2 seroconversion (Yu 2001, Hofer 2011). However, a negative impact of interferon was not seen in a large multicenter trial (Schwarze-Zander 2006). Proposed pathomechanisms Up to now, the fundamental chicken or egg dilemma remains unsolved: whether HPgV viremia is an epiphenomenon or the cause for an improved outcome of HIV infection. A major drawback of the first studies was the lack of any pathophysiologic concept. Meanwhile many different hypotheses have been postulated about direct inhibitory effects of HPgV on HIV replication, about competition of both viruses at certain steps of action during the replication cycle, and about immunomodulatory mechanisms in the host induced by HPgV. After more than two decades of research, it has been shown that more than one way leads to Rome. The knowledge about the pathophysiology of HPgV coinfection in HIV looks rather like a varied bunch of pleiotropic effects of numerous different modes of (inter-)action. The modulating effects of HPgV on HIV disease (Table 3) have be explained by attachment or entry inhibition, downregulation of CD4- and chemokine receptors including upregula- tion of their ligands, enhancement of innate immunity, downregulation of immune activation and apoptosis, and modulation of T cell responses. The elucidation of the underlying molecular pathomechanisms is still fragmentary. However, HPgV treads several independent pathways, using E2-protein, NS5A- protein, and Anti-E2-antibodies. Hence it might be speculated, that mankind shares a long coevolution together with HPgV and retroviruses, which could explain why HIV – in contrast to SIV in other primates – until recently was not able to establish a stable endemic. IL-2, IL-12) and PDCs (CD80+ pDCs) Stapleton 2009 mediated by NS5A) less increase of Th2- cytokines (IL-4, IL-10) Deceleration of In HPgV viremic HIV+ HPgV viremia reduces Maidana-Giret increased T cellular pts less expression of IL-2 production and 2009 immune activation CD38+, CCR5+, CD69, IL-2 induced T cell Bhattarai 2012a and CD25 on T cells proliferation Increase of double DNTCs are associated HPgV viremia associated Bhattarai 2012c negative T cells (DNTC: with decreased immune with higher levels of Petitjean 2012 CD3+/CD4-/CD8-) activation immunosuppressive cytokines (TGF-ß, IL-10) Reduction of NK-, Decreased expression of Stapleton 2013 B cell and monocyte CD69 (NK-cells), CD86 (B activation cells) and CCR5 (monocytes) Inhibition of Anti-E2-antibodies Inhibition of HIV by Mohr 2010 HIV-attachment precipitate and neutralise attachment-inhibition (Anti-HPgV-E2- HIV particles in vitro and to target cells but not antibodies) inhibit CCR5- and CXCR4- by entry inhibition tropic HIV replication PDCs, plasmacytoid dendritic cells Human Pegivirus HPgV Infection 471 Hypothetically in the past spread of HIV could have been limited by two other viral diseases, both formerly highly prevalent in Africa where HIV had its origin: The chemokine receptor inhibition by HPgV might have prevented transmission, espe- cially vertical transmission, which is a result of perinatal HPgV transmission in HIV+ mothers (Handelsmann 2007, Bhanich-Suparol 2009). On the other side periodical epidemics of pox might have killed efficiently any human host of HIV, because a fatal course in pox is common especially in cases with preexisting cellular immun- odeficiency. The possible result of this two competing coinfections: HIV was – until recently – not able to establish a stable endemic in humans over a long time. The story of HPgV coinfection in HIV started with observational epidemiology and revealed an unexpected clinical observation: HPgV presents as a non-pathogenic virus in humans and as a beneficial coinfection in HIV+ individuals. At this point science started at bedside and went to bench in the last two decades. A puzzling diversity of pathomechanisms had been described meanwhile and may have raised more questions