HIV AIDS opportunistic infections: Difference between revisions

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**[[Primaquine]] plus [[clindamycin]] ('''BI''') (the clindamycin component can be administered intravenously for more severe cases.<ref name="pmid8086551">{{cite journal |author=Black JR, Feinberg J, Murphy RL, Fass RJ, Finkelstein D, Akil B, Safrin S, Carey JT, Stansell J, Plouffe JF |title=Clindamycin and primaquine therapy for mild-to-moderate episodes of Pneumocystis carinii pneumonia in patients with AIDS: AIDS Clinical Trials Group 044 |journal=Clin. Infect. Dis. |volume=18 |issue=6 |pages=905–13 |year=1994 |month=June |pmid=8086551 |doi= |url=http://www.cid.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=8086551 |accessdate=2012-04-07}}</ref>
**[[Primaquine]] plus [[clindamycin]] ('''BI''') (the clindamycin component can be administered intravenously for more severe cases.<ref name="pmid8086551">{{cite journal |author=Black JR, Feinberg J, Murphy RL, Fass RJ, Finkelstein D, Akil B, Safrin S, Carey JT, Stansell J, Plouffe JF |title=Clindamycin and primaquine therapy for mild-to-moderate episodes of Pneumocystis carinii pneumonia in patients with AIDS: AIDS Clinical Trials Group 044 |journal=Clin. Infect. Dis. |volume=18 |issue=6 |pages=905–13 |year=1994 |month=June |pmid=8086551 |doi= |url=http://www.cid.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=8086551 |accessdate=2012-04-07}}</ref>
**Atovaquone suspension ('''BI''')  (this is less effective than TMP-SMX for mild-to-moderate disease but has fewer side effects).
**Atovaquone suspension ('''BI''')  (this is less effective than TMP-SMX for mild-to-moderate disease but has fewer side effects).
*Patients should be tested for G6PD deficiency whenever possible before administration of primaquine.
*Patients should be tested for [[G6PD]] deficiency whenever possible before administration of primaquine.


==Related Chapters==
==Related Chapters==

Revision as of 14:30, 7 April 2012

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief:, Ujjwal Rastogi, MBBS [2]

Overview

Before the widespread use of potent combination antiretroviral therapy (ART), opportunistic infections (OIs), which have been defined as infections that are more frequent or more severe because of immunosuppression in HIV-infected persons, were the principal cause of morbidity and mortality in this population. In the early 1990s, the use of chemoprophylaxis, immunization, and better strategies for managing acute OIs contributed to improved quality of life and improved survival.[1] However, the widespread use of ART starting in the mid-1990s has had the most profound influence on reducing OI-related mortality in HIV-infected persons in those countries in which these therapies are accessible and affordable.

Etiology

Despite the availability of ART in the United States and other industrialized countries, OIs continue to cause considerable morbidity and mortality for three primary reasons:

  • Many patients are unaware of their HIV infection and seek medical care when an OI becomes the initial indicator of their disease.
  • Certain patients are aware of their HIV infection, but do not take ART because of psychosocial or economic factors.
  • Certain patients are prescribed ART, but fail to attain adequate virologic and immunologic response because of factors related to adherence, pharmacokinetics, or unexplained biologic factors.[2][3]

Thus, although hospitalizations and deaths have decreased since the implementation of ART, OIs remain a leading cause of morbidity and mortality in HIV-infected persons.[4][5][6]

Pathophysiology

Recognizing that the relation between OIs and HIV infection is bidirectional is important. HIV leads to immunosuppression that allows opportunistic pathogens to cause disease in HIV-infected persons. OIs and other coinfections that might be common in HIV-infected persons, such as sexually transmitted infections, can also have adverse effects on the natural history of HIV infection. Certain OIs are associated with reversible increases in circulating viral load and these increases could lead to accelerated HIV progression or increased transmission of HIV. Thus, although chemoprophylaxis and vaccination directly prevent pathogen-specific morbidity and mortality, they might also contribute to reduced rate of progression of HIV disease. For instance, randomized trials using trimethoprim-sulfamethoxazole (TMP-SMX) have documented that chemoprophylaxis can both decrease OI-related morbidity and improve survival.

