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Primary Care Approach To Managing The HIV Patient
- 1. Primary Care Approach To The HIV Patient Tahseen J. Siddiqui, M.D., M.R.C.P Medical Director, Infectious Disease/HIV/STD Prevention & Care Program Jackson Park Hospital & Medical Center Chicago
- 3. EPIDEMIOLOGY Global Distribution of HIV Officially, there are 1,710 people living with HIV in Pakistan today, a nation of over 140 million. However, given the taboo nature of the subject, few infected people disclose their status. Some experts estimate the true number of HIV-positive people to be closer to 80,000. Around 2.5 million people in India are living with HIV.
- 4. Increase In HIV Cases
- 5. USA STATES Geographical Distribution of HIV/AIDS (2003) 72% of all AIDS cases to date have been reported from just ten states New York - /66,311 California - /55,612 Florida 32,196 / 42,861 Texas 20,820 /29,958 New Jersey 15,192/ 16,969 Illinois - /14,241 Georgia - /13,963 Maryland - /12,830 North Carolina 11,118 /6,519 Total 172,714 /393,375
- 6. Racial & Gender Differences
- 7. HIV/AIDS Diagnoses among Adults and Adolescents, by Transmission Category — 33 States, 2001–2004 MSM 61% IDU 16% Heterosexual 17% MSM/IDU 5% Other 1% Males (n ≈ 112,000) Females (n ≈ 45,000) Heterosexual 76% IDU 21% Other 3% MMWR, Nov 18, 2005
- 8. Changing Faces of HIV/AIDS No Longer A Disease of Gay Men And Drug Abusers
- 9. Modes Of Transmission A GUIDE TO THE CLINICAL CARE OF WOMEN WITH HIV Epidemiology and Natural History of HIV Infection in Women
- 10. HIV TRANSMISSION (Average, per episode, involving HIV-infected source patient ) HCV 3% and HBV 30% risk by needle stick injury 24% Vertical (no prophylaxis) 10 0.67% IDU needle sharing 9 4 case reports Female-female orogenital 8 0.06% Receptive oral (male) 7 0.03 – 0.14% Insertive vaginal intercourse 6 0.1 – 0.2% Receptive vaginal intercourse 5 0.06% Insertive anal intercourse 4 1% Receptive anal intercourse 3 0.09% Mucocutaneous (blood) 2 0.3% Percutaneous (blood) 1
- 13. HIV Cycle
- 14. HIV Timeline UNTREATED NATURAL HISTORY
- 15. HIV NATURAL HISTORY Based On CD4 Cell Count & Viral Load
- 16. Primary HIV Infection (4-12 weeks post infx) Seroconversion Illness, Acute Retroviral Syndrome (‘Bad Flu’)
- 19. HIV Presents To Dermatologist Kaposi's sarcoma SEROCONVERSION ILLNESS Herpes Simplex Herpes Zoster ( Shingles ) Molluscum Contagiosum Kaposi's sarcoma
- 20. HIV Presents To Dermatologist Warts Oral 'Hairy' Leukoplakia Oral Candidiasis 'Thrush' onchomycosis Bacillary angiomatosis psoriasis Seborrheic dermatitis HSV Crypto disseminated
- 21. HIV Presents To Pulmonologist PCP Military TB Kaposi's sarcoma
- 22. HIV Presents To Gastroenterologist Candida esophagitis (HSV) esophagitis CMV Proctitis Primary gastric lymphoma Kaposi's sarcoma – GI lesions
- 26. Metabolic Abnormalities Changes in glucose and lipids occur early after the initiation of therapy and before the development of body shape changes.