than answers. For more detailed information to the complex role of HPgV in the pathophysiology of HIV-infection it is referred to recent reviews of the scientific literature in this evolving field of infectiology (Bhattarai 2012a, Chiveiro 2015, Maidana Giret 2012, Schwarze-Zander 2012, Shankar 2011). How to deal with HPgV coinfection in clinical practice? Beyond the tales of a potentially beneficial infection the impact of HPg-Virus may be in understanding the pathophysiology of virus to virus- and virus to host-inter- actions rather than in a hypothetical role in clinical practice: 1. Until now it is not recommended to test HIV+ patients for their HPgV serostatus nor for HPgV replication by PCR beyond clinical studies. But some authors claim such tools for clinical practice (Battharai 2012b). HIV+ patients should be informed that – at least in adults (Tenckhoff 2012) – there is no evidence that (an artificial) HPgV infection, which happens after HIV sero- conversion will be of benefit in the course of HIV infection. It cannot be predicted whether an infection with HPgV will remain chronically replicative. Coinfections with HPgV in an in vitro model show evidence for an inhibition of HIV replication when HPgV infection occurs before HIV infection but not later (Xiang 2001). In addi- tion the substantial risks of any mucosal or parenteral inoculation with infectious materials from human sources should be considered carefully. There is no evidence to support the deferral of HCV therapy in HIV/HCV/HPgV coinfected patients, although interferon therapy can terminate chronic HPgV repli- cation. Whether DAAs may be as well active against the closely related flavivirus HPgV must be elucidated by further (in vitro)studies. Over the last two decades we have accrued some fascinating insights into possible mechanisms of HIV and HPgV inter- action and the roles that individual host factors may play. At present, HPgV gives us the opportunity to obtain insight into clinically relevant regulation pathways of HIV. This may help us develop auxiliary therapeutic concepts. These concepts may be both clinically and therapeutically promising because an additional benefit of HPgV remains evident in several studies after the initiation of ART. Ratification vote on taxonomic proposals to the International Committee on Taxonomy of Viruses. Analysis of GB virus C infection among HIV-HCV coinfected patients. GB virus C envelope protein E2 inhibits TCR- induced IL-2 production and alters IL-2-signaling pathways. J Immunol 2012b;189:2211-6 Bhattarai N, Rydze RT, Chivero ET, Stapleton JT. GB Virus C Viremia Is Associated With Higher Levels of Double- Negative T Cells and Lower T-Cell Activation in HIV-Infected Individuals Receiving Antiretroviral Therapy. J Infect Dis 2012c; 206:1469-1472 Berenguer M, Terrault NA, Piatak M, et al. Hepatitis G virus infection in patients with hepatitis C virus infection undergoing liver transplantation. GB virus C genotype 2 predominance in a hepatitis C virus/HIV infected population associated with reduced liver disease. No influence of GB virus C replication on the prognosis in a cohort of HIV-1- infected patients. Mother-to-child transmission of GB virus C in a cohort of women coinfected with GB virus C and HIV in Bangkok, Thailand. JID 2009:227-35 Bjorkman P, Flamholc L, Naucler A, Molnegren V, Wallmark E, Widell A. GB virus C during the natural course of HIV-1 infection: viremia at diagnosis does not predict mortality. Chang Q, McLinden JH, Stapleton JT, Sathar MA, Xiang J. Expression of GB virus C NS5A protein from genotypes 1, 2, 3 and 5 and a 30 aa NS5A fragment inhibit human immunodeficiency virus type 1 replication in a CD4+ T- lymphocyte cell line. Tropism of Human Pegivirus (formerly known as GB virus C/Hepatitis G virus)and host immunomodulation: insights into a highly successful viral infection. American Journal of the Medical Sciences 1893;10:487-511.