Historical Perspective

The first guidelines for Prophylaxis against Pneumocystis carinii Pneumonia for persons infected with the human immunodeficiency virus became the first HIV-related treatment guideline published by the U.S. Public Health Service in 1989. This report was followed by guideline on prevention of Mycobacterium avium complex (MAC) disease in 1993.

Treatment

Initiation of ART in the Setting of an Acute OI (Treatment-Naïve Patients)

When an acute OI is present, initiation of ART is usually expected to improve immune function and contribute to faster resolution of the OI.

Initiation of ART has been documented to be effective for OIs for which effective therapy does not exist; cryptosporidiosis, microsporidiosis, and progressive multifocal leukoencephalopathy (PML) might resolve or at least stabilize after the institution of effective ART. For kaposi's sarcoma (KS), initiation of ART has been documented to lead to resolution of lesions in the absence of specific therapy for the sarcoma.[7]

Benefits of ART in preventing OI:

The initiation of ART in the setting of an acute OI also has preventive benefit; a second OI is less likely to occur if ART is started promptly rather than delaying the initiation of ART.

Disadvantages:

Starting ART in the setting of an acute OI has several potential disadvantages.

  • Severely ill patients might not absorb ART drugs, leading to subtherapeutic serum levels and the development of antiretroviral drug resistance.
  • ART toxicities might be confused with disease manifestations or toxicities associated with drugs used for treating patients with an OI. Drug-drug interactions among ART and anti-OI drugs might be difficult to manage.
  • Renal or hepatic dysfunction during acute OIs might make dosing of ART drugs difficult to estimate.
  • IRIS events can occur and cause manifestations that are difficult to distinguish from other clinical conditions.

When to start the therapy?

For above mentioned reasons, no consensus has been reached concerning the optimal time to start ART in the setting of a recently diagnosed OI. However, one recently completed randomized clinical trial has demonstrated a clinical and survival benefit of starting ART early, within the first 2 weeks, of initiation of treatment for an acute OI, excluding TB.[8]

Management of Acute OIs in Patients Receiving ART

OIs that occur after patients have been started on ART can be categorized into three groups.

  • The first group includes OIs that occur shortly after initiating ART (within 12 weeks).
    • These cases might be subclinical infections that have been unmasked by early immune reconstitution or simply OIs that occurred because of advanced immunosuppression and are not considered to represent early failure of ART. Many of these cases represent IRIS.[9][10]
    • When an OI occurs within 12 weeks of starting ART, treatment for the OI should be started and ART should be continued.
  • The second group includes OIs that occur >12 weeks after initiation of ART among patients with suppressed HIV ribonucleic acid. levels and sustained CD4+ counts >200 cells/µL[11][12] Determining whether these represent a form of IRIS rather than incomplete immunity with the occurrence of a new OI is difficult.
    • When an OI occurs despite complete virologic suppression (i.e., late OI), therapy for the OI should be initiated and ART should be continued.
    • If the CD4+ response to ART has been suboptimal, modification of the ART regimen may be considered, although no evidence exists to indicate that changing the ART regimen in this setting will improve the CD4+ response.
  • The third group includes OIs that occur among patients who are experiencing virologic and immunologic failure while on ART. These represent clinical failure of ART.
    • When an OI occurs in the setting of virologic failure, OI therapy should be started, antiretroviral resistance testing should be performed, and the ART regimen should be modified, if possible, to achieve better virologic control.

Special Considerations During Pregnancy

Physiologic changes during pregnancy can complicate the recognition of OIs and complicate pharmacokinetics. Factors to consider include the following:

  • Increased cardiac output by 30%--50% with concomitant increase in glomerular filtration rate and renal clearance.
  • Increased plasma volume by 45%--50% while red cell mass increases only by 20%--30%, leading to dilutional anemia.
  • Tidal volume and pulmonary blood flow increase, possibly leading to increased absorption of aerosolized medications. The tidal volume increase of 30%--40% should be considered if ventilatory assistance is required.
  • Placental transfer of drugs, increased renal clearance, altered gastrointestinal absorption, and metabolism by the fetus might affect maternal drug levels.
  • Limited pharmacokinetic data are available; use usual adult doses based on current weight, monitor levels if available, and consider the need to increase doses if the patient is not responding as expected.

