Posts filed under ‘HIV/SIDA Trastornos Oseos’

2016 BHIVA GUIDELINES for the treatment of HIV-1-positive Adults with antiretroviral therapy

The British HIV Association

Writing Group

Laura Waters (Chair)

N Ahmed, B Angus, M Boffito, M Bower, D Churchill, D Dunn, S Edwards, C Emerson, S Fidler, †M Fisher, R Horne, S Khoo, C Leen, N Mackie, N Marshall, F Monteiro, M Nelson, C Orkin, A Palfreeman, S Pett, A Phillips, F Post, A Pozniak, I Reeves, C Sabin, R Trevelion, J Walsh, E Wilkins, I Williams, A Winston

†Professor Martin Fisher died in April 2015 – he made a significant contribution to these, many other guidelines and our speciality as a whole – he is greatly missed.


The overall purpose of these guidelines is to provide guidance on best clinical practice in the treatment and management of adults with HIV infection on antiretroviral therapy (ART).

The scope includes: (i) guidance on the initiation of ART in those previously naïve to therapy; (ii) support of people living with HIV (PLWH) on treatment; (iii) management of individuals experiencing virological failure; and (iv) recommendations in specific populations where other factors need to be taken into consideration.

The guidelines are aimed at clinical professionals directly involved with and responsible for the care of adults with HIV infection, and at community advocates responsible for promoting the best interests and care of HIV-positive adults. They should be read in conjunction with other published BHIVA guidelines.

The 2016 interim update to the 2015 BHIVA antiretroviral guidelines has been published online to include tenofovir-alafenamide/emtricitabine as a preferred NRTI backbone for first-line therapy. Changes were based on new data and the consensus opinion of the writing committee. All changes to the guideline are highlighted and include updates to the chronic kidney disease and bone disease sections of special populations and some small changes to managing virological failure. The next formal update to the guidelines in anticipated in 2017.



December 3, 2016 at 9:33 am

Human Immunodeficiency Virus and Total Joint Arthroplasty: The Risk for Infection Is Reduced

Journal of Arthroplasty October 2016 V.31 N.10 P.2146–2151

Mohammad Ali Enayatollahi, Dermot Murphy, Mitchell G. Maltenfort, Javad Parvizi


Highly active antiretroviral therapy (HAART) has changed the face of human immunodeficiency virus (HIV) and allowed patients to live for many decades. HIV and HAART are known risk factors for osteonecrosis of bone, osteopenia, and osteoporosis. Therefore, the demand for total joint arthroplasty (TJA) in HIV-infected patients is on the rise. We attempted to determine whether modern treatments for HIV have impacted the rate of periprosthetic joint infection (PJI).


Conducting a systematic review, 25 studies with a total of 722 TJAs were identified. We extracted data on rates of PJI after primary TJA in HIV-infected patients with and without hemophilia and data on administration of HAART at the time of arthroplasty.


Three hundred eighty-one TJAs were performed in 293 patients with HIV infection without hemophilia. The follow-up ranged between 1.5 months and 11 years. Nine patients developed PJI. In patients with both HIV and hemophilia, 341 primary TJAs were performed. Forty-five received treatment for PJI. Follow-up ranged between 1 year and 26 years. Rates of PJI were 2.28% and 10.98% for HIV-only patients and patients with HIV and hemophilia, respectively. This difference was statistically significant (P < .0001) with a 5.28 odds ratio for hemophilia. HAART was associated with fewer infections overall (odds ratio, 0.12).


The rates of PJI after TJA in HIV-only patients are lower than those in patients with both HIV and hemophilia. Treatment of patients with HAART and optimization of underlying comorbidities appears to lower the rate of PJI in this patient population.



November 2, 2016 at 12:48 pm

Hepatitis C virus coinfection as a risk factor for osteoporosis and fracture

Current Opinion In HIV and AIDS May 2016 V.11 N.3 P.285–293

Bedimo, Roger; Maalouf, Naim M.; Re, Vincent Lo III

aInfectious Diseases Section, Medical Service, Veterans Affairs North Texas Healthcare System

bDivision of Infectious Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center

cEndocrine Section, Medical Service, Veterans Affairs North Texas Healthcare System

dDivision of Mineral Metabolism, Department of Internal Medicine, and the Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas

eDivision of Infectious Diseases, Department of Medicine

fDepartment of Biostatistics and Epidemiology, Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA

Purpose of review

With increased survival of HIV-infected patients, osteoporotic fractures have developed as a major cause of morbidity in these patients, and chronic hepatitis C virus (HCV) coinfection has emerged as a significant contributor to this increased fracture risk. The present article reviews the epidemiologic and clinical evidence for osteoporosis and increased fracture risk among HIV/HCV coinfected patients, and potential mechanisms for these outcomes with HCV coinfection.

