HIV Infection Presenting as Haemophagocytic Syndrome

The authors describe a case of a 48-year-old man who presented with four weeks of fever, generalized malaise, weight loss, right upper quadrant abdominal pain and hepatosplenomegaly. He evolved with pancytopenia, bone marrow haemophagocytosis and hyperferritinaemia. Recent diagnosis of HIV infection, with the exclusion of other plausible causes, prompted the diagnosis of haemophagocytic syndrome (HPS) secondary to HIV. Despite intensive care support and initiation of antiretroviral therapy, the patient died. HPS diagnosis secondary to HIV alone demands the exclusion of all the other secondary causes. The best approach includes early diagnosis and specific treatment of the associated cause, whenever possible.

Lymphadenopathy after Initiating HAART in an HIV-positive Patient with Kaposi's Sarcoma: a Case of Multicentric Castleman's Disease

We present the case of a 33-year-old lady who was diagnosed with disseminated Kaposi’s sarcoma and HIV infection. The patient improved on highly active antiretroviral therapy (HAART), however, nine days into treatment, she became febrile and dyspnoeic and developed tender cervical and axillary lymphadenopathy. Despite treatment for suspected sepsis and immune reconstitution, she died in intensive care. Lymph node biopsies revealed coexistent Castleman’s disease and Kaposi’s sarcoma. Initiation of HAART can be rarely associated with unmasking and rapid progression of Castleman’s disease, a phenomenon called immune reconstitution. Urgent investigation and treatment with agents such as steroids and cytotoxic drugs can be life-saving.

Ischemic Stroke as the Initial Manifestation of Neurosyphilis in a Young Adult Patient Positive for Human Immunodeficiency Virus

A 31-year-old man with pontine infarction was referred to our hospital for further evaluation and treatment. At admission, his neurological examination was unremarkable. No lymphadenopathy or skin lesions were found. The Treponema pallidum haemagglutination test, rapid plasma regain test and fluorescent treponemal antibody absorption test of immunoglobulin G were positive in both serum and cerebrospinal fluid (CSF). CSF analysis showed lymphocytic pleocytosis. The patient had male-to-male sexual contact and was found to be HIV positive. Physicians should be aware that acute ischaemic stroke may be the first manifestation of neurosyphilis in a young adult, especially with HIV infection.

Immunologic Storm Simulating Systemic Lupus Erythematosus Following Parvovirus B19 Infection

Background: The appearance of symptoms compatible with systemic autoimmune diseases has been described in relation to several viral infections like HIV, cytomegalovirus and especially PVB19, depending on the evolution of the immunological condition of the host and their age. We present a young immunocompetent male patient, with clinical manifestations simulating systemic lupus erythematosus (SLE) with important activation of cytokines. Methods: For quantification of the different cytokines in plasma, a commercially available multiplex bead immunoassay, based on the Luminex platform (Cat # HSCYTO-60SK-08, Milliplex® MAP High Sensitivity, Millipore), was used according to the manufacturer’s instructions. All samples were run in duplicate and the data (mean fluorescence intensity) were analyzed using a Luminex reader. The mean concentration was calculated using a standard curve. Results: The clinical evolution was favourable without the need for any specific treatment, showing complete recovery after two months. Whilst the symptoms and viral charge were disappearing, the anti-DNA continued to increase and we demonstrate important activation of IL-10, IL-6 and TNFα cytokines as a result of a hyperstimulating response by an immunocompetent hyperfunctional system, which persists after clinical improvement. We should emphasize the behaviour of two cytokines: IL-12p70 and IL-2, which showed opposite tendencies. Conclusions: Viral infections, especially PVB19, can produce or simulate several autoimmune diseases as a hyperstimulation response from an immunocompetent hyperfunctional system. Consequently, a persistent increase of autoantobodies and important activation of cytokines, even after clinical improvement and seroconversion, can be demonstrated.