Also in regards with risk in Fetus, pregnancy should not preclude usual diagnostic evaluation when an OI is suspected.[13][14][15] Experience with use of magnetic resonance imaging (MRI) in pregnancy is limited, but no adverse fetal effects have been noted.[13]

Guidelines

Disease Specific Recommendations

Pneumocystis Pneumonia

Preventing Exposure

Certain authorities might recommend that persons who are at risk for PCP not share a hospital room with a patient who has PCP, a recommendations based on animal studies and anecdotal human experience. Data are insufficient to support this recommendation as standard practice (CIII).

Preventing Disease
Initiating Primary Prophylaxis
  • HIV-infected adults and adolescents, including pregnant women and those on ART, should receive chemoprophylaxis against PCP if they have a CD4+ count of <200 cells/µL (AI) or a history of oropharyngeal candidiasis (AII).[16][17]
  • Persons who have a CD4+ cell percentage of <14% or a history of an AIDS-defining illness, but do not otherwise qualify, should be considered for prophylaxis (BII). [16][17]
  • When monitoring CD4+ counts frequently (e.g., every 1--3 months) is not possible, initiating chemoprophylaxis at a CD4+ count of >200, but <250 cells/µL, also should be considered (BII). [17]
  • TMP-SMX is the recommended prophylactic agent (AI).[18][19][20] One double-strength tablet daily is the preferred regimen (AI). However, one single-strength tablet daily also is effective and might be better tolerated than one double-strength tablet daily (AI).[20] One double-strength tablet three times weekly also is effective (BI)[21]. TMP-SMX at a dose of one double-strength tablet daily confers cross-protection against toxoplasmosis[22] and selected common respiratory bacterial infections.[18][23] Lower doses of TMP-SMX also likely confer such protection. For patients who have an adverse reaction that is not life threatening, chemoprophylaxis with TMP-SMX should be continued if clinically feasible; for those who have discontinued such therapy because of an adverse reaction, reinstituting TMP-SMX should be strongly considered after the adverse event has resolved (AII). Patients who have experienced adverse events, including fever and rash, might better tolerate reintroduction of the drug with a gradual increase in dose (i.e., desensitization), according to published regimens (BI) [24][25] or reintroduction of TMP-SMX at a reduced dose or frequency (CIII); as many as 70% of patients can tolerate such reinstitution of therapy.[23]
  • If TMP-SMX cannot be tolerated, alternative prophylactic regimens include dapsone (BI)[18], dapsone plus pyrimethamine plus leucovorin (BI)[26][27][28], erosolized pentamidine administered by the Respirgard II nebulizer (manufactured by Marquest, Englewood, Colorado) (BI)[19], and atovaquone (BI)[29][30] Atovaquone is as effective as aerosolized pentamidine[29] or dapsone (BI) [30] but is substantially more expensive than the other regimens. For patients seropositive for Toxoplasma gondii who cannot tolerate TMP-SMX, recommended alternatives to TMP-SMX for prophylaxis against both PCP and toxoplasmosis include dapsone plus pyrimethamine plus leucovorin (BI)[26][27][28], erosolized pentamidine administered by the Respirgard II nebulizer (manufactured by Marquest, Englewood, Colorado) (BI)[19], and atovaquone (BI)[29][30] or atovaquone with or without pyrimethamine plus leucovorin (CIII).
  • Oral pyrimethamine plus sulfadoxine also has activity in preventing PCP (CIII)[31][32][33] This combination should not be used in patients with hypersensitivity to sulfonamides. Pyrimethamine plus sulfadoxine has an increased risk for severe cutaneous reactions, including Stevens-Johnson syndrome[34], and the long half-life of both pyrimethamine and sulfadoxine will result in a delayed clearance when the drug is stopped. Largely because TMP-SMX has superior safety, widespread availability, and is low cost, oral pyrimethamine plus sulfadoxine should be used rarely in the United States (CIII).
  • The following regimens cannot be recommended as alternatives because data regarding their efficacy for PCP prophylaxis are insufficient:
    • Aerosolized pentamidine administered by other nebulization devices.
    • Intermittently administered parenteral pentamidine.
    • Oral clindamycin plus primaquine.

However, clinicians might consider using these agents in unusual situations in which the recommended agents cannot be administered (CIII).