Recent findings

Epidemiologic studies suggest that HIV/HCV coinfected patients exhibit a three-fold increased fracture incidence compared with uninfected controls, and 1.2–2.4-fold increased fracture risk compared with HIV monoinfected patients. Recent reports suggest that chronic HCV coinfection is independently associated with reduced bone mineral density in HIV, but that it is not associated with significantly increased bone turnover. The deleterious impact of chronic HCV on BMD and fracture risk occurs even in the absence of advanced liver fibrosis or cirrhosis. New tools to assess bone quality, including the trabecular bone score, high-resolution peripheral quantitative computed tomography, and in-vivo microindentation, may help improve understanding of the mechanisms of HCV-associated skeletal fragility. The impact of approved antiosteoporosis medications and direct-acting antivirals for the treatment of chronic HCV infection on patients’ bone health remain to be studied.


Chronic HCV infection is an independent risk factor for osteoporosis and fractures among HIV-infected patients, even before the development of cirrhosis. The underlying mechanisms are being unraveled, but major questions persist regarding the optimal evaluation and management of bone health in HIV/HCV coinfected patients.




August 2, 2016 at 1:24 pm

The protease inhibitors and HIV-associated bone loss

Current Opinion In HIV and AIDS May 2016 V.11 N.3 P. 333–342

Moran, Caitlin A.; Weitzmann, M. Neale; Ofotokun, Ighovwerha

aDepartment of Medicine, Division of Infectious Diseases, Emory University School of Medicine

bGrady Healthcare System, Atlanta

cDepartment of Medicine, Division of Endocrinology, Metabolism & Lipids, Emory University School of Medicine, Atlanta

dAtlanta Department of Veterans Affairs Medical Center, Decatur, Georgia, USA

Purpose of review

HIV infection is an established risk factor for osteoporosis and bone fracture. Combination antiretroviral therapy (cART) increases bone resorption leading to an additional 2–6% bone mineral density (BMD) loss within the first 1–2 years of therapy. Although tenofovir disoproxil fumarate is often blamed for antiretroviral drug-associated bone loss, evidence abounds to suggest that other agents, including the protease inhibitors (PIs), have adverse bone effects. In the current review, we examine bone loss associated with protease inhibitor use, describing the relative magnitude of bone loss reported for individual protease inhibitors. We also review the potential mechanisms associated with protease inhibitor-induced bone loss.

Recent findings

As a class, protease inhibitors contribute to a greater degree of bone loss than other anchor drugs. HIV disease reversal and the associated immune reconstitution following cART initiation play an important role in protease inhibitor-mediated bone loss in addition to plausible direct effects of protease inhibitors on bone cells.


Protease inhibitors remain an important component of cART despite their adverse effects on bone. A better understanding of factors that drive HIV/cART-induced bone loss is needed to stem the rising rate of fracture in the HIV-infected population.



August 2, 2016 at 8:22 am

Tenofovir and bone health

Current Opinion In HIV and AIDS May 2016 V.11 N.3 P.326–332

Grant, Philip M.; Cotter, Aoife G.

aDivision of Infectious Diseases; Department of Medicine; Stanford University, Palo Alto, CA, USA

bHIV Molecular Research Group, School of Medicine & Medical Science, University College Dublin

cDepartment of Infectious Diseases, Mater Misericordiae University Hospital, Dublin, Ireland

Purpose of review

With continued improvements to the antiviral efficacy and tolerability of antiretroviral therapy, long-term safety of antiretroviral therapy has become paramount. Low bone mineral density and fragility fractures are more common in HIV-infected individuals than in the general population. The aims of this review are to describe potential mechanisms underlying the adverse effects of tenofovir on bone, clinical studies of tenofovir disoproxil fumarate (TDF) and bone, and more recent bone data on tenofovir alafenamide.

