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Morrissette DL purchase generic suhagra on-line erectile dysfunction statistics 2014, Skinner MH order suhagra in united states online impotence your 20s, Hoffman BB cheap suhagra 100mg online erectile dysfunction injection therapy, Levine RE cheap suhagra 100mg free shipping impotence icd 9, Davidson JM. Effects of antihypertensive drugs atenolol and nifedipine on sexual function in older men: a placebo-controlled, crossover study. Comparative effects of pindolol and hydrochlorothiazide in black hypertensive patients. Mulcahy D, Crake T, Crean P, Keegan J, Wright C, Fox KM. Therapeutic implications of dynamic coronary stenosis in patients with single vessel coronary artery disease. Nifedipine versus propranolol treatment for unstable angina in the elderly. Double-blind study with propranolol and LB-46 in angina pectoris. Prospective randomized comparison of antiarrhythmic therapy versus first- line radiofrequency ablation in patients with atrial flutter. 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Pahor M, Psaty BM, Alderman MH, Applegate WB, Williamson JD, Furberg CD. Therapeutic benefits of ACE inhibitors and other antihypertensive drugs in patients with type 2 diabetes. Diuretic-based treatment and cardiovascular events in patients with mild renal dysfunction enrolled in the systolic hypertension in the elderly program. Palmer AJ, Fletcher AE, Rudge PJ, Andrews CD, Callaghan TS, Bulpitt CJ. Quality of life in hypertensives treated with atenolol or captopril: a double-blind crossover trial. Effects of diltiazem, metoprolol, enalapril and hydrochlorothiazide on frequency of ventricular premature complexes. The effects of replacing beta-blockers with an angiotensin converting enzyme inhibitor on the quality of life of hypertensive patients. Beta blockers Page 113 of 122 Final Report Update 4 Drug Effectiveness Review Project 323. Parikka H, Toivonen L, Heikkila L, Virtanen K, Jarvinen A. Comparison of sotalol and metoprolol in the prevention of atrial fibrillation after coronary artery bypass surgery. Pasta L, Pagliaro L, SImonetti R, Maringhini A, Marceno M, al. Propranolol for prevention of upper GI rebleeding in cirrhosis. Beta blockade to prevent atrial dysrhythmias following coronary bypass surgery. The problems of morbidity and therapy in borderline hypertension. Schweizerische Medizinische Wochenschrift Journal Suisse de Medecine. Penzien DB, Holroyd K, Cordingley G, Wagner M, Jackson B. Propranolol in the treatment of migraine headache: a meta-analytic review of the research literature. Perez V, Puiigdemont D, Gilaberte I, Alvarez E, Artigas F, Grup de Recerca en Trastorns A. Efficacy and safety of atenolol, enalapril, and isradipine in elderly hypertensive women. Effects of beta receptor antagonists on left ventricular function in patients with clinical evidence of heart failure after myocardial infarction. A double-blind comparison of metoprolol and xamoterol. Effects of beta receptor antagonists in patients with clinical evidence of heart failure after myocardial infarction: double blind comparison of metoprolol and xamoterol. Reduction of enzyme levels by propranolol after acute myocardial infarction. A comparison of a hydrochlorothiazide plus triamterene combination (Dyazide) and atenolol in the treatment of patients with mild hypertension: a multicentre study in general practice. Pomier-Layrargues G, Villeneuve JP, Willems B, Huet PM, Marleau D. Systemic and hepatic hemodynamics after variceal hemorrhage: effects of propranolol and placebo. Portegies MCM, Brouwer J, Van de Ven LLM, Viersma JW, Lie KI. Effects of bisoprolol and isosorbide dinitrate on the circadian distribution of myocardial ischemia. Current Therapeutic Research, Clinical & Experimental. Blood pressure and mood responses in hypertensive patients on antihypertensive medications. Journal of the American Academy of Nurse Practitioners. Beta blockers Page 114 of 122 Final Report Update 4 Drug Effectiveness Review Project 339. Poulter NR, Sanderson JE, Thompson AV, Sever PS, Chang CL. Comparison of nifedipine and propranolol as second line agent for hypertension in black Kenyans. Low-dose combination therapy as first-line hypertension