DOI: 10.1097/01.aids.0000237380.54186.35
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PMID: 16847419
Issn Print: 0269-9370
Publication Date: 2006/07/13
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Excerpt
We describe the first case of a severe cytomegalovirus-associated haemorrhagic colitis during acute HIV infection.
Patient A.B., a 35-year-old woman, had a history of Hodgkin's lymphoma, splenectomy, chemotherapy and roentgen therapy in 1984. On 11 March 2005 she presented with a sore throat, maculopapular rash associated with cervical and axillary lymphoadenopathy and elevation of liver enzymes. Fifteen days later oral aphtous ulcers and fever appeared. By 12 April 2005 she was HIV positive with a Western blot pattern of response to the two main determinants (p24, gp160) alone. The source was heterosexual contact. The CD4 T-cell count was 1305 cells/μl and the HIV-RNA viral load exceeded 750 000 copies/ml (polymerase chain reaction HIV-RNA Amplicor Monitor; Roche, Branchburg, New Jersey, USA). Jaundice, generalized lymphadenopathy, hepatomegaly, numerous deep oral ulcers, and tachycardia were present. Blood analyses showed anaemia, thrombocytopenia, neutropenia, lymphocytosis, hyperbilirubinemia, hypoalbuminemia and an important elevation of all liver enzymes. A whole-body computed tomography scan showed a muff-like thickening of the colic wall. Three days later intravenous gancyclovir therapy was started upon suspicion of disseminated cytomegalovirus infection, but the patient rapidly worsened, with uncontrollable intestinal bleeding, life-threatening anaemia, hypotension, and anuria. On 20 April 2005, she underwent colonoscopy, which revealed a massive quantity of deep bleeding ulcers, with a ‘shirt-button’ shape, in a hyperplasic mucosal surface. A subtotal colectomy was performed. On 22 April 2005, cytomegalovirus antigen (50 cells/ml) was detected in the blood, and immunohistochemistry showed the presence of the virus in intestinal biopsies. Intravenous gancyclovir was continued, resulting in the disappearance of cytomegalovirus antigen from the blood, regression of fever, aphtous ulcers, hepatitis and anaemia, and an improvement in her general condition. On 6 May 2005, she started oral gancyclovir, but presented with gastrointestinal intolerance both to it and to oral valgancyclovir, thus she continued the maintenance phase with cidofovir. HAART (tenofovir plus lamivudine plus boosted fosamprenavir) was started on 2 May 2005. After discharge, the patient continued to be prophylaxed with cidofovir and cotrimoxazole.
Cytomegalovirus and HIV-specific (env and gag) cytokine (IL-10 and IFN-γ) production and CD4 and CD8 cell post-thymic maturation pathways were checked at two time points: before starting HAART and after 4 months of therapy. After 4 months of HAART: (i) cytomegalovirus and HIV-specific IL-10 synthesis was reduced with a consequent increase in the IFN-γ: IL-10 ratio; (ii) HIV and cytomegalovirus-specific naive CD4 T cells increased, whereas effector memory and terminally differentiated CD4 T cells were reduced; and (iii) HIV and cytomegalovirus-specific naive CD8 T cells were reduced, whereas HIV and cytomegalovirus-specific effector memory and terminally differentiated CD8 T cells were increased.
On 28 October 2005, the patient presented with hepatitis. Serology for hepatotropic viruses and parasites were negative. The withdrawal of ritonavir did not produce any result, but the discontinuation of HAART led to a rapid normalization of liver enzymes. On the basis of the immunological results, the prophylaxis with cidofovir and cotrimoxazole was interrupted to improve hepatic function. The patient started a new HAART regimen (zidovudine plus lamivudine plus tenofovir) on 14 December 2005, when HIV viremia was 48 000 copies/ml.
