HIV-oireet (englanniksi)

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Signs and symptoms

The most common symptoms associated with PHI are fever,
night sweats,
arthralgia,
myalgia,
malaise,
headache,
nausea,
vomiting,
diarrhea, and
anorexia.

Commonly reported signs include
pharyngitis,
rash,
weight loss,
lymphadenopathy,
leukopenia, and
thrombocytopenia, in addition to
meningitis,
neuropathy, and
encephalopathy


The acute HIV infection rash is a very common manifestation, occurring in over 50% of cases as reported in most series.[25] This rash classically appears as a maculopapular eruption primarily on the upper trunk (Fig. 1), neck, and face, is nonpruritic and nonscaling, and generally disappears within 2 to 3 weeks.[26,27] Less commonly, it manifests as roseola-like or vesiculopapular (Table 1).[28,29] to other viral- and drug-induced exanthemas.[30,31] Exanthematous skin rash commonly associated with primary HIV-infection. This patient's rash is concentrated on his upper back.

Neurologic manifestations such as lymphocytic meningitis, encephalopathy, and polyneuropathy are frequently reported as symptoms of PHI.[32-34]. Ho and colleagues[35] described acute infection of the central nervous system (CNS) with demonstration of virus in the cerebrospinal fluid (CSF) coincident with seroconversion for HIV and a syndrome of acute self-limited aseptic meningitis. Since then, this syndrome has been reported frequently. Encephalitis with seizures was described in 1985 in a small case series published in Lancet.[33] Subsequent case reports have described other neurologic manifestations at the time of seroconversion -- namely, Guillain-Barré syndrome, facial nerve palsy, acute myelopathy, brachial neuritis, and a ganglioneuronitis causing ataxic neuropathy (Table 2).[28,36-39]

Opportunistic infections have been reported at the time of acute seroconversion, presumably secondary to the profound immunosuppression that can occur during this period. Multiple cases of oral and esophageal candidiasis have been described in association with a transient, severe loss of CD4 cells.[2,40-43]Several studies have also reported a higher incidence of non-candidal esophageal ulcerations, raising the possibility that such mucosal ulceration may provide a favorable local environment for the growth of Candida species.[44-46] There have also been case reports of Pneumocystis carinii pneumonia occurring during PHI, in addition to cases of cytomegalovirus (CMV) colitis, cerebral toxoplasmosis, and tuberculosis (Table 3).[2,47,48]

More unusual manifestations of acute HIV infection have included clinical hepatitis,[49] acute pneumonitis,[50] lymphocytic alveolitis,[51] aplastic anemia,[52] vasculitis,[53] and 1 case each of rhabdomyolysis, nephrosis, and renal failure[54]. In a review of 31 cases of symptomatic PHI, Kinloch-de Loes and coworkers[10] noted that 43.3% of their patients developed oral or genital mucosal ulcerations, and that those patients were more likely to have acquired their infection sexually. The 5 IVDUs in their series had no mucocutaneous ulcerations, raising the possibility that these lesions are a result of direct viral inoculation. In another study by Rabeneck and associates,[55] electron microscopy of tissue taken from esophageal ulcerations in 8 homosexual men during PHI revealed viral particles, which also supports this theory.

Typical laboratory abnormalities seen at the time of PHI include transient leukopenia, lymphopenia, and thrombocytopenia with inversion of the ratio of helper to suppressor cells. Some patients also develop anemia and elevated transaminases. CSF analysis often reveals a pleocytosis with elevated protein levels.[8,24]



Clinical Features

Symptomatic PHI occurs in 53% to 92% of patients.[4-6]. However, the criteria used to define an acute retroviral syndrome vary among studies, as does the method of reporting symptoms. Therefore, when these symptom rates are compared with the rates of similar symptoms in seronegative control subjects, the incidence of symptomatic PHI is closer to 34% to 53% in some studies.[7,8] The clinical syndrome of PHI has been described in all of the major risk groups, including homosexual men,[9,10] intravenous drug users (IVDUs),[11] blood transfusion and transplant recipients,[12-15] health care workers with needle stick injuries,[16-18] and heterosexuals.[19]

Symptoms associated with seroconversion were first reported in 1984,[16] and the clinical syndrome of PHI was subsequently described in 1985.[11,20] When the Centers for Disease Control and Prevention (CDC) published their updated classification system for human T-cell lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV) infections in 1986, "acute infection" was defined as "a mononucleosislike syndrome, with or without aseptic meningitis, associated with seroconversion for HTLV-III/LAV antibody."[21]Since that time, however, it has become clear that the clinical manifestations of primary HIV infection are protean and can include opportunistic infections. While the denotation of PHI as a mononucleosis-like illness encompasses many of the more common manifestations of the syndrome, the definition of acute HIV-1 disease needs to be broadened.[22] Only 1 case of symptomatic primary HIV-2 infection has been reported in the literature.[23] Very little has been written regarding the manifestations of PHI in children.

After exposure to HIV, there is an incubation period of approximately 2 to 6 weeks before symptoms occur. It is often difficult, using standard ELISA and Western blot methods, to determine whether someone is in the "window" period before the production of IgG antibody; however, a number of other serologic assays can be used.HIV-specific IgM antibody, p24 antigen levels, HIV-1 DNA and RNA levels, and viral isolation by culture have all been used to establish the diagnosis of PHI. Typically, the time between infection and detection of antibodies by ELISA is 1 to 2 months. The acute syndrome lasts 1 to 6 weeks and is usually self-limited.[5]

http://www.medscape.com/viewarticle/416697_2

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