treatment for blacks and nonblacks. The Systolic Hypertension in the Elderly Program (SHEP): an intervention trial on isolated systolic hypertension. Clinical & Experimental Hypertension - Part A, Theory & Practice. The influence of atenolol and propafenone on QT interval dispersion in patients 3 months after myocardial infarction. International Journal of Clinical Pharmacology & Therapeutics. Effect of partial agonist activity in beta blockers in severe angina pectoris: a double blind comparison of pindolol and atenolol. The prophylactic value of propranolol in angina pectoris. Radevski IV, Valtchanova SP, Candy GP, Tshele EF, Sareli P. Comparison of acebutolol with and without hydrochlorothiazide versus carvedilol with and without hydrochlorothiazide in black patients with mild to moderate systemic hypertension. Calcium blockers and beta blockers: alone and in combination. A double-blind comparison of a beta- blocker and a potassium channel opener in exercise induced angina. Rainwater J, Steele P, Kirch D, LeFree M, Jensen D, Vogel R. Effect of propranolol on myocardial perfusion images and exercise ejection fraction in men with coronary artery disease.
The FA justify the broad use of this regimen outside of clinical trials purchase suhagra 100 mg amex erectile dysfunction fix. Infusion reactions (fever discount 100mg suhagra erectile dysfunction drugs over the counter canada, chills order suhagra line erectile dysfunction systems, and skin reactions) occurred primarily during the ﬁrst infusions of alemtu- An alternative idea was to replace ﬂudarabine in the FCR regimen zumab and were mild in the majority of patients buy suhagra overnight erectile dysfunction in a young male. Although 80% of with pentostatin (PCR) to reduce myelotoxicity. In a phase 3 patients were CMV IgG-positive before treatment, there were only 2 randomized trial comparing FCR with PCR in previously untreated subclinical CMV reactivations. The primary grade 3/4 hematologi- or minimally treated CLL patients, there were no statistical differ- cal events were transient, including leukocytopenia (44%) and ences between treatments in OS or response rates. Stable CD4 T-cell counts ( 200/ l) trial did not demonstrate a lower infection rate with PCR. Bendamustine has been also combined with rituximab (BR) in 81 Two phase 3 trials tested alemtuzumab in combination with FC patients with relapsed CLL. One trial comparing FCA with FCR in bendamustine on days 1 and 2 and 375 mg/m2 of rituximab on day 0 frontline therapy was closed prematurely due to the higher toxicity 140 American Society of Hematology and treatment-related mortality observed in the FCA arm. The recent results obtained with single-agent ibrutinib in therapeutic efﬁcacy of FCR was clearly superior to FCA. In this refractory or relapsed patients with a del(17p) showed an ORR of trial, alemtuzumab was given subcutaneously. A second random- 68%, with a PFS at 26 months of 57% and an OS of 70%. FA (n 168) resulted in better PFS stem cell transplantation should still be offered and discussed in than ﬂudarabine monotherapy (n 167; median 23. Adverse events occurred in 161 (98%) of 164 patients in the frontline treatment may be repeated if the duration of the ﬁrst FA group and 149 (90%) of 165 in the ﬂudarabine alone group. The choice becomes more difﬁcult and limited in grade 1 or 2 infusion-related adverse reactions (62% vs 13%). Major treatment-refractory CLL, in patients relapsing within 24 months of grade 3 or 4 toxicities in the FA and monotherapy groups were treatment, or in patients with the chromosomal aberration del(17p). The following (59% vs 68%), thrombocytopenia (11% vs 17%), and anemia (9% options exist as a relapse therapy for patients no longer responding vs 17%). The incidence of serious adverse events was higher in the to chemoimmunotherapy with rituximab: (1) alemtuzumab alone or FA group (33% vs 25%); deaths due to adverse events were similar in combinations, in particular with high-dose steroids26,51,54; (2) com- between the 2 groups (6% vs 12%). The combination of alemtuzumab and methylprednisolone was tested in the UK CLL206 The choice of one of these options depends on the ﬁtness of the trial on 17 untreated and 22 previously