- 27. HIV- HAART Vs HEART
- 28. Metabolic Abnormalities HIV Infection Itself Increase the Risk of Diabetes relative risk of 3.32
- 34. Rapid Diagnosis Four FDA-approved Rapid HIV Tests Results are available in 10-20 min 99.7 (99.0 – 100) 99.8 (99.3 – 100) 100 (99.5 – 100) 100 (99.5 – 100) Uni-Gold Recombigen - whole blood - serum/plasma 100 (99.7-100) 99.8 (99.6 – 99.9) 99.9 (99.6 – 99.9) 99.6 (98.5 - 99.9) 99.3 (98.4 - 99.7) 99.6 (98.5 - 99.9) OraQuick Advance - whole blood - oral fluid - plasma Specificity (95% C.I.) Sensitivity (95% C.I.) 99.9 (99.8 – 100) 100 (99.9 – 100) 100 (99.7 – 100) Multispot - serum/plasma - HIV-2 99.1 (98.8 – 99.4) 98.6 (98.4 – 98.8) 99.8 (99.2 – 100) 99.8 (99.0 – 100) Reveal G2 - serum - plasma Specificity (95% C.I.) Sensitivity (95% C.I.)
- 36. Treatment With HAART (Highly Active Antiretroviral Therapy) *The pre-HAART era (1994-1995) *Early-HAART (1996-1997) *Late-HAART (1998 onwards) Incidence of AIDS was about 50% lower in late-HAART when compared with early-HAART. The incidence of death also decreased significantly Median survival on HAART is now ~ 25 years
- 37. ‘ COSTS’ Of HAART *Price Tag *Side Effects *Resistance Globally, more than 90 percent of HIV-positive patients do not have access to HAART
- 38. When to Start HAART Chronic Infection Treatment should be offered, with consideration of pros and cons Any value >200 cells/µL but <350 cells/µL Asymptomatic Treat Any value <200 cells/µL Asymptomatic, AIDS Treat Any value Any value Symptomatic (AIDS, severe symptoms) Recommendation Plasma HIV RNA CD4 + T Cell Count Clinical Category
- 39. When to Start HAART Chronic Infection Defer therapy <100,000 copies/mL CD4 + T cells >350 cells/µL Asymptomatic Most clinicians recommend deferring therapy; some will treat >100,000 copies/mL >350 cells/µL Asymptomatic Recommendation Plasma HIV RNA CD4 + T Cell Count Clinical Category
- 41. BASELINE EVALUATION Pap smear/Anal Pap/STD screening Vaccination; (annual Influenza/ Pneumovax 3-5 y/ HBV series/ HPV (revaccinate once CD4>200) In addition: • Resistance testing (Genotype/Phenotype) in chronically infected patients prior to initiating antiretroviral therapy • Chest x-ray if clinically indicated. G6PD (in selected patients) PPD (annually) Serologies : RPR, toxoplasma IgG, hepatitis A, hepatitis B, hepatitis C CMV, varicella-zoster virus (if no history of chickenpox or shingles), Lipid profile : total cholesterol, HDL, LDL, triglycerides CBC/Diff CMP: including liver and renal function CD4 count/Viral load (2-8 w after initiating therapy then after every 3-4 months) Confirm HIV (ELISA and Western blot)
- 45. Thanks
Hinweis der Redaktion
- These charts illustrate the risk behaviors reported by persons newly diagnosed with HIV or AIDS in recent years (2001 through 2004) in the 33 states with name-based HIV/AIDS reporting. They represent new diagnoses – not necessarily new or recent infections. Approximately 29% of these new cases were among women. Injection drug use accounts for approximately 20% of cases among both men and women. The route of infection among the majority (61%) of men was male-to-male sexual contact. The majority (76%) of females with HIV/AIDS diagnosed were exposed through high-risk heterosexual contact.
- 1. Bell DM. Am J Med 1997;102(suppl 5B):9--15. 2. Ippolito G et al. Arch Int Med 1993;153:1451--8. 3. Am J Epidemiology 1999;150:306-11. 4. Am J Epidemiology 1999;150:306-11. 5. MMWR 47;RR-17, 1998. 6. NEJM 336(15):1072-8. (rates in Europe & U.S.) 7. Am J Epidemiology 1999;150:306-11. 8. Rothenberg RB et al. AIDS 1998;12:2095-2105. 9. MMWR 47;RR-17, 1998. 10. ACTG 076
- The primary goal of the new initiative – to reduce HIV transmission – is not new. AHP emphasizes the use of proven public health approaches to reduce incidence and the spread of disease. The initiative consists of four priority strategies: Make voluntary testing a routine part of medical care. Implement new models for diagnosing HIV infections outside medical settings. Prevent new infections by working with persons diagnosed with HIV. Further decrease perinatal HIV transmission.
