Mr. O is a 29-year-old white man with a history of unprotected anal intercourse with multiple partners. He has noticed some oral lesions and weight loss. He is quite worried and wants to know if he is infected with HIV.
Prioritizing the Differential Diagnosis
Mr. O presents with weight loss and significant HIV risk factors. Men who have sex with men (MSM) are at very high risk for acquiring HIV infection, especially if they have multiple partners and do not use condoms consistently. Mr. O is well aware of his high-risk behavior and is rightly concerned that his weight loss and oral lesions may suggest HIV infection. He comes to your office to be tested for HIV.
This discussion will focus on his chief concern: whether he has acquired HIV infection.
Mr. O's past medical history is remarkable for a history of syphilis and gonorrhea. Physical exam reveals a thin white man. He is 6' tall and weighs 140 pounds. HEENT exam reveals white coating on the palate consistent with thrush. Cardiac and pulmonary exam are unremarkable.
|Is the clinical information sufficient to make a diagnosis? If not, what other information do you need?|
Leading Hypothesis: HIV Infection
Chronic HIV infection may present in a myriad of ways. Many patients are asymptomatic in spite of long-standing HIV infection and even advanced immune deficiency. Other patients have conditions that suggest possible HIV infection but are frequently encountered in non–HIV-infected persons (eg, tuberculosis (TB), idiopathic thrombocytopenic purpura, nephropathy, cardiomyopathy, unexplained chronic diarrhea, herpes zoster, non-Hodgkin lymphoma). HIV infection may be diagnosed only after a patient seeks medical attention for an opportunistic infection or malignancy that is highly suggestive of severe T-cell immunodeficiency (eg, oral candidiasis, pneumocystosis, cryptococcosis, Kaposi sarcoma, primary CNS lymphoma). Nonspecific skin findings, such as severe or refractory seborrheic dermatitis, psoriasis, and prurigo nodularis (see below for skin findings in HIV infected patients), may suggest the diagnosis.
In December 2007, about 33.2 [30.6–36.1] million people were reported living with HIV worldwide (Table 5–1).
Rates vary dramatically by gender and ethnicity (Figure 5–1).
The Center for Disease Control and Prevention (CDC) estimates that at the end of 2003 the total number of persons in the United States living with HIV was > 1 million (1,039,000–1,185,000). Approximately 25% are unaware that they are infected.
HIV is a retrovirus. The viral enzyme reverse transcriptase uses the viral RNA genome as a template for production of DNA that is integrated into the cell genome.
The HIV virus carries 3 enzymes: reverse transcriptase, integrase, and protease; all 3 enzymes are targets of highly effective inhibitors.
The virus is present in blood, semen, and vaginal fluid.
Common modes of transmission include male to male sexual transmission (62% of cases), needle sharing among injection drug users (17% of cases), heterosexual transmission (13% of cases), and vertical transmission from mother to child.
Low viral loads decrease the rate of sexual transmission. Presence of sexually transmitted diseases (STDs), especially those that cause genital ulceration, increase the risk.
Transmission through blood transfusion has been greatly reduced by blood product screening, implemented in 1985. Current risk associated with blood transfusion is ≈ 1/1,800,000 units in the United States with the current use of donor screening, and blood testing for HIV 1 and 2.
The highest risk of sexual transmission is among patients with unprotected receptive anal intercourse, sex-for-hire workers, sexual contacts of sex-for-hire workers, and individuals with multiple sexual partners.
The HIV surface protein GP 120 selectively binds first to the CD4 T receptor (main HIV receptor), then to one of two chemokine receptors (CCR5 or CXCR4) on CD4 T positive lymphocytes (helper cells).
HIV replicates mostly in activated CD4 T cells.
In acute HIV infection, there is a very rapid decrease in the CD4 T lymphocytes in the gut associated lymphoid tissues (GALT) but only a moderate and partially reversible decrease in the CD4 T lymphocyte count in the blood.
In chronic HIV infection, there is a very slowly progressive decrease in the CD4 T lymphocyte count in the blood. This reflects about 2 billion cells destroyed and replaced every day. Both HIV-infected CD4 T lymphocytes and noninfected CD4 T lymphocytes are activated and destroyed.
In most infected individuals, CD4 T cell death eventually outstrips CD4 T cell production, resulting in progressive depletion of CD4 helper lymphocytes in the blood.
When the absolute CD4 T lymphocyte count falls below 200/mcL, the patient is said to have immunologic AIDS.
A small percentage of infected individuals do not drop their CD4 counts over time (long-term nonprogressors).
CD4 T cell counts below 200/mcL render patients susceptible to a wide array of opportunistic infections and malignancies.
The HIV virus mutates frequently.
A high rate of mutations occurs because the reverse transcriptase enzyme is error prone and HIV replicates very rapidly (10 billion new viruses a day.)
This allows for the rapid development of genetic variants.
Effective therapy requires complete or near complete suppression of viral replication to prevent the production of mutations associated with drug resistance (see below).
Stages of HIV infection include viral transmission, primary infection, seroconversion, clinically latent period, early symptomatic HIV infection, AIDS and advanced HIV infection.
May be asymptomatic but up to 70% of patients may experience a “mononucleosis syndrome” with fever, rash, sore throat, diarrhea, lymphadenopathy, arthralgia, headache, and flu-like symptoms. Acute HIV infection should be considered when a mononucleosis syndrome fails to show evidence of infection by Epstein-Barr virus (EBV) (negative heterophile antibody, negative EBV viral capsid antibody (VCA) IgM) or cytomegalovirus (CMV) (negative CMV IgM).
Standard HIV enzyme immunoassay (EIA) and Western blot tests require ...
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