Harry TC, Stuart H, Wright M, Williams M, Brett B; International Conference on AIDS (15th : 2004 : Bangkok, Thailand).
Int Conf AIDS. 2004 Jul 11-16; 15: abstract no. B10268.
Bure Clinic,James Paget Healthcare NHS Trust, Great Yarmouth, United Kingdom
Background: A 26 years old white female was diagnosed HIV-1 in October 1995. Baseline CD4 count was 50 cells/ mu l. She started AZT, DDI in November 1995. Treatment was modified due to drug reactions from 1996 - 2001. After Virco VirtualPhenotype she started D4T, DDI & Tenofovir in June 2002. Presentation: Viral load in June 2002 was 6.20 log 10 copies /ml and CD4 T lymphocyte count was<10 cells/ mu l. Full blood count, liver function test, urea & electrolytes were normal. She weighed 62 kg. She was admitted unwell in November 2002, severely jaundiced with vomiting, nausea and dyspnoeic at rest. Bilirubin levels were 364 mumol/ml, blood pH was 7.02 and pCO2 was 0.8. Virological screen for hepatitis were normal. A diagnosis of severe lactic acidosis, secondary to mitochondrial dysfunction and hepato-toxicity was made and her anti-retroviral therapy was stopped. She was transferred to the ICU and her convalescence was turbulent. She was discharged December 2002 after 42 days weighing 35 kg and had amenorrhoea. She was seen in January 2003 and was no longer jaundiced. She weighed 44 kg and was on drug holidays. In May 2003 she weighed 56 kg and repeat Virco VirtualPhenotype showed (TAM), 41, 67, 215 including 44, 184,103, 181, 10, 36, 71 & 90. Subcutaneous T20, 3TC, Fosamprenavir, Ritonavir and D4Twas started. Outcome: In November 2003, CD4 count was 250 cells/ mul and she had a 4 log [down arrow]in viral load. She now weighed 59 kg and LFT, U & E was normal. She was well and her menstrual periods were normal. Conclusion: Lactic acidosis if associated with mitochondrial dysfunction and hepato-toxicity has a high mortality. Our patient survived with discontinuation of antiretroviral drugs, haemofiltration and supportive measures. Use of DDI, D4T& Tenofovir is associated with mitochondrial toxicity & lactic acidosis. T-20 fusion inhibitor contributed to the efficacy in viral suppression and immune reconstitution.
Publication Types:
Keywords:
- Acidosis, Lactic
- Antiretroviral Therapy, Highly Active
- CASP4 protein, human
- CD4 Lymphocyte Count
- CD4-Positive T-Lymphocytes
- Caspases
- Didanosine
- Drug Therapy, Combination
- Female
- HIV Envelope Protein gp41
- HIV-1
- Humans
- Lamivudine
- Nucleosides
- Peptide Fragments
- Stavudine
- Viral Load
- Zidovudine
- drug therapy
- enfuvirtide
- immunology
- therapy
- virology
Other ID:
UI: 102276417
From Meeting Abstracts