Recent finding

Several studies have demonstrated an approximately 1–3% greater bone mineral density loss with TDF compared with other agents. Recent studies with tenofovir alafenamide have shown improved bone (and renal) safety with similar virologic efficacy when compared to TDF.


Given these findings, TDF-containing regimens may be gradually replaced with non-TDF containing regimens for the treatment of HIV infection, especially in those at higher risk for fragility fracture.



August 2, 2016 at 8:21 am

Which HIV patients should be screened for osteoporosis: an international perspective

Current Opinion In HIV and AIDS May 2016 V.11 N.3 P.268–276

Alvarez, Elena; Belloso, Waldo H.; Boyd, Mark A

aHIV Molecular Research Group, School of Medicine, University College Dublin, Dublin, Ireland

bInfectious Diseases and Clinical Pharmacology Sections, Internal Medicine Service, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina

cThe Kirby Institute for Infection and Immunity in Society, University of New South Wales, Sydney, Australia

dSchool of Medicine, Hacettepe University, Ankara, Turkey

eDepartment of Infectious Diseases at Peking Union Medical College Hospital, Beijing, China

fInfectious Diseases Institute (IDI) HIV outpatient clinic at Mulago Hospital Complex, Makerere University College of Health Sciences, Kampala, Uganda

gMoscow Regional AIDS Centre, Moscow, Russia

hInfectious Diseases Unit Hospital Clinic – Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain

iICH Study Center, Hamburg, Germany

jToronto General Research Institute (TGRI), University Health Network (NHN), Toronto General Hospital, Toronto, Canada

kDivision of Endocrinology, Diabetes & Metabolism, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

lMater Misericordiae University Hospital, Department of Infectious Diseases, Dublin, Ireland

Purpose of review

This review provides international insights into the real-world clinical approach to screening for bone mineral density (BMD) and osteoporosis in people living with HIV (PLWH) using opinions from HIV physicians from key regions around the world.

Recent findings

Although a significant proportion of PLWH are aged over 50, the relative importance of low BMD to clinical care differs significantly between countries and regions, based on factors such as the population at risk, access to adequate screening resources, and physicians’ knowledge. Generally, management of osteoporosis in PLWH follows similar principals as for the general population, with risk factors for fracture combined with measurement of BMD by dual energy X-ray absorptiometry in algorithms such as Fracture Risk Assessment Tool, designed to provide an overall risk estimation. Although in most regions age is considered among the most important factors contributing to low BMD and fractures, considerable country and region-specific factors become apparent, such as malnutrition, inactivity and impact of comorbidities, substance abuse, and increasing use of tenofovir disoproxil fumarate.


These opinions highlight the diversity that still exists in the approach to the long-term management of PLWH and highlight challenges facing development of consensus guidelines that can be effectively implemented worldwide.



July 31, 2016 at 9:33 pm

How to predict the risk of fracture in HIV?

Current Opinion In HIV and AIDS May 2016 V.11 N.3 P.261–267

Yin, Michael T.; Falutz, Julian

aDivision of Infectious Diseases, Columbia University Medical Center, New York, New York, USA

bChronic Viral Illness Service, Division of Infectious Diseases, McGill University Health Center, Montreal, Quebec, Canada

Purpose of review

Skeletal fractures are more common in HIV, and impact the medical, functional and economic status of frequently vulnerable patients. Identifying asymptomatic patients with low bone mineral density (BMD)/osteoporosis requiring intervention can be expected to reduce fracture risk and complications. Clinical tools are available to determine fracture risk in the general population and are being evaluated in HIV patients. The FRAX® calculator, incorporating demographics and risk factors for osteoporosis, with or without BMD results, has been investigated most often in HIV patients.

Recent findings

The few published studies that have calculated the 10-year FRAX® risk for both major osteoporosis and hip fractures without BMD generally show limited precision in predicting the presence of osteoporosis severe enough to initiate treatment. It remains uncertain whether using HIV as a secondary risk factor and adding dual X-ray absorptiometry (DXA)-BMD information improves case-finding compared with using DXA results only. Not incorporating risks relevant to aging HIV patients such as antiretroviral exposure, hepatitis C virus coinfection and history of falls is other potential limitation.


Accurate screening tools using clinical risk factors alone to determine fracture risk in HIV are not yet available. Further research and validation studies are necessary.



July 31, 2016 at 9:32 pm

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