Aminotransferases would appear to be enjoying something of a renaissance – if the number of journal articles in which they feature is a reliable indicator. As if we are not exposed to enough borderline raised results as it is, the aminotransferases have now been accorded predictive powers. A recent paper can be cited as the cause for the floodgates to open even more with respect to an increasing number of requests (Hepatology 2008;47:880–7) as reviewed in a commentary in the Lancet (Lancet 2008;37:1822–3). The humble aminotransferases (which have undergone numerous name changes since) were first identified as markers of liver damage in the 1950s and have been a staple of the routine biochemistry profile since then. The article in Hepatology argues that they can be used to predict mortality in the subsequent decade on the basis of a study of a cohort of patients attending the Mayo Clinic in 1995. Their results were abstracted from the laboratory database and the patients followed-up for the next 11 yr. Increases in aspartate aminotransferase between one and two times of normal were associated with a standardized mortality ratio of 1.32. The higher the increment so the greater the odds stacked against you. Alanine aminotransferase (ALT) results which were more than twice normal (a common enough finding in my experience of patients attending primary care) were associated with a ratio of 1.51. Similar inferences were made from data obtained for German construction workers in 1998 and in the widely referenced population study undertaken in South Korea (Br Med J 2004;328:983–6). No one disputes that increases in the aminotransferases are linked to coronary artery disease via the metabolic syndrome and might also be indicative of alcohol abuse. The Lancet commentary debates whether there is a case for population screening to identify individuals with increased aminotransferases who would be targeted for clinical intervention. Given the plethora of scenarios in which aminotransferases are increased – raised body mass index, hepatitis, strenuous exercise, thyroid disease, etc., the advice would be caution (thankfully). Repeated measurements often fail to confirm the original abnormality in up to one-third of cases. Conversely, the low ALT observed in extreme old ages doubles the risk of mortality. But really is that not over-stating the glaringly obvious – the longer we live, the closer we move towards the ‘great laboratory in the sky’ whatever the ALT?

Nor is the other end of the age-spectrum spared. The authors of a recent study (Arch Dis Child 2007;92:1109–12) were all too aware of the plethora of literature on ‘transaminitis’ in asymptomatic adults, so much so that they referenced 10 articles in the bibliography. The credence given to marginal disturbances would have been of concern some time ago, but the chemistries on modern analytical platforms are now so robust that small increments can indeed be regarded as clinically significant – the exclusion of all possible in vivo and in vitro interference not withstanding. Their study design was based on the recruitment of infants and children with isolated increases in the aminotransferases of 1.5 times of the upper limit of normal. The definition of normal was somewhat problematic however, as this was actually not specified – rather there was a discussion of literature sources of reference ranges some of which were more than 25 years old. The authors were of the opinion that infants less than 1-yr-old have higher ALT than older children. A total of 72 infants and children under the age of 4 yr who exhibited an increased aminotransferase of more than 3 months duration in the absence of cholestasis were followed-up for a period of up to 3 yr. The majority (73.6%) demonstrated a normalization of the enzyme activity within the study period. The authors were confident that an isolated increase in aminotransferases in thriving infants with no evidence of cholestasis is a benign, self-limiting phenomenon. This outcome will come as a relief to parents who will be spared the anguish of up to nine collections of blood (as documented in the paper) from their healthy infants in order to confirm it. As a final comment on ‘transaminitis’ in the older child, one referenced study implicated obesity as a major culprit.

And finally, something all together different … the recreational drug users in Leipzig in the former DDR got something more than they bargained for – in reality they were distinctly short-changed – in their purchases of marijuana (N Engl J Med 2008;358:1641–2). There has been a recent epidemic of lead-poisoning in the city. The patients (29 over a period of 3–4 months) had the classical signs and symptoms of the poisoning – cramps, nausea, vomiting, neurological symptoms and the tell-tale ‘Burton's line’. There were some pretty impressive blood lead results – the highest being >20 μmol/L (if my mental arithmetic is correct). The astute physicians made a prompt diagnosis in most cases and initiated chelation therapy. However, the source of the poisoning was a mystery. The patients ‘profiles’ were studied and shown to share similarities of being young, unemployed or students ( is one synonymous with the other in the eyes of the German law- enforcers?), smoked and had body jewellery. The renowned German means of interrogation elicited a marijuana habit. The material was found on analysis by atomic absorption to contain elemental lead – further inspection revealed that the marijuana had been ‘cut’ with lead to increase its weight. The average lead content was 10% by weight which increased the dealers profit further to the tune of 1000 €/kg. Heavy, man…………………………………………….…