- The decision to begin therapy for the asymptomatic patient is complex and must be made in the setting of careful patient counseling and education. Considerations of initiating antiretroviral therapy should be primarily based on the prognosis of disease-free survival as determined by baseline CD4 + T cell count [27-29] ( Figure A ; and Table 3a, 3b ) . Also important are baseline viral load [27-29] , readiness of the patient to begin therapy; and assessment of potential benefits and risks of initiating therapy for asymptomatic persons, including short-and long-term adverse drug effects; the likelihood, after counseling and education, of adherence to the prescribed treatment regimen. Recommendations vary according to the CD4 count and viral load of the patient, as follows. <200 CD4 + T cell count, with AIDS-defining illness, or symptomatic. Randomized clinical trials provide strong evidence of improved survival and reduced disease progression by treating symptomatic patients and patients with <200 CD4 + T cells/mm 3 [30-33]. Observational cohorts indicate a strong relationship between lower CD4 + T cell counts and higher plasma HIV RNA levels in terms of risk for progression to AIDS for untreated persons and antiretroviral naïve patients beginning treatment. These data provide strong support for the conclusion that therapy should be initiated in patients with CD4 + T cell count <200 cells/mm 3 ( Figures A and Table 3a ) (AI) [27, 28]. 200-350 CD4 + T cell count, patient asymptomatic. The optimal time to initiate antiretroviral therapy among asymptomatic patients with CD4 + T cell counts >200 cells/mm 3 is unknown. For these patients, the strength of the recommendation for therapy must balance other considerations, such as patient readiness for treatment and potential drug toxicities. After considering available data in terms of the relative risk for progression to AIDS at certain CD4 + T cell counts and viral loads, and the potential risks and benefits associated with initiating therapy, most specialists in this area believe that the evidence supports initiating therapy in asymptomatic HIV-infected persons with a CD4 + T cell count of 200-350 cells/mm 3 (BII) . There is a paucity of data from randomized, controlled trials concerning clinical endpoints (e.g., the development of AIDS-defining illnesses or death) for asymptomatic persons with >200 CD4 + T cells/mm 3 to guide decisions on when to initiate therapy. Observational data from cohorts of HIV-infected persons provide some guidance to assist in risk assessment for disease progression. … . While there are clear strengths to these observational data, there are also important limitations. Uncontrolled confounding factors could impact estimates in both studies. Furthermore, neither study provides direct evidence on the optimum CD4 + T cell count to begin therapy. Such data will have to come from studies that follow patients who start therapy at different CD4 + T-cell counts above 200 cells/mm 3 and compare them with a similar group of patients (e.g., with similar CD4 + T cell count and HIV RNA level) who defer treatment. To completely balance the benefits and risks of therapy, follow-up will have to examine progression to AIDS, major toxicities, and death. >350 CD4 + T cell count, patient asymptomatic. There is little evidence on the benefit of initiating therapy in asymptomatic patients with CD4 + T cell count > 350 cells/mm 3 . Most clinicians would defer therapy. • The deferred treatment approach is based on the recognition that robust immune reconstitution still occurs in the majority of patients who initiate treatment while CD4 + T cell counts are in the 200–350 cells/mm 3 range. Also, toxicity risks and adherence challenges generally outweigh the benefits of initiating therapy at CD4 + T cell counts >350 cells/mm 3 . In the deferred treatment approach, increased levels of plasma HIV RNA (i.e., >100,000 copies/mL) are an indication for monitoring of CD4 + T cell counts and plasma HIV RNA levels at least every three months, but not necessarily for initiation of therapy. For patients with HIV RNA <100,000 copies/mL, therapy should be deferred (DII) . • In the early treatment approach, asymptomatic patients with CD4 + T cell counts >350 cells/mm 3 and levels of plasma HIV RNA >100,000 copies/mL would be treated because of the risk for immunologic deterioration and disease progression (CII) . An estimate of the short term risk of AIDS progression may be useful in guiding clinicians and patients as they weigh the risks and benefits of initiating versus deferring therapy in this CD4 cell range. As cited above, Table 3b provides an analysis of data from the CASCADE Collaboration, demonstrating the risk of AIDS progression within 6 months for different strata of CD4 + T cell count, viral load, and age. As seen in Table 3b , a 55 year old with a CD4 + T cell count of 350 and a HIV viral load of 300,000 copies/ml has a 5% chance of progression in 6 months, compared with a 1.2% chance for a similar patient with a viral load of 3000 copies/mL.