In the HIV-1 phylogeny generic 100mg kamagra oral jelly otc impotence reasons, the different subtypes coalesce to a common ancestor that probably occurred near the origin of the HIV-1 epidemic 256 CHAPTER 15 A E C G H F B D 10% Figure 15 buy kamagra oral jelly with visa erectile dysfunction 47 years old. The bar shows the length along branches corresponding to 10% diver- gence in sequence kamagra oral jelly 100 mg cheap erectile dysfunction medscape. From McCutchan (1999), with permission from Johns Hop- kins University Press. Various studies estimate that the ancestor occurred during thefirsthalf of the twentieth century (Korber et al. Comparison of HIV-1 subtypes may not be the appropriate scale at which to study the correlation between amino acid substitutions and fit- ness. The subtypes are to some extent separated geographically and may not compete directly. Even within regions, HIV-1 continues to spread to naive hosts, so escape from immune memory at a few key antibody epi- topes would not dominate the relative success of lineages. It would be interesting to see the shapes of HIV-1 phylogenies based on samples collected over several years from a single region. In the other shapes, the signal of differential success would usu- ally not be strong enough to associate particular substitutions with the survival of a lineage. However, the dominance of a single lineage as in figure 15. This corresponds to a star phylogeny when drawn as infig. Some ex- tinctions occur in this case, but many different lineages have survived to the present. Ineachtimeperiod, a single lineage gives rise to all survivors a few generations into the future. Powerful epidemics that start from just a few individuals also give rise to skewed phylogenetic trees, but the progenitors of those epidemics may simply have been lucky and may show no tendency to carry particular traits. INFLUENZA Influenza A phylogenies have just the sort of shape that could allow correlation between particular substitutions and fitness. They as- signed each variable amino acid site to zero or more of four different sets: 18 sites were positively selected with dN significantly greater than dS,16siteswereassociated with the receptor binding site of the HA1 258 CHAPTER 15 Shd5: positively selected Har3: receptor binding Sant: fastest evolving NY15: antibody epitopes Shd5 Sant Har3? Shd5 Har3 NY15 Sant NY15 * 5 nucleotide substitutions Figure 15. The tree on the left shows evolutionary relationships between isolates from subtype H3 from 1983 to 1994. The horizontal axis measures the number of nucleotide sub- stitutions between isolates, which correlates closely with time. Thus, the lower isolates come from earlier seasons, with time increasing up and to the right. The bold line shows the single lineage that succeeded through time. The asterisk shows another lineage that succeeded for about five years after its divergence from the main line, but eventually died out. See the text for a description of the labeled isolates (filled circles) and how the left tree was used to predict evolution in theupperpartofthe right tree, which contains the data from 1983 to 1994 plus three additional years from 1994 to 1997. MEASURING SELECTION 259 surface, 20 sites evolved relatively faster than the other sites, and 41 sites were in or near the well-known antibody epitope domains A and B. Suppose amino acid changes in one of thefour sets consistently cor- related with the ultimate success of a lineage. Then, at any time, one could predict which of the currently circulating isolates would be most closely related to the progenitor of future lineages. In particular, those lineages with the most amino acids that had recently changed at the key sites would be most likely to succeed. In influenza, success probably occurs by escaping the host’s immunological antibody memory caused by recent epidemics. Variant sites near key antibody epitopes would be good candidates to produce antibody escape. In other words, those sites with amino acid replacements favored by selection in the past also provided the best in- formation about which amino acid changes would lead to success in the future. Instead, they used data from 1983 to 1997 to form eleven retrospective tests. A ret- rospective test analyzed data from 1983 to year x and predicted subse- quent evolution in the years following x,wherex varied between 1986 and 1997. The bold line along the left marks the single dominant “trunk” lineage. At the question mark, just before 1994, the data can no longer resolve the trunk lineage because several variants cocirculated at thattimeandthetrunkcanberesolved only after one knows which of those lineages succeeded. The filled circles show four isolates from 1994 that represented the four classifications for variable amino acids. Shd5 (A/Shangdong/5/94) represented the lineagewiththegreatest number of recent amino acid changes at sites that had been positively selected in the past, as inferred from the 1983–1997 data. The Har3 (A/Harbin/3/94) lineage had variant amino acids near the receptor binding site. The Sant (A/Santiago/7198/ 94) lineage had variant amino acids at those sites that had evolved rap- idly in the past. The NY15 (A/New York/15/94) lineage had variant sites in or near antibody epitopes A and B. Those data show which of the 1994 lineages succeeded and which died out. Suc- cessful prediction means choosing the isolate closest on the tree (most alike genetically) with the lineagethatcontinues along the trunk and gives rise to the future population. It turned out that Shd5 was closest to the successful trunk lineage among the candidates. In other words, the most changes in previously positively selected sites predicted which lineage succeeded in subsequent years. In nine of those elevenyears,thelineage that contained the most changes relative to its ancestor at the eighteen positively se- lected sites identified the section of the tree from which the future trunk emerged. The sites in the antibody epitopes only identified seven of eleven trunk lineages, and the other amino acid sets did worse. Thus, positive selection provided the best signal for which amino acid changes correlated most closely with fitness. The epidemic strains con- tained amino acid replacements at a small number of sites that had previously been identified as crucial for escape from monoclonal anti- bodies. It would be interesting to compare these two methods in a single study of the same evolving parasite population. Substitutions at these positively selected sites correlated with the future success of MEASURING SELECTION 261 lineages during the years of sampling, 1983–1997. In the future, will these eighteen sites continue to be the primary target of selection? On the one hand, the eighteen sites may indeed be the most important for escape from protective antibodies.