Discontinuing Primary Prophylaxis
  • Primary pneumocystis prophylaxis should be discontinued for adult and adolescent patients who have responded to ART with an increase in CD4+ counts to >200 cells/µL for >3 months (AI). In observational and randomized studies supporting this recommendation, the majority of patients were taking antiretroviral regimens that included a protease inhibitor (PI), and the majority had a CD4+ count of >200 cells/µL for >3 months before discontinuing PCP prophylaxis.[35][36] The median CD4+ count at the time prophylaxis was discontinued was >300 cells/µL, most had a CD4+ cell percentage of >14 %, and many patients had a sustained suppression of HIV plasma RNA levels below detection limits of the assay employed. Median follow-up was 6 - 19 months.
  • Discontinuing primary prophylaxis among these patients is recommended because prophylaxis adds limited disease prevention (i.e., for PCP, toxoplasmosis, or bacterial infections).[36][37]
  • Prophylaxis should be reintroduced if the CD4+ count decreases to <200 cells/µL (AIII).
Treatment of Disease
  • TMP-SMX is the treatment of choice (AI).[38] The dose must be adjusted for abnormal renal function. Multiple randomized clinical trials indicate that TMP-SMX is as effective as parenteral pentamidine and more effective than other regimens. Adding leucovorin to prevent myelosuppression during acute treatment is not recommended because of questionable efficacy and some evidence for a higher failure rate (DII). Oral outpatient therapy of TMP-SMX is highly effective among patients with mild-to-moderate disease (AI).
  • Mutations associated with resistance to sulfa drugs have been documented, but their effect on clinical outcome is uncertain. Patients who have PCP despite TMP-SMX prophylaxis are usually effectively treated with standard doses of TMP-SMX (BIII).
  • Patients with documented or suspected PCP and moderate-to-severe disease, as defined by room air pO2 <70 mm Hg or arterial-alveolar O2 gradient >35 mm Hg, should receive adjunctive corticosteroids as early as possible, and certainly within 72 hours after starting specific PCP therapy (AI).[39][40][41][42][43] If steroids are started at a later time, their benefits are unclear, although the majority of clinicians would use them in such circumstances for patients with moderate-to-severe disease (BIII). Methylprednisolone at 75% of the respective prednisone dose can be used if parenteral administration is necessary.
  • Alternative therapeutic regimens for mild-to-moderate disease include :
    • Dapsone and TMP (BI) (this regimen might have similar efficacy and fewer side effects than TMP-SMX but is less convenient because of the number of pills).[44][45]
    • Primaquine plus clindamycin (BI) (the clindamycin component can be administered intravenously for more severe cases.[46]
    • Atovaquone suspension (BI) (this is less effective than TMP-SMX for mild-to-moderate disease but has fewer side effects).
  • Patients should be tested for G6PD deficiency whenever possible before administration of primaquine.