treated patients with patient, the availability of some drugs, and the prognostic risk of the del(17p). The ORR and CR rate were 85% and 36% in the whole leukemia as deﬁned by molecular cytogenetics. According to cohort and 88% and 65% in treatment naive patient group, recommendations of a European Group for Blood and Marrow respectively. Some of the new Given the impressive number of novel drugs, the right choice of drugs, in particular ibrutinib or ABT-199, show good responses in treatment for a given CLL patient has become a task that requires these patients and could become an additional option in the very experience, a good clinical assessment of the patient, and an near future. The following parameters should be considered before recommending a treatment for CLL56: New drugs targeting pathogenic pathways of CLL (1) the clinical stage of disease, (2) the ﬁtness of the patient, (3) the cells genetic risk of the leukemia, and (4) the treatment situation (front- There are an increasing number of interesting new compounds in line vs second-line, response vs nonresponse of the last treatment). With the use of these 4 parameters, the following recommendations The common denominator of these compounds is that their mecha- can be given (Figure 1A,B): nism of action targets a relatively speciﬁc signaling abnormality or redirects the immune system against CLL cells. A detailed descrip- Frontline treatment (Figure 1A). In a patient with advanced tion of these fascinating agents is beyond the scope of this article. In this situation, patients need to be evaluated of clinical development and shows that these agents may yield high for their physical condition (or comorbidity). For patients in good response rates above 50% even in relapsed and refractory CLL physical condition (“go go”), as deﬁned by a normal creatinine patients. Some of these agents (eg, obinutuzumab, CART19, clearance and a low score at the “cumulative illness rating scale” 57 ABT-199, idelalisib, and ibrutinib) currently elicit the greatest (CIRS), patients should be offered chemoimmunotherapies such enthusiasm and hope both among CLL patients and their treating as FCR or FR to achieve sustained remissions. Patients with a somewhat impaired physical condition (“slow go”) may be offered either CLB in combination with an anti-CD20 New anti-CD20 antibodies antibody42 or a dose-reduced ﬂudarabine-containing regimen with a Obinutuzumab (GA101). The aim of therapy in this situation is symptom monoclonal antibody obinutuzumab showed impressive results in control. In general, these regimens all yield cellular cytotoxicity, low complement-dependent cytotoxicity activ- response rates above 50%, but the TTP tends to be shorter than 2 ity, and increased direct cell death induction. Treatment algorithm for CLL patients in frontline (A) and second-line (B) indications. Al indicates alemtuzumab; R, rituximab; O, ofatumumab; F, ﬂudarabine; C, cyclophosphamide; Mab, monoclonal antibody; Dex, dexamethasone; and Allo-SCT, allogeneic stem cell transplantation. Please note that performing an allogeneic transplantation usually requires the induction of a PR or CR before the procedure. Major side effects included infections, neutropenia, thrombocytope- Results of a planned interim analysis of the CLL11 trial have been nia, and tumor lysis syndrome, all of which resolved. There were no recently reported and conﬁrmed the very promising activity of dose-limiting toxicities. Encouraging results were reported in the obinutuzumab in CLL. Infusion-related reactions occurred in 5 patients, Idelalisib (CAL-101). Class I PI3Ks regulate cellular functions but were mild. All (PI3K ) is restricted to cells of hematopoietic origin, where it plays subjects completed therapy. CRs were documented in 2 patients and a key role in B-cell proliferation and survival. After a median follow-up of 23 months from start of pathway is constitutively activated and dependent on PI3K. Targeting of BCR signaling as a therapeutic strategy in CLL. Red symbols and letters indicate new therapeutics as discussed in the text. CAL-101 is an oral PI3K isoform–selective inhibitor that promotes ibrutinib on 85 patients with relapsed or refractory CLL or small apoptosis in primary