All but 2 of these studies used gemfibrozil; the others used bezafibrate plus simvastatin 20 mg and fenofibrate plus pravastatin 20 mg or simvastatin 10 mg buy kamagra oral jelly 100mg with amex erectile dysfunction yoga youtube. Some of the studies did not report whether the creatine kinase elevation was symptomatic or if treatment was discontinued as a result order kamagra oral jelly 100mg on line erectile dysfunction doctors in houston tx. In 1 of the included studies purchase kamagra oral jelly 100 mg fast delivery erectile dysfunction treatment chennai, a patient tolerated the combination of pravastatin and gemfibrozil for 4 years, and then developed myopathy with clinically important elevation in creatine kinase after being switched to simvastatin. Statins used were lovastatin in 21 cases, simvastatin in 4 cases, cerivastatin in 3 cases, and atorvastatin in 1 case. Time to developing rhabdomyolysis was rapid Statins Page 68 of 128 Final Report Update 5 Drug Effectiveness Review Project (17% within 2 weeks and 93% within 12 weeks) and the onset of symptoms ranged from 36 hours to 36 weeks. No case reports of severe myopathy or rhabdomyolysis in patients receiving pravastatin or fluvastatin combined with a fibrate were found. Similarly, there were no reports of severe myopathy or rhabdomyolysis in a different trial evaluating combination of pravastatin and 280 gemfibrozil. However, cases of pravastatin or fluvastatin combined with a fibrate resulting in 218 rhabdomyolysis have been reported. First, included trials tended to exclude patients who had risk factors or comorbidities for developing adverse outcomes. Therefore, data based on these trials likely underestimate rates of adverse events in the broader population. Also, some of the included studies did not report numbers and reasons for study withdrawal and were not of the best quality. We identified 2 observational studies that found statin-fibrate combination therapy to 226, 272 have higher rates of rhabdomyolysis compared with statin monotherapy. Data collected in these studies included the time period when cerivastatin was on the market and when serious adverse events were being reported. The inclusion of cerivastatin in both studies could have inflated rates observed, so results should be considered with caution. A retrospective cohort study of 252 460 patients using claims data from 11 managed 226 health care plans found 24 cases of hospitalized rhabdomyolysis occurring during treatment. The average incidence of rhabdomyolysis requiring hospitalization was 0. When taken in combination with a fibrate, statins were associated with a higher incidence of hospitalized rhabdomyolysis of 5. The study of health plan claims data referred to above reported cases of rhabdomyolysis with the combination of a statin 226 and a fibrate. The cohort represented 7300 person-years of combined therapy with statins and fibrates (gemfibrozil or fenofibrate). There were 8 cases of rhabdomyolysis with combination therapy. There were no cases with pravastatin; fluvastatin and lovastatin were excluded from the analysis because usage was very low. Another retrospective review from the US Food and Drug Administration’s adverse events reporting system found 866 cases of rhabdomyolysis, of which 44% were related to statin- 272 gemfibrozil combination therapy and 56% with statin monotherapy. Almost half of the monotherapy cases and about 75% of combination therapy cases were believed to be from cerivastatin. When individual statins were stratified based on mono-or combination therapy, the crude reporting rates for rhabdomyolysis per an estimated 100 000 prescriptions over marketing years (1988-July 2001) was higher with statin-gemfibrozil combinations than statin monotherapy. The crude reporting rates for combination compared with monotherapy were: lovastatin (2. In addition to the above observational studies, we found 2 retrospective reviews using the US Food and Drug Administration’s adverse event reporting system to compare rates of 275, 276 rhabdomyolysis between statin-fenofibrate and statin-gemfibrozil combination therapies. Both studies found fewer reports or lower rates of rhabdomyolysis associated with statin- 276 fenofibrate use than statin-gemfibrozil use. The number of cases reported in the Jones study Statins Page 69 of 128 Final Report Update 5 Drug Effectiveness Review Project for statin-fenofibrate compared with statin-gemfibrozil was 0. Since data from the US Food and Drug Administration database are dependent on volunteer reports of adverse events, rates may be an underestimation of “actual” events for either combination therapies and results should be considered carefully. Of the 12 publications that reported harms associated with statin-fibrate therapy, the 273, 274, 277 remaining publications showed variable rates of elevated liver transaminase or creatine kinase elevations with combination statin-fibrate usage compared with placebo, statin, or fibrate monotherapies. The evidence base was limited and results should be interpreted carefully. A