Related Chapters

Reference

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  10. ↑ Race EM, Adelson-Mitty J, Kriegel GR, Barlam TF, Reimann KA, Letvin NL, Japour AJ (1998). "Focal mycobacterial lymphadenitis following initiation of protease-inhibitor therapy in patients with advanced HIV-1 disease". Lancet. 351 (9098): 252–5. doi:10.1016/S0140-6736(97)04352-3. PMID 9457095. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
  11. ↑ Currier JS, Williams PL, Koletar SL, Cohn SE, Murphy RL, Heald AE, Hafner R, Bassily EL, Lederman HM, Knirsch C, Benson CA, Valdez H, Aberg JA, McCutchan JA (2000). "Discontinuation of Mycobacterium avium complex prophylaxis in patients with antiretroviral therapy-induced increases in CD4+ cell count. A randomized, double-blind, placebo-controlled trial. AIDS Clinical Trials Group 362 Study Team". Ann. Intern. Med. 133 (7): 493–503. PMID 11015162. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
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  13. ↑ 13.0 13.1 "ACOG Committee Opinion. Number 299, September 2004 (replaces No. 158, September 1995). Guidelines for diagnostic imaging during pregnancy". Obstet Gynecol. 104 (3): 647–51. 2004. PMID 15339791. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
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  15. ↑ Adelstein SJ (1999). <236::AID-TERA9>3.0.CO;2-6 "Administered radionuclides in pregnancy". Teratology. 59 (4): 236–9. doi:10.1002/(SICI)1096-9926(199904)59:4<236::AID-TERA9>3.0.CO;2-6. PMID 10331526. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
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  21. ↑ El-Sadr WM, Luskin-Hawk R, Yurik TM, Walker J, Abrams D, John SL, Sherer R, Crane L, Labriola A, Caras S, Pulling C, Hafner R (1999). "A randomized trial of daily and thrice-weekly trimethoprim-sulfamethoxazole for the prevention of Pneumocystis carinii pneumonia in human immunodeficiency virus-infected persons. Terry Beirn Community Programs for Clinical Research on AIDS (CPCRA)". Clin. Infect. Dis. 29 (4): 775–83. doi:10.1086/520433. PMID 10589887. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
  22. ↑ Carr A, Tindall B, Brew BJ, Marriott DJ, Harkness JL, Penny R, Cooper DA (1992). "Low-dose trimethoprim-sulfamethoxazole prophylaxis for toxoplasmic encephalitis in patients with AIDS". Ann. Intern. Med. 117 (2): 106–11. PMID 1351371. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  23. ↑ 23.0 23.1 Hardy WD, Feinberg J, Finkelstein DM, Power ME, He W, Kaczka C, Frame PT, Holmes M, Waskin H, Fass RJ (1992). "A controlled trial of trimethoprim-sulfamethoxazole or aerosolized pentamidine for secondary prophylaxis of Pneumocystis carinii pneumonia in patients with the acquired immunodeficiency syndrome. AIDS Clinical Trials Group Protocol 021". N. Engl. J. Med. 327 (26): 1842–8. doi:10.1056/NEJM199212243272604. PMID 1448121. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
  24. ↑ Para MF, Finkelstein D, Becker S, Dohn M, Walawander A, Black JR (2000). "Reduced toxicity with gradual initiation of trimethoprim-sulfamethoxazole as primary prophylaxis for Pneumocystis carinii pneumonia: AIDS Clinical Trials Group 268". J. Acquir. Immune Defic. Syndr. 24 (4): 337–43. PMID 11015150. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
  25. ↑ Leoung GS, Stanford JF, Giordano MF, Stein A, Torres RA, Giffen CA, Wesley M, Sarracco T, Cooper EC, Dratter V, Smith JJ, Frost KR (2001). "Trimethoprim-sulfamethoxazole (TMP-SMZ) dose escalation versus direct rechallenge for Pneumocystis Carinii pneumonia prophylaxis in human immunodeficiency virus-infected patients with previous adverse reaction to TMP-SMZ". J. Infect. Dis. 184 (8): 992–7. doi:10.1086/323353. PMID 11574913. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