CLL cells in a time- and dose-dependent lymphocytic lymphoma, the majority of whom had high-risk manner without inducing apoptosis in normal T cells or natural disease, were published recently. CAL-101 inhibits CLL cell chemotaxis toward CXCL12 (predominantly grade 1 or 2) and included transient diarrhea, and CXCL13 and migration beneath stromal cells (pseudoemperip- fatigue, and upper respiratory tract infection. CAL-101 also down-regulates the secretion of chemokines the majority being PRs (68%). Most interestingly, the response was in stromal cocultures and after BCR triggering. At 26 inhibits BCR- and chemokine-receptor-induced AKT and MAP months, the estimated PFS rate was 75% and the OS rate was 83%. In a phase 1 clinical trial in 54 heavily pretreated and high-risk CLL patients, idelalisib showed acceptable toxicity, positive pharmacody- Bcl-2 inhibitors namic effects, and favorable clinical activity (ie, a high level of Proteins in the B-cell CLL/lymphoma 2 (Bcl-2) family are key lymph node regression and prolonged duration of symptomatic regulators of the apoptotic process. Of the 28 patients with PRs, 6 showed persistent lymphocyto- the latter is an established mechanism whereby cancer cells evade sis. The majority of patients (81%) showed a lymph node response apoptosis. Bcl-2, the founding member of this protein family, is ( 50% reduction in the nodal sum of the product of greatest encoded by the BCL2 gene, which was initially described in diameter). Side effects were mild, with follicular lymphoma as a protein in translocations involving chromo- fatigue, diarrhea, pyrexia, rash, and upper respiratory tract infec- somes 14 and 18. More importantly, there were no dose-limiting toxicities. Results on idelalisib in combination with Bcl-2 inhibitors ABT-263 (Navitoclax) and ABT-199. ABT- rituximab, ofatumumab, or bendamustine/rituximab were presented 263 is a small-molecule Bcl-2 family protein inhibitor that binds in preliminary form and showed encouraging results. For example, a with high afﬁnity (Ki 1 nM) to multiple antiapoptotic Bcl-2 trial using a combination of idelalisib and rituximab as a frontline family proteins, including Bcl-XL, Bcl-2, Bcl-w, and Bcl-B, and has therapy in 64 patients yielded an ORR of 97% with 19% CRs. Initial studies showed very promising effects were mild, with 23% diarrheas as the only relevant CTC results for this drug as a single agent. Therefore, the compound was reengineered to Ibrutinib (formerly called PCI-32765). BTK leads to down- create a highly potent, orally bioavailable, and Bcl-2-selective stream activation of cell survival pathways such as NF- B and inhibitor, ABT-199. A single dose molecule inhibiting BTK that plays a role in the signal transduction of ABT-199 in 3 patients with refractory CLL resulted in tumor of the BCR. Inhibition of BTK might induce apoptosis in B-cell lysis within 24 hours. ABT-199 yielded an ORR of Hematology 2013 143 144 American Society of Hematology 85%, with 13% CRs and 72% PRs. Interestingly, 88% and 75% of leukapheresis were transduced with a lentivirus encoding anti-CD19 patients with a del(17p) and F-refractory CLL, respectively, achieved scFv linked to 4-1BB and CD3-z signaling domains. These data indicate that selective pharmacological T cells were expanded and activated ex vivo by exposure to inhibition of Bcl-2 holds great promise for the treatment of CLL. Ten patients have received CART19 cells; 9 adults of median age 65 years (range, 51-78) were treated for relapsed, refractory CLL and 1 7-year-old was treated for relapsed Immunomodulatory drugs refractory acute lymphoblastic leukemia (ALL). Lenalidomide has shown encouraging results in 76 patients had a deletion of the p53 gene. All CLL patients received the treatment of high-risk patients, including carriers of a del(17p).
