PubMed · 15588451
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2004. Piscator.. https://doi.org/10.1258/0004563042466811
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Lactic acidosis is a rare but potentially life-threatening complication of antiretroviral therapy (ART) and is commonly considered in the differential diagnosis of patients on ART. In the developing world, definitive diagnosis by laboratory measurement of lactate may be impossible. Point-of-care devices are available that provide simple, accurate measurements of lactic acid levels at relatively low cost. Their use in an HIV treatment programme in rural Haiti has greatly assisted clinical decision-making in patients with symptoms suggestive of lactic acidosis.
The recommendations made in this review are based on the current clinical knowledge with regard to the origin and therapy of lipodystrophy. They should be regarded as provisional and will change with expanding knowledge. The recommendations for treating dyslipidaemia in particular are oriented closely on the American recommendations of the National Cholesterol Education Program (NCEP III), and may be regarded both by HIV practitioners and patients as excessive and too rigid. The therapeutic goals of the NCEP in the first intervention studies in HIV-positive individuals were only achieved for a small proportion of the HIV patients. In addition, preliminary results suggest a potentially higher risk of adverse events in HIV-patients under statins or fibrates. The clinical efficacy of interventions with lipid lowering drugs has not been validated in HIV-seropositive patients. However, therapeutic decisions so far have been based on data obtained in non-HIV cardiovascular intervention studies. With more and more results becoming available from the HIV patient population a revision of these recommendations will be required.
Cerebral tissue acidosis following ischemia or traumatic brain injury contributes to cytotoxic brain edema formation. In vitro lactacidosis induces swelling of glial cells by intracellular Na+- and Cl--accumulation by the Na+/H+-antiporter, Cl-/HCO3--antiporters and the Na+-K+-2Cl--cotransport. The present study aimed to elucidate whether mechanisms of lactacidosis-induced glial swelling are dependent on intra- or extracellular Ca2+-ions. Therefore, C6 glioma cells were exposed to a lactacidosis of pH 6.2 in standard or calcium-free medium and following intracellular calcium chelation. Cell volume and intracellular pH were assessed by flow cytometry. Lactacidosis of pH 6.2 induced a prompt and sustained swelling of suspended C6 glioma cells reaching a maximum of 128% within 60 min. Omission of Ca2+ from the suspension medium strongly attenuated cell swelling while chelation of intracellular Ca2+ had no effects. Intracellular acidosis was not affected by either treatment. The present data show a strong dependency of lactacidosis-induced glial swelling upon extracellular Ca2+ while intracellular acidosis is not affected by omission of [Ca2+]e. Therefore, our data suggest that the Na+-K+-2Cl--cotransporter, the only so far known transporter involved in cell volume regulation but not in pHi regulation during lactacidosis, is activated in a [Ca2+]e-dependent manner.