  26. ↑ 26.0 26.1 Podzamczer D, Salazar A, Jiménez J, Consiglio E, Santín M, Casanova A, Rufí G, Gudiol F (1995). "Intermittent trimethoprim-sulfamethoxazole compared with dapsone-pyrimethamine for the simultaneous primary prophylaxis of Pneumocystis pneumonia and toxoplasmosis in patients infected with HIV". Ann. Intern. Med. 122 (10): 755–61. PMID 7717598. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  27. ↑ 27.0 27.1 Opravil M, Hirschel B, Lazzarin A, Heald A, Pechère M, Rüttimann S, Iten A, von Overbeck J, Oertle D, Praz G (1995). "Once-weekly administration of dapsone/pyrimethamine vs. aerosolized pentamidine as combined prophylaxis for Pneumocystis carinii pneumonia and toxoplasmic encephalitis in human immunodeficiency virus-infected patients". Clin. Infect. Dis. 20 (3): 531–41. PMID 7756472. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
  28. ↑ 28.0 28.1 Girard PM, Landman R, Gaudebout C, Olivares R, Saimot AG, Jelazko P, Gaudebout C, Certain A, Boué F, Bouvet E (1993). "Dapsone-pyrimethamine compared with aerosolized pentamidine as primary prophylaxis against Pneumocystis carinii pneumonia and toxoplasmosis in HIV infection. The PRIO Study Group". N. Engl. J. Med. 328 (21): 1514–20. doi:10.1056/NEJM199305273282102. PMID 8479488. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
  29. ↑ 29.0 29.1 29.2 Chan C, Montaner J, Lefebvre EA, Morey G, Dohn M, McIvor RA, Scott J, Marina R, Caldwell P (1999). "Atovaquone suspension compared with aerosolized pentamidine for prevention of Pneumocystis carinii pneumonia in human immunodeficiency virus-infected subjects intolerant of trimethoprim or sulfonamides". J. Infect. Dis. 180 (2): 369–76. doi:10.1086/314893. PMID 10395851. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
  30. ↑ 30.0 30.1 30.2 El-Sadr WM, Murphy RL, Yurik TM, Luskin-Hawk R, Cheung TW, Balfour HH, Eng R, Hooton TM, Kerkering TM, Schutz M, van der Horst C, Hafner R (1998). "Atovaquone compared with dapsone for the prevention of Pneumocystis carinii pneumonia in patients with HIV infection who cannot tolerate trimethoprim, sulfonamides, or both. Community Program for Clinical Research on AIDS and the AIDS Clinical Trials Group". N. Engl. J. Med. 339 (26): 1889–95. doi:10.1056/NEJM199812243392604. PMID 9862944. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
  31. ↑ Schürmann D, Bergmann F, Albrecht H, Padberg J, Wünsche T, Grünewald T, Schürmann M, Grobusch M, Vallée M, Ruf B, Suttorp N (2002). "Effectiveness of twice-weekly pyrimethamine-sulfadoxine as primary prophylaxis of Pneumocystis carinii pneumonia and toxoplasmic encephalitis in patients with advanced HIV infection". Eur. J. Clin. Microbiol. Infect. Dis. 21 (5): 353–61. doi:10.1007/s10096-002-0723-3. PMID 12072919. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
  32. ↑ Payen MC, De Wit S, Sommereijns B, Clumeck N (1997). "A controlled trial of dapsone versus pyrimethamine-sulfadoxine for primary prophylaxis of Pneumocystis carinii pneumonia and toxoplasmosis in patients with AIDS". Biomed. Pharmacother. 51 (10): 439–45. PMID 9863502. Retrieved 2012-04-06.
  33. ↑ Schürmann D, Bergmann F, Albrecht H, Padberg J, Grünewald T, Behnsch M, Grobusch M, Vallée M, Wünsche T, Ruf B, Suttorp N (2001). "Twice-weekly pyrimethamine-sulfadoxine effectively prevents Pneumocystis carinii pneumonia relapse and toxoplasmic encephalitis in patients with AIDS". J. Infect. 42 (1): 8–15. doi:10.1053/jinf.2000.0772. PMID 11243747. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
  34. ↑ Navin TR, Miller KD, Satriale RF, Lobel HO (1985). "Adverse reactions associated with pyrimethamine-sulfadoxine prophylaxis for Pneumocystis carinii infections in AIDS". Lancet. 1 (8441): 1332. PMID 2860516. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  35. ↑ Dworkin MS, Hanson DL, Kaplan JE, Jones JL, Ward JW (2000). "Risk for preventable opportunistic infections in persons with AIDS after antiretroviral therapy increases CD4+ T lymphocyte counts above prophylaxis thresholds". J. Infect. Dis. 182 (2): 611–5. doi:10.1086/315734. PMID 10915098. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
  36. ↑ 36.0 36.1 Mussini C, Pezzotti P, Govoni A, Borghi V, Antinori A, d'Arminio Monforte A, De Luca A, Mongiardo N, Cerri MC, Chiodo F, Concia E, Bonazzi L, Moroni M, Ortona L, Esposito R, Cossarizza A, De Rienzo B (2000). "Discontinuation of primary prophylaxis for Pneumocystis carinii pneumonia and toxoplasmic encephalitis in human immunodeficiency virus type I-infected patients: the changes in opportunistic prophylaxis study". J. Infect. Dis. 181 (5): 1635–42. doi:10.1086/315471. PMID 10823763. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
