The lipid profile is important in the risk assessment for cardiovascular disease. The lipid profile includes total cholesterol, high-density lipoprotein (HDL)-cholesterol, triglycerides (TGs) and low-density lipoprotein (LDL)-cholesterol (LDL-C). LDL-C has traditionally been calculated using the Friedewald equation (invalid with TGs greater than 4.5 mmol/L and is based on the assumption that the ratio of TG to cholesterol in very- low-density lipoprotein (VLDL) is 5 when measured in mg /dL). LDL-C can be quantified with a reference method, beta-quantification involving ultracentrifugation and this is unsuitable for routine use. Direct measurement of LDL-C was expected to provide a solution with high TGs. However, this has some challenges because of a lack of standardisation between the reagents and assays from different manufacturers as well as the additional costs. Furthermore, mild hypertriglyceridaemia also distorts direct LDL-C measurements. With the limitations of the Friedewald equation, alternatives have been derived. Newer equations include the Sampson-National Institutes of Health (NIH) equation 2 and the Martin-Hopkins equation. The Sampson-NIH2 equation was derived using beta-quantification in a population with high TG and multiple least squares regression to calculate VLDL-C, using TGs and non-HDL-C as independent variables. These data were used in a second equation to calculate LDL-C. The Sampson-NIH2 equation can be used with TGs up to 9 mmol/L. The Martin-Hopkins equation uses a 180 cell stratification of TG/non-HDL-C to determine the TG:VLDL-C ratio and can be used with TGs up to 4.5 mmol/L. Recently, an extended Martin-Hopkins equation has become available for TGs up to 9.04 mmol/L.This article discusses the best practice approach to calculating LDL-C based on the available evidence.

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Ketamine, a dissociative anaesthetic drug, acts on the central nervous system (CNS) primarily through antagonism of the n-methyl-d-aspartate (NMDA) receptor.[1] Methods of administration include intravenous, intramuscular, snorting, and smoking. [2] Intranasal use which has a very rapid onset of action is common amongst recreational users. [3] Ketamine may be used as an anti-depressant and for recovery from drug abuse.[1] Doses used in abuse are significantly higher than for therapy.[3] For recreational use the usual intranasal dose is 50 mg with abusers regularly using multiple doses to prolong intoxication.

Introduction: Liddle syndrome is an autosomal dominantly inherited disorder usually arising from single mutations of the genes that encode for the alpha, beta and gamma epithelial sodium channel (ENaC) subunits. This leads to refractory hypertension, hypokalaemia, metabolic alkalosis, hyporeninaemia and hypoaldosteronism, through over-activation of the ENaC.Case presentation: We describe a 5-day old neonate who presented with severe hypernatraemic dehydration requiring admission to Steve Biko Academic Hospital in South Africa in 2012. Further evaluation revealed features in keeping with Liddle syndrome. Two compound heterozygous mutations located at different subunits encoding the ENaC were detected following genetic sequencing done in 2020. The severe clinical phenotype observed here could be attributed to the synergistic effect of these known pathological mutations, but may also indicate that one of the other variants detected has hitherto undocumented pathological effects.Management and outcome: This child’s treatment course was complicated by poor adherence to therapy, requiring numerous admissions over the years. Adequate blood pressure control was achieved only after the addition of amiloride at the end of 2018, which raised the suspicion of an ENaC abnormality.Conclusion: To our knowledge, this is the first Liddle syndrome case where a combined effect from mutations resulted in severe disease. This highlights the importance of early recognition and management of this highly treatable genetic disease to prevent the grave sequelae associated with long-standing hypertension. Whole exome sequencing may assist in the detection of known mutations, but may also unveil new potentially pathological variants.What this study adds: This study highlights the importance of developing a high index of suspicion of tubulopathy such as Liddle syndrome for any child presenting with persistent hypertension associated with hypokalaemic metabolic alkalosis.