The latent reservoirs At this point in time order 100mg suhagra with visa erectile dysfunction vitamin b12, eradication of HIV buy suhagra 100 mg fast delivery erectile dysfunction shake drink, the removal of all HIV from the body purchase suhagra 100mg free shipping valium causes erectile dysfunction, is a theoretical goal order suhagra 100 mg impotence only with wife. The main reason is that latently HIV-infected cells comprise a life- long reservoir (Saksena 2003). Even after years of suppression, viral transcription can be detected (Finzi 1999, Furtado 1999, Sigal 2011). This is particularly true in blood cells, but also in the lymph nodes and in sperm (Lafeuillade 2001, Nunnari 2002), where HIV may persist hiding from immune recognition (Fukazawa 2015). Replication also takes place in cells of the gastrointestinal tract, even if no virus is detected in the blood. Even after myoablative chemotherapy and autologous stem cell transplantation, latent reservoirs persist (Cillo 2013). After stopping ART in such patients, a rebound is seen rapidly (Henrich 2013+2014), and possibly occurs at multiple sites (Rothenberger 2015). In addition, latently infected reservoirs consist of very heterogenic cell populations, among the T memory and stem cells (Buzon 2014). The stability of these cells is probably independent of residual virus replication. Theoretically, how long does it take until the last latently infected cells are removed? The calculated time to eradication of these reservoirs was 73. Even in patients with no measurable blips during at least three years of stable ART and with a tendency for a more rapid decrease of viral load, the time to eradication was 51. Virus in resting CD4 memory cells with minimal evolution persists, even after close to 9 years on ART (Nottet 2009). Moreover, recent research suggest that the latent reservoir is larger than previously thought (Dolgin 2013). Intensification strategies Many studies have investigated whether viral decay rates can be improved or whether any change at all can be effected by intensifying therapy. Different strategies were tried, such as additional administration of integrase or entry inhibitors, but also of other compounds to try to to empty the latent reservoirs. Mega-HAART, entry and/or integrase inhibitors In a trial with patients with good viral suppression and additional PIs or NNRTIs in their ART, an ultrasensitive single copy assay showed no further reduction of viral load by intensification (Dinoso 2009). The level of viral load depends not so much on the applied regime, but on on the pre-therapeutical setpoint (Maldarelli 2007). Additional administration of the entry inhibitor T-20 did not show any effects either (Ghandi 2010). Resting T cells are also not affected by T-20 nor by a combination with valproic acid (Archin 2010). Goals and principles of therapy 161 Maraviroc, as a potential immune-modulating CCR5 antagonist, was also investi- gated as an intensification strategy. One study showed no relevant effects on the latent reservoirs (Puertas 2014) and other studies showed no or even unfavorable effects on immune activation (Sauzullo 2010, Wilkin 2010, Hunt 2013). One study with acutely infected patients showed hardly any effect either on virologic or immunologic parameters (Evering 2010). Another carefully designed study with 40 patients with acute HIV infection compared a triple regime plus raltegravir plus maraviroc with a classic triple regimen. Intensive therapy showed no advantages regarding residual viremia or the degree of immune reconstitution or immune acti- vation (Markowitz 2014). Obviously it is not a question of the number of ARVs. Hopes for additional effects of the integrase inhibitor raltegravir were raised by a study in which treatment-naïve patients on a raltegravir regimen achieved a viral load below detection significantly more rapidly than those on efavirenz (Murray 2007). Several prospective studies in which raltegravir was added to an existing ART showed no additional antiviral effect by means of ultrasensitive viral load assays (Gandhi 2009, MacMahon 2010, Gandhi 2012). Immune activation was also not influenced by raltegravir (Luna 2009, Massanella 2011). Results are contradictory regarding the question of whether proviral DNA decreases more rapidly. While two small studies showed positive effects (Arponen 2008, Reigadas 2010), several larger studies did not confirm these results (Buzon 2010, Hatano 2011, Chege 2012). Several studies showed an increase of episomal DNA while on raltegravir. This DNA, also referred to as 2-long terminal repeat (2-LTR) circular, develops when integrase