pooled analysis evaluated the frequency of creatine kinase elevations in Novartis- 274 funded trials in which fluvastatin was administered in combination with fibrates. Of 1017 patients treated with combination therapy, 493 received bezafibrate, 158 fenofibrate, and 366 gemfibrozil. Results were not reported separately by type of fibrate. There were no significant differences in the frequency of creatine kinase elevations among the group on combination therapy and patients taking placebo, fibrates only, or fluvastatin only. Similarly, there were no large differences in liver function tests or creatine kinase levels found between the atorvastatin-fenofibrate treatment 273, group and atorvastatin or fenofibrate monotherapy groups in 2 short-term (8-16 week) studies. A prospective observational cohort study followed 252 patients who were prescribed a statin combined with gemfibrozil for a mean of 2. Creatine kinase levels, aminotransferase levels, and any reports of muscle soreness or weakness were monitored. One presumed case of myositis occurred in a patient who took simvastatin for 1 year. The patient had previously taken pravastatin combination therapy for 4 years without incident. An asymptomatic 5-fold rise in alanine aminotransferase was observed in 1 patient, and 2 other patients had an alanine aminotransferase elevation between 2 and 3 times the upper limit of normal. The statin involved in these cases is not specified. Because of the nature of adverse effect reporting and the available evidence, whether one statin is safer than the other with regard to combination therapy with fibrates is still unclear. The US Food and Drug Administration has approved the following recommendations when combining fibric acid derivatives or niacin with a statin: • Atorvastatin: Weigh the potential benefits and risks and closely monitor patients on combined therapy. Statins Page 70 of 128 Final Report Update 5 Drug Effectiveness Review Project • Rosuvastatin: Avoid the combination with fibrates unless the benefit outweighs the risk and limit doses to 10 mg if combined with gemfibrozil. In the systematic review by Shek in 2001, 8 patients in 3 of the 36 included studies discontinued the combination therapy due to significant elevation in liver transaminases (alanine aminotransferase and aspartate aminotransferase). In most of the other studies, there were only reports of subclinical (<3 times the upper limit of normal) elevation in alanine aminotransferase or aspartate aminotransferase. Conclusions regarding the safety of different statins in the liver were not made.

Effectiveness outcomes: Outcomes that are generally important to patients and caregivers buy kamagra oral jelly 100mg free shipping erectile dysfunction treatment penile implants, such as quality of life kamagra oral jelly 100 mg without a prescription erectile dysfunction rap, responder rates discount kamagra oral jelly 100 mg on-line erectile dysfunction liver, number and length of hospitalizations, and ability to work. Data on effectiveness outcomes usually comes from longer-term studies of a “real-world” population. Effect size/estimate of effect: The amount of change in a condition or symptom because of a treatment (compared to not receiving the treatment). It is commonly expressed as a risk ratio (relative risk), odds ratio, or difference in risk. Efficacy: The extent to which an intervention produces a beneficial result under ideal conditions in a selected and controlled population. DRIs, AIIRAs, and ACE-Is Page 119 of 144 Final Report Drug Effectiveness Review Project Equivalence level: The amount which an outcome from two treatments can differ but still be considered equivalent, as in an equivalence trial, or the amount which an outcome from treatment A can be worse than that of treatment B but still be considered noninferior, as in a noninferiority trial. Equivalence trial: A trial designed to determine whether the response to two or more treatments differs by an amount that is clinically unimportant. This lack of clinical importance is usually demonstrated by showing that the true treatment difference is likely to lie between a lower and an upper equivalence level of clinically acceptable differences. Exclusion criteria: The criteria, or standards, set out before a study or review. Exclusion criteria are used to determine whether a person should participate in a research study or whether an individual study should be excluded in a systematic review. Exclusion criteria may include age, previous treatments, and other medical conditions. External validity: The extent to which results provide a correct basis for generalizations to other circumstances. For instance, a meta-analysis of trials of elderly patients may not be generalizable to children. Fixed-effect model: A model that calculates a pooled estimate using the assumption that all observed variation between studies is due to by chance. Studies are assumed to be measuring the same overall effect. Fixed-dose combination product: A formulation of two or more active ingredients