ABSTRACT
It will be obvious from the foregoing that type IV hyperlipoproteinaemia is heterogeneous and unlikely to have any single metabolic cause. Despite methodological difficulties associated with the interpretation of the results of experiments in which triglyceride turnover or VLDL apo B turnover have been investigated,79,80 it is evident that in most patients with type IV hyperlipoproteinaemia the cause is an increased input of hepatic VLDL into the circulation.65,81-92
Since the triglyceride removal mechanism is readily saturable, its capacity becomes a more significant factor in patients in whom increases in production are extreme. Often, too, some partial defect in catabolism or a catabolic rate towards the lower end of the normal distribution seems to be present,93-96 which in the absence of any increase in production would be insufficient to take the serum triglyceride concentration out of the normal range. The so-called familial endogenous hypertriglyceridaemia may be an expression of a more marked catabolic defect,88 and it is in this type of patient that some additional stimulus to triglyceride production, such as alcohol, oestrogen administration or diabetes mellitus, or some further slowing of catabolism, such as β-blockade, hypothyroidism or diabetes mellitus, may lead to the progression of relatively mild type IV hyperlipoproteinaemia to the type V phenotype with its attendant risk of acute pancreatitis.97