inhibitors block the DNA integration process into the chromatin. Evidence of this episomal DNA (2-LTR circles) in approximately 30% of patients receiving raltegravir plus effective ART, shows that an active viral increase was stopped (Buzon 2010, Reigadas 2010, Llibre 2012, Hatano 2013). A recent study, however, found no increased 2-LTR circles during raltegravir intensification (Besson 2012). Another study demonstrated that resting CD4 T cells were not achieved with raltegravir or with a combination that included valproic acid (Archin 2010) (see below). Sites such as the CNS or gut are not influenced (Yukl 2010, Lee 2011, Yilmaz 2011). Intensification or extension to a four- or five-drug therapy has not had meaningful results. Therefore, the old “Kick and Kill” strategy is being revived, in which infected cells are first activated in hope of them being recognized by the immune system and killed more rapidly (Deeks 2012). Several attempts to empty viral reservoirs using different methods (IL-2, hydroxyurea or OKT) have not been successful (Kulkosky 2002, Pomerantz 2002). A pilot study on valproic acid, an epileptic drug, caused a stir in the summer of 2005. Implemented as an inhibitor of histone deacetylase 1 (HDAC), it suggested a clearance of HIV from resting T cells (Lehrmann 2005). In three out of four patients the number of infected resting CD4 T cells decreased significantly and half-life was reduced to 2-3 months compared to other studies showing a longer half-life of 44 months on ART (Siciliano 2003). Smaller follow-up studies (Steel 2006, Siliciano 2007, Archin 2010) did not confirm these results. More recently, a randomized crossover study finally put an end to the discussion, showing no effect at all of valproic acid in 56 patients (Routy 2010). With the end of valproate, more selective and possibly more potent HDAC inhibitors are being investigated. Results are conflicting (Archin 2012, Blazkova 2012). Vorinostat, an agent that has been approved as a treatment of malignant mesothe- lioma, was active in one study in vivo (Archin 2012) but failed to do so in another (Elliott 2013). Vorinostat was able to increase HIV transcription (“kick”), but without 162 ART “kill” – the pool of latently infected cells was not reduced. Romidepsin seems to be more effective (Wei 2013, Søgaard 2014) and is tested as well as panobinostat and other HDACi (Edelstein 2009, Rasmussen 2013). Further chemical classes able to acti- vate latent infected cells are quinolone derivatives (Xing 2012) protein phosphatase- 1 targeting compounds (Tyagi 2015) or disulfiram (Spival 2012). It may be necessary to activate HIV-specific CTLs (Shan 2012, Deng 2014) for the “kill” part. There are attempts with therapeutical vaccines that simultaneously improve HIV-specific immune response (Garcia 2012). Recently it was shown that acutely infected patients retain a broad-spectrum viral-specific CTL response and that appropriate boosting of this response may be required for the elimination of the latent reservoir (Deng 2015). Attempts with immunoglobins (Lindkvist 2009) or broadly neutralizing antibodies are also being postulated. Even the old substance interferon is being discussed again as an immune modulator (Sandler 2014). In one study 9 out of 20 patients receiv- ing pegylated interferon during a HAART interruption, demonstrated viral load levels below 400 copies/ml after 12 weeks of IFN monotherapy (Azzoni 2013). Gentherapeutic approaches are also under investigation. In a pilot trial, the infusion of autologous, gene-modified CD4 T cells in which the CCR5 gene was rendered per- manently dysfunctional by a zinc-finger nuclease was safe (Tebas 2014). The observed relative survival advantage of the gene-modified cells during treatment interruption suggests that genome editing at the CCR5 locus confers a selective advantage to CD4 T cells in patients infected with HIV. Many more approaches are under investiga- tion, the most promising among them are: a) zinc-finger nucleases that can efficiently excise integrated HIV-1 from the human genome in infected cells b) “designer” T cells that can target and kill HIV Env-expressing cells and thus improve the HIV-specific immune response (Sahu 2013, Yang 2014) c) induction