combined in a single dosage form available in certain fixed doses. Forest plot: A graphical representation of the individual results of each study included in a meta- analysis and the combined result of the meta-analysis. The plot allows viewers to see the heterogeneity among the results of the studies. The results of individual studies are shown as squares centered on each study’s point estimate. A horizontal line runs through each square to show each study’s confidence interval—usually, but not always, a 95% confidence interval. The overall estimate from the meta-analysis and its confidence interval are represented as a diamond. The center of the diamond is at the pooled point estimate, and its horizontal tips show the confidence interval. Funnel plot: A graphical display of some measure of study precision plotted against effect size that can be used to investigate whether there is a link between study size and treatment effect. Half- life: The time it takes for the plasma concentration or the amount of drug in the body to be reduced by 50%. Harms: See Adverse Event DRIs, AIIRAs, and ACE-Is Page 120 of 144 Final Report Drug Effectiveness Review Project Hazard ratio: The increased risk with which one group is likely to experience an outcome of interest. For example, if the hazard ratio for death for a treatment is 0. Head-to-head trial: A trial that directly compares one drug in a particular class or group with another in the same class or group. Health outcome: The result of a particular health care practice or intervention, including the ability to function and feelings of well-being. For individuals with chronic conditions – where cure is not always possible – results include health-related quality of life as well as mortality. Heterogeneity: The variation in, or diversity of, participants, interventions, and measurement of outcomes across a set of studies. I2: A measure of statistical heterogeneity of the estimates of effect from studies. I2 is the proportion of total variability across studies that is due to heterogeneity and not chance. It is calculated as (Q-(n- 1))/Q, where n is the number of studies. Incidence: The number of new occurrences of something in a population over a particular period of time, e. Indication: A term describing a valid reason to use a certain test, medication, procedure, or surgery. In the United States, indications for medications are strictly regulated by the Food and Drug Administration, which includes them in the package insert under the phrase "Indications and Usage". Indirect analysis: The practice of using data from trials comparing one drug in a particular class or group with another drug outside of that class or group or with placebo and attempting to draw conclusions about the comparative effectiveness of drugs within a class or group based on that data. For example, direct comparisons between drugs A and B and between drugs B and C can be used to make an indirect comparison between drugs A and C. Intention to treat: The use of data from a randomized controlled trial in which data from all randomized patients are accounted for in the final results. Trials often incorrectly report results as being based on intention to treat despite the fact that some patients are excluded from the analysis. Internal validity: The extent to which the design and conduct of a study are likely to have prevented bias. Generally, the higher the interval validity, the better the quality of the study publication. Inter-rater reliability: The degree of stability exhibited when a measurement is repeated under identical conditions by different raters. Intermediate outcome: An outcome not of direct practical importance but believed to reflect outcomes that are important. For example, blood pressure is not directly important to patients but DRIs, AIIRAs, and ACE-Is Page 121 of 144 Final Report Drug Effectiveness Review Project it is often used as an outcome in clinical trials because it is a risk factor for stroke and myocardial infarction (hear attack). Masking: See Blinding Mean difference: A method used to combine measures on continuous scales (such as weight) where the mean, standard deviation, and sample size are known for each group. Meta-analysis: The use of statistical techniques in a systematic review to integrate the results of included studies. Although the terms are sometimes used interchangeably, meta-analysis is not synonymous with systematic review. However, systematic reviews often include meta-analyses. Meta-regression: A technique used to explore the relationship between study characteristics (for example, baseline risk, concealment of allocation, timing of the intervention) and study results (the magnitude of effect observed in each study) in a systematic review. Mixed treatment comparison meta analysis: A meta-analytic technique that simultaneously compares multiple treatments (typical 3 or more) using both direct and indirect evidence. The multiple treatments form a network of treatment comparisons.

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