Deficiency of 2,3-Dimethoxy-5-Methyl-6-Decaprenyl-1,4-Benzoquinone (Mitoquinone) and Hyperlactic Acidosis in Human Immunodeficiency Virus (HIV) Patients with Head and Neck Squamous Cell Carcinoma (HNSCC) Treated with Nucleoside Reverse Transcriptase Inhibitor (NRTI)-Based HAART and Chemoradiation.

Mitoquinone is a nutrient obtained fromm food and produced in small amounts by the body with a crucial component of oxidative phosphorylation process in the mitochondria generating adenosine triphosphate (ATP). Deficiency of mitoquinone has been described based on failure of biosynthesis caused by gene mutation, inhibition of biosynthesis by HMG coA reductase(statins), compromisal of immune system function in breast cancer and acquired immunodeficiency syndrome (AIDS). Patients with (HNSCC) coinfected with HIV and deficient of mitoquinone, progress more rapidly to AIDS and when treated with statins for dyslipidemia, mitoquinone can become severely depressed and cause serious fatal type B lactic acidosis requiring emergent interventions. Correction of mitoquinone deficiency by supplementing mitoquinone may prevent and reverse the lactic acidosis seen in NRTI-based HAART (Highly Active Antiretroviral Therapy) allowing more effective chemoradiation with less side effects of mucositis, anemia and dermatitis. We present a case of a 44 year old female with HIV disease who developed a right tongue base squamous cell carcinoma (T2N0M0) lesion with trismus, elevated epstein-barr virus DNA (EBVDNA-PCR), dyslipidemia, and renal insufficiency was worked up and staged and treatment started with radiation therapy (XRT). No platinum chemotherapy given due to severe renal disease). Seven weeks of radiation therapy was given with interruption caused by grade II-III mucositis overcome by mitoquinone adjuvant therapy. Immune parameters CD4+ level initially was 71/cumm (10%) with a CD4/CD8 ratio 0f 0.17 and CD16+, CD56+ of 143/cumm (20%). A good response to XRT with less trismus and tumour shrinkage but soon after XRT she developed lactic acidosis with evidence of mitoquinone deficiency, 2.45 mmol/L and 0.4 mg/L respectively. Apolipoprotein A-1 level decreased along with high density lipoprotein-cholesterol (HDL-C). Statin therapy was started and lactic acidosis persisted with no further deteriorations of parameters. Lactic acidosis and mucositis (grade I) improved with mitoquinone supplements. The CD4+ level increased to 132/cumm (20%) and CD16+, CD56+ increased to 298/cumm (26%). CONCLUSIONS:HIV disease patients with HNSCC malignancy and mitoquinone deficiency may be at increase risk for mitochondrial DNA toxicity, chemoradiation side effects and severe lactic acidosis when treated with NRTI-based HAART, statins and XRT. Mitoquinone supplementation may prevent and reverse fatal lactic acidosis, modulate immune status and improve response to chemoradiation therapy, survival and quality of life.