- Three NNRTIs (namely, delavirdine, efavirenz, and nevirapine) are currently marketed for use. NNRTI-based regimens are commonly prescribed as initial therapy for treatment-naïve patients. In general, these regimens have the advantage of lower pill burden as compared to most of the PI-based regimens. Use of NNRTI-based regimens as initial therapy can preserve the PIs for later use, reducing or delaying patient exposure to some of the adverse effects more commonly associated with PIs. The major disadvantage of currently available NNRTIs is their low genetic barrier for development of resistance. These agents only require a single mutation to confer resistance, and cross resistance often develops across the entire class. As a result, patients who fail this initial regimen may lose the utility of other NNRTIs and/or may transmit NNRTI-resistant virus to others. Based on clinical trial results and safety data, the Panel recommends the use of efavirenz as the preferred NNRTI as part of initial antiretroviral therapy (AII) . The exception is during pregnancy (especially during the first trimester) or in women who are planning to conceive or women who are not using effective and consistent contraception. Nevirapine may be used as an alternative to efavirenz as the initial NNRTI-based regimen. (BII) Close monitoring of liver enzymes and skin rash should be undertaken during the first 18 weeks of nevirapine therapy, particularly, in female patients with CD4 + T-cell count >250 cells/mm 3 prior to therapy initiation. Among these three agents, delavirdine appears to have the least potent antiviral activity. As such, it is not recommended as part of an initial regimen. (DII) PI-based regimens (1or 2 PIs + 2 NRTIs) revolutionized the treatment of HIV infection, leading to sustained viral suppression, improved immunologic function, and prolonged patient survival. Since their inception in the mid-1990s, much has been learned about their efficacy as well as some short term and long term adverse effects. To date, eight PIs have been approved for use in the United States. Each agent has its own unique characteristics based on its clinical efficacy, adverse effect profile, and pharmacokinetic properties. The characteristics, advantages, and disadvantages of each PI can be found in Tables 6 & 12 . In selecting a PI-based regimen for a treatment-naïve patient, factors such as dosing frequency, food and fluid requirements, pill burden, drug interaction potential, baseline hepatic function, and toxicity profile should be taken into consideration. A number of metabolic abnormalities, including dyslipidemia, fat maldistribution, and insulin resistance, have been associated with PI use. The eight PIs differ in their propensity to cause these metabolic complications. At this time, the extent to which these complications may result in adverse long term consequences, such as increased cardiac events in chronically-infected patients, is unknown. The potent inhibitory effect of ritonavir on the cytochrome P450 3A4 isoenzyme has allowed the addition of low dose ritonavir to other PIs as a “pharmacokinetic booster” to increase drug exposure and prolong serum half-lives of the active PIs. This allows for reduced dosing frequency and pill burden, and in the case of indinavir, the addition of low dose ritonavir eliminates the need for food restrictions. All these advantages may improve overall adherence to the regimen. The increased trough concentration (C min ) may improve the antiretroviral activity of the active PIs, which is most beneficial in cases where the patient harbors HIV-1 strains with reduced susceptibility to the PI [61-63]. The major drawbacks associated with this strategy are the potential for increased risk of hyperlipidemia and a greater potential of drug-drug interactions from the addition of ritonavir. The Panel considers lopinavir/ritonavir as the preferred PI for the treatment-naive patient (AII) . Discussed below, this recommendation is based on clinical trial data for virologic potency, barrier for virologic resistance, and patient tolerance. However, there are limited data on the comparative efficacy of lopinavir/ritonavir with other ritonavir-boosted regimens. Alternative PIs are listed in Table 5 and discussed below in greater detail and may include atazanavir (BII) , fosamprenavir (BII) , or nelfinavir (CII) as sole PI, or ritonavir-boosted fosamprenavir (BII) , indinavir (BII) , or saquinavir (BII) .