of broadly neutralizing antibodies that can effectively suppress viremia in untreated patients (Horwitz 2013). Within the next years, we will see more and more patients classified as post-treatment controllers or “functionally cured”. However, this will apply only to a small group of patients. Latently infected cells differ minutely from non-infected cells, which cannot be easily discerned via those methods available in most clinics. Washing out the reser- voirs or eliminating all the infected memory cells has either been unsuccessful or too toxic. Removing the HIV genome from infected cells with special recombinants has been successful in the laboratory and in the animal model (Hauber 2013); but there is still a long way to go before this can be used in the clinic (Sarkar 2007). Given the complexity of the immune system which is far away from being com- pletely understood, a solution for the majority of the patients is a distant prospect. Evidence for the cure of HIV infection by CCR5 32/ 32 stem cell trans- plantation. Early ART Intervention Restricts the Seeding of the HIV Reservoir in Long-lived Central Memory CD4 T Cells. Antiretroviral intensification and valproic acid lack sustained effect on residual HIV-1 viremia or resting CD4+ cell infection. Administration of vorinostat disrupts HIV-1 latency in patients on ART.
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Prevalence of dilated car- diomyopathy in HIV-infected African patients not receiving HAART: a multicenter, observational, prospective, cohort study in Rwanda. Wever-Pinzon O, Bangalore S, Romero J, Silva EJ, Chaudhry FA. Inotropic contractile reserve can risk-stratify patients with HIV cardiomyopathy: a dobutamine stress echocardiography study. Comparison of Rates of Death Having Any Death-Certificate Mention of Heart, Kidney, or Liver Disease Among Persons Diagnosed with HIV Infection with Those in the General US Population, 2009-2011. Diabetes mellitus, preexisting coronary heart disease, and the risk of subse- quent coronary heart disease events in patients infected with HIV: the data collection on adverse events of anti- hiv drugs (D:A:D Study). Circulation 2009, 17;119:805-811 Worm SW, Sabin C, Weber R et al. Risk of myocardial infarction in patients with HIV infection exposed to spe- cific individual antiretroviral drugs from the 3 major drug classes: the data collection on adverse events of anti- HIV drugs (D:A:D) study. In situ detection of human cytomegalovirus immediate-early gene tran- scripts within cardiac myocytes of patients with HIV-associated cardiomyopathy. Pulmonary arterial hypertension related to HIV infection: improved hemo- dynamics and survival associated with antiretroviral therapy. HIV and Respiratory Diseases MARKUS UNNEW EHR, MARTIN HOW ER, BERNHARD SCHAAF The spectrum of lung diseases in encompasses typical HIV-related complications such as TB and PCP, bacterial pneumonia, lymphomas and HIV-associated pulmonary hypertension, but also includes usual respiratory problems like acute bronchitis and asthma (see Table 1). Due to the better management of HIV+ people, comorbidities of the older patient become more important, such as COPD, bronchial carcinomas and lung fibrosis (Staitieh 2014, Feldman 2014). With ART, PCP and TB have become less frequent and pulmonary mortality has decreased (Grubb 2006, Morris 2011). HIV influences toll-like receptors and other factors of immune function that increase the risk of pneumonia (Morris 2011). Particularly in patients with respiratory pro- blems and advanced immune deficiency, it is essential to take all differential diag- noses into consideration, of which this chapter presents an outline. PCP, myco- bacterial infections and pulmonary hypertension are covered in detail in other chapters. Table 1: Pulmonary complications in HIV+ patients Infections Neoplasia Other Pneumocystis jiroveci Kaposi sarcoma (KS) Lymphocytic interstitial pneumonia (LIP) Non-Hodgkin lymphoma Non-specific interstitial pneumonia (NSIP) Bacterial pneumonia Hodgkin lymphoma Cryptogenic organizing pneumonia (COP) S. Cryptococcus neoformans Histoplasma capsulatum Toxoplasma gondii Talking with the patient The most important question: What is the immune status?