  37. ↑ Lopez Bernaldo de Quiros JC, Miro JM, Peña JM, Podzamczer D, Alberdi JC, Martínez E, Cosin J, Claramonte X, Gonzalez J, Domingo P, Casado JL, Ribera E (2001). "A randomized trial of the discontinuation of primary and secondary prophylaxis against Pneumocystis carinii pneumonia after highly active antiretroviral therapy in patients with HIV infection. Grupo de Estudio del SIDA 04/98". N. Engl. J. Med. 344 (3): 159–67. doi:10.1056/NEJM200101183440301. PMID 11172138. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
  38. ↑ Hughes W, Leoung G, Kramer F, Bozzette SA, Safrin S, Frame P, Clumeck N, Masur H, Lancaster D, Chan C (1993). "Comparison of atovaquone (566C80) with trimethoprim-sulfamethoxazole to treat Pneumocystis carinii pneumonia in patients with AIDS". N. Engl. J. Med. 328 (21): 1521–7. doi:10.1056/NEJM199305273282103. PMID 8479489. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
  39. ↑ Nielsen TL, Eeftinck Schattenkerk JK, Jensen BN, Lundgren JD, Gerstoft J, van Steenwijk RP, Bentsen K, Frissen PH, Gaub J, Orholm M (1992). "Adjunctive corticosteroid therapy for Pneumocystis carinii pneumonia in AIDS: a randomized European multicenter open label study". J. Acquir. Immune Defic. Syndr. 5 (7): 726–31. PMID 1613673. |access-date= requires |url= (help)
  40. ↑ Bozzette SA, Sattler FR, Chiu J, Wu AW, Gluckstein D, Kemper C, Bartok A, Niosi J, Abramson I, Coffman J (1990). "A controlled trial of early adjunctive treatment with corticosteroids for Pneumocystis carinii pneumonia in the acquired immunodeficiency syndrome. California Collaborative Treatment Group". N. Engl. J. Med. 323 (21): 1451–7. doi:10.1056/NEJM199011223232104. PMID 2233917. Retrieved 2012-04-07. Unknown parameter |month= ignored (help)
  41. ↑ Montaner JS, Lawson LM, Levitt N, Belzberg A, Schechter MT, Ruedy J (1990). "Corticosteroids prevent early deterioration in patients with moderately severe Pneumocystis carinii pneumonia and the acquired immunodeficiency syndrome (AIDS)". Ann. Intern. Med. 113 (1): 14–20. PMID 2190515. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  42. ↑ Gallant JE, Chaisson RE, Moore RD (1998). "The effect of adjunctive corticosteroids for the treatment of Pneumocystis carinii pneumonia on mortality and subsequent complications". Chest. 114 (5): 1258–63. PMID 9823998. Retrieved 2012-04-07. Unknown parameter |month= ignored (help)
  43. ↑ Briel M, Boscacci R, Furrer H, Bucher HC (2005). "Adjunctive corticosteroids for Pneumocystis jiroveci pneumonia in patients with HIV infection: a meta-analysis of randomised controlled trials". BMC Infect. Dis. 5: 101. doi:10.1186/1471-2334-5-101. PMC 1309617. PMID 16271157. Retrieved 2012-04-07.
  44. ↑ Safrin S, Finkelstein DM, Feinberg J, Frame P, Simpson G, Wu A, Cheung T, Soeiro R, Hojczyk P, Black JR (1996). "Comparison of three regimens for treatment of mild to moderate Pneumocystis carinii pneumonia in patients with AIDS. A double-blind, randomized, trial of oral trimethoprim-sulfamethoxazole, dapsone-trimethoprim, and clindamycin-primaquine. ACTG 108 Study Group". Ann. Intern. Med. 124 (9): 792–802. PMID 8610948. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  45. ↑ Medina I, Mills J, Leoung G, Hopewell PC, Lee B, Modin G, Benowitz N, Wofsy CB (1990). "Oral therapy for Pneumocystis carinii pneumonia in the acquired immunodeficiency syndrome. A controlled trial of trimethoprim-sulfamethoxazole versus trimethoprim-dapsone". N. Engl. J. Med. 323 (12): 776–82. doi:10.1056/NEJM199009203231202. PMID 2392131. Retrieved 2012-04-07. Unknown parameter |month= ignored (help)
  46. ↑ Black JR, Feinberg J, Murphy RL, Fass RJ, Finkelstein D, Akil B, Safrin S, Carey JT, Stansell J, Plouffe JF (1994). "Clindamycin and primaquine therapy for mild-to-moderate episodes of Pneumocystis carinii pneumonia in patients with AIDS: AIDS Clinical Trials Group 044". Clin. Infect. Dis. 18 (6): 905–13. PMID 8086551. Retrieved 2012-04-07. Unknown parameter |month= ignored (help)
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