Primary HIV infection masquerading as Munchausen’s syndrome
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《性传输感染》
Departments of Genitourinary Medicine and Virology, Brighton and Sussex University Hospitals NHS Trust, Brighton, East Sussex, BN2 5BE, UK
Keywords: Munchausen’s syndrome; HIV
Since 1986 there have been several case reports describing factitious HIV infection.1 We have seen two acute presentations where the patients claimed to have chronic HIV infection, were found to be HIV antibody negative but on closer evaluation were found to be seroconverting with primary HIV infection (PHI). We believe that the patients were motivated by the psychological need to assume the sick role, fulfilling the principal feature of a factitious disorder, rather than malingering.
Case 1
A 40 year old homosexual man presented to HIV services with an acute diarrhoeal illness, claiming to have been diagnosed as HIV positive at another hospital 2 years previously. A third generation HIV test, Abbott AxSYM HIV 1/2 gO (antibody only), was negative. He returned 1 month later, still denying any sexual risk, and requested a repeat HIV test, which was again antibody negative but reactive with the fourth generation assay, Abbott HIV Ag/Ab Combo (antibody and p24 antigen combined).
Case 2
A 39 year old homosexual man presented to the accident and emergency department with fever, ulcerative gingivitis, and maculopapular rash, claiming to have been diagnosed HIV positive 4 years previously. He reported safer sex with 30 casual male partners in the previous 3 months and stated that his regular male partner was HIV negative. He was found to have had four negative HIV tests in the previous 2 years at this hospital and numerous negative HIV tests at other hospitals. The third generation HIV test was negative. The following day, however, a fourth generation test was reactive.
Comment
The ability to diagnose PHI has always required a high index of suspicion and a keenly taken history, and if missed the next opportunity for testing may not be until years later when the patient presents in ill health, with symptomatic HIV or even AIDS.2 Clearly, a missed diagnosis of PHI may have a deleterious effect on the individual’s prognosis, but there may also be significant public health consequences, as early infection is a core factor in the propagation of an epidemic3,4 because of high viral burden and de facto risk taking sexual behaviour. Indeed, early detection of PHI probably represents the single most important method of slowing the spread of HIV within populations, with mathematical modelling indicating that eliminating high infectivity in early infection has more effect than at any other disease stage.5
Thus, the diagnosis of PHI in at-risk individuals has considerable advantages in both individual and public heath terms. These two cases demonstrate how easy it can be to disregard such patients as having factitious HIV infection and are a gentle reminder that a negative antibody test does not necessarily exclude PHI. Healthcare professionals must continue to be alert to the less common clinical manifestations of PHI, be aware of the particular assays used in their own laboratory, and because no combination of symptoms is 100% sensitive or specific, diagnostic procedure must be broad and inclusive.6
References
Churchill DR, De Cock KM, Miller RF. Feigned HIV infection/AIDS: malingering and Munchausen’s syndrome. Genitourin Med 1994;70:314–16.
Castilla J, Sobrino P, De La Fuente L, et al. Late diagnosis of HIV infection in the era of highly active antiretroviral therapy: consequences for AIDS incidence. AIDS. 2002;16 :1945–51.
Vernazza PL, Eron JJ, Fiscus SA, et al. Sexual transmission of HIV: infectiousness and prevention. AIDS 1999;13:155–66.
Leynaert B, Downs AM, de Vincenzi I. Heterosexual transmission of human immunodeficiency virus: variability of infectivity throughout the course of infection. European Study Group on Heterosexual Transmission of HIV. Am J Epidemiol 1998;148:88–96.
Koopman JS, Jacquez JA, Welch GW, et al. Role of the Primary Infection in epidemics of HIV infection in gay cohorts. J Acquir Immune Defic Syndr 1994;7:1169–8.
Kahn JO, Walker BD. Acute human immunodeficiency virus type 1 infection. N Engl J Med 1998;339:33–9.(D Pao, D McElborough and )
Keywords: Munchausen’s syndrome; HIV
Since 1986 there have been several case reports describing factitious HIV infection.1 We have seen two acute presentations where the patients claimed to have chronic HIV infection, were found to be HIV antibody negative but on closer evaluation were found to be seroconverting with primary HIV infection (PHI). We believe that the patients were motivated by the psychological need to assume the sick role, fulfilling the principal feature of a factitious disorder, rather than malingering.
Case 1
A 40 year old homosexual man presented to HIV services with an acute diarrhoeal illness, claiming to have been diagnosed as HIV positive at another hospital 2 years previously. A third generation HIV test, Abbott AxSYM HIV 1/2 gO (antibody only), was negative. He returned 1 month later, still denying any sexual risk, and requested a repeat HIV test, which was again antibody negative but reactive with the fourth generation assay, Abbott HIV Ag/Ab Combo (antibody and p24 antigen combined).
Case 2
A 39 year old homosexual man presented to the accident and emergency department with fever, ulcerative gingivitis, and maculopapular rash, claiming to have been diagnosed HIV positive 4 years previously. He reported safer sex with 30 casual male partners in the previous 3 months and stated that his regular male partner was HIV negative. He was found to have had four negative HIV tests in the previous 2 years at this hospital and numerous negative HIV tests at other hospitals. The third generation HIV test was negative. The following day, however, a fourth generation test was reactive.
Comment
The ability to diagnose PHI has always required a high index of suspicion and a keenly taken history, and if missed the next opportunity for testing may not be until years later when the patient presents in ill health, with symptomatic HIV or even AIDS.2 Clearly, a missed diagnosis of PHI may have a deleterious effect on the individual’s prognosis, but there may also be significant public health consequences, as early infection is a core factor in the propagation of an epidemic3,4 because of high viral burden and de facto risk taking sexual behaviour. Indeed, early detection of PHI probably represents the single most important method of slowing the spread of HIV within populations, with mathematical modelling indicating that eliminating high infectivity in early infection has more effect than at any other disease stage.5
Thus, the diagnosis of PHI in at-risk individuals has considerable advantages in both individual and public heath terms. These two cases demonstrate how easy it can be to disregard such patients as having factitious HIV infection and are a gentle reminder that a negative antibody test does not necessarily exclude PHI. Healthcare professionals must continue to be alert to the less common clinical manifestations of PHI, be aware of the particular assays used in their own laboratory, and because no combination of symptoms is 100% sensitive or specific, diagnostic procedure must be broad and inclusive.6
References
Churchill DR, De Cock KM, Miller RF. Feigned HIV infection/AIDS: malingering and Munchausen’s syndrome. Genitourin Med 1994;70:314–16.
Castilla J, Sobrino P, De La Fuente L, et al. Late diagnosis of HIV infection in the era of highly active antiretroviral therapy: consequences for AIDS incidence. AIDS. 2002;16 :1945–51.
Vernazza PL, Eron JJ, Fiscus SA, et al. Sexual transmission of HIV: infectiousness and prevention. AIDS 1999;13:155–66.
Leynaert B, Downs AM, de Vincenzi I. Heterosexual transmission of human immunodeficiency virus: variability of infectivity throughout the course of infection. European Study Group on Heterosexual Transmission of HIV. Am J Epidemiol 1998;148:88–96.
Koopman JS, Jacquez JA, Welch GW, et al. Role of the Primary Infection in epidemics of HIV infection in gay cohorts. J Acquir Immune Defic Syndr 1994;7:1169–8.
Kahn JO, Walker BD. Acute human immunodeficiency virus type 1 infection. N Engl J Med 1998;339:33–9.(D Pao, D McElborough and )