Abayomi O. Akanji

About 15% of the adult Kuwaiti population has type 2 diabetes and over 50% are hyperlipidaemic by current diagnostic criteria. Not surprisingly, coronary heart disease (CHD) is the leading cause of death in Kuwait. Reports from coronary care units in Kuwait suggest that 40–80% of the CHD patients were diabetic and 50–80% hyperlipidaemic. The pattern worldwide is similar. International guidelines have therefore consistently recognised diabetes as a major risk factor for CHD. In our Lipid Clinic population in Kuwait, about 30% are diabetic. The commonest lipid abnormalities seen in Kuwaiti diabetic patients, as elsewhere, are hypertriglyceridaemia with low HDL levels and variable LDL levels. About 75% of the subjects had either mixed hyperlipidaemia or predominant hypertriglyceridaemia. There are possibly some compositional changes in LDL in the diabetic subjects in that there were important differences in the statistical relationships between LDL and HDL and their respective apolipoproteins – apo B and apo A-1 in diabetic as compared to non-diabetic subjects. Other important observations made in diabetic subjects in Kuwait are: (i) similar serum Lp (a) levels and pattern of apo(a) polymorphism with non-diabetic subjects, with no demonstrable relationship between serum levels of Lp(a) and insulin/insulin sensitivity, although with CHD, Lp(a) levels were increased; (ii) diabetic hyperlipidaemic subjects had elevated PAI-1 levels with significant correlations between blood PAI-1 and insulin levels suggesting underlying insulin resistance (syndrome X). Various landmark trials of cholesterol-lowering therapies in the prevention of CHD have consistently demonstrated near-normalization of the increased CHD risk in diabetes. Our experience in Kuwait suggests that diabetic patients and others with mixed hyperlipidaemia benefit from tight glycaemic control, appropriate advice on diet and exercise with regular reinforcement by continuing contact with professional dietitians and regular availability of drugs where prescribed. Often, it is the regular compliance with medication that is important, rather than the specific medication used particularly where HMG CoA reductase inhibitors (statin drugs) are not always available. A useful guideline for management of dyslipidaemia in diabetes is suggested.

Objective: To evaluate the role of serum troponin I (TnI) estimations in the early risk stratification of patients with acute coronary syndromes (ACS) subsequently diagnosed as acute myocardial infarction (AMI) or unstable angina (UA). Subjects and Methods: Blood samples were collected from 86 patients admitted to the Coronary Care Unit of the Mubarak Al-Kabeer Hospital, Kuwait, with a diagnosis of ACS on admission (TnI-1) and after 8 h (TnI-2) and 16 h (TnI-3). Blood was also collected from 38 age-matched healthy controls for comparison. Serum TnI was measured by paramagnetic particle chemiluminescent immunoassay. Results: Serum TnI of 0.3 ng/ml gave a >80% certainty of diagnosis of AMI. Also, TnI-2 Conclusion: In the evaluation of ACS, admission and 8-hour serum TnI 0.3 ng/ml on admission and increasing rapidly by 8 h is likely AMI, and serum TnI >0.05 and <0.3 ng/ml on admission with a mild increase by 8 h is likely due to UA.

Background: In patients with metabolic and nutritional disorders such as diabetes and hyperlipidaemia, where strict compliance to advice on timing and composition of food intake is important, the prolonged daylight fasting during the month of Ramadan could produce undesirable biochemical consequences. Aim: The study aimed to compare pre- and post-Ramadan lipid and lipoprotein profiles in stable Kuwaiti hyperlipidaemic subjects attending a Lipid Clinic. Subjects and methods: The study population comprised 64 adult Kuwaitis (33 M, 31 F) who had been attending a Lipid Clinic for at least 12 months and were considered stable, without any acute systemic illness. At each clinic visit, the following parameters were measured: weight, total cholesterol (TC), triglycerides (TG), HDL, LDL, apo A-1, apo B, glucose and uric acid. These biochemical parameters were measured by routine automated analyzer techniques. The pre-Ramadan values comprised the means of two measurements taken at about 3 month and 1 month before commencement of Ramadan. Post-Ramadan values were obtained within 1 month of the end of the Ramadan fast. The parameters so obtained were compared in the whole group, and then according to gender, glycaemic status and modality of treatment (diet alone or with a fibrate or statin). Results and discussion: In the nondiabetic subjects, apo A-1 and apo A-1/apo B and apo A-1/HDL ratios were increased post-Ramadan (PPEuropean Journal of Clinical Nutrition (2000) 54, 508–513

It is well recognized that blood lipoprotein A [Lp(a)] levels constitute an important risk factor for atherosclerotic vascular disease. In some populations, mainly Caucasian, Lp(a) levels and coronary heart disease (CHD) risk are determined by the pattern of apolipoprotein a [apo(a)] polymorphism. It is currently unclear if these observations apply to other populations and ethnic groups. The aim of the current study is to determine to what extent known apo(a) polymorphisms associate with development of CHD in a Kuwaiti Arab population. Serum Lp(a) levels were measured by enzyme-linked immunosorbent assay and apo(a) isoforms determined by a high-resolution sodium dodecyl sulphate/agarose gel electrophoresis with immunoblotting in two groups of Kuwaiti subjects: healthy controls ( n = 140) and subjects with CHD ( n=140). Blood lipids and anthropometric parameters were also determined in these subjects by standard methods. Serum Lp(a) levels were greater in those with CHD than in those in the healthy group ( P<0·001). There was no consistent trend in the pattern of serum Lp(a) levels found with specific apo(a) isoforms in either group of subjects. There was, therefore, no simple relationship between the isoform pattern (and number of kringle-IV repeats) and serum Lp(a) concentration, unlike in certain other populations. Additionally, almost identical proportions of subjects in either group had singlebanded (homozygous, ~ 70%), double-banded (heterozygous, ~ 23%) and no-band (null, ~ 7%) phenotypes. The distribution of the five identified isoforms (F, S1, S2, S3 and S4) also was almost identical for both groups of subjects, whether homozygous or heterozygous, and whether classified into fast-moving (F, S1 and S2) or slow-moving (S3 and S4) isoforms. We conclude that the frequency and pattern of distribution of apo(a) phenotypes did not differ significantly between healthy control Kuwaiti Arab subjects and those with CHD. It is thus unlikely that an individual's apo(a) phenotype can predict both serum Lp(a) level and risk for CHD, irrespective of race and/or ethnic grouping.

Blood lipoprotein(a) Lp(a) concentrations are an important risk factor for atherosclerosis. The basis for this atherogenic property of Lp(a) and the factors that influence its cross-population levels, however, remain poorly understood. To investigate the relationship between serum Lp(a) and metabolic and anthropometric parameters in a healthy Kuwaiti population. Cross-sectional study. 177 (72 male, 105 female) randomly recruited healthy Kuwait Arabs aged 17-60 y Metabolic parameters in serum: Lp(a), apo(a) phenotypes, lipids and lipoproteins, glucose and urate. Anthropometric parameters: body mass index (BMI) and waist:hip-ratio (WHR). The distribution of Lp(a) concentrations was positively skewed (median 153 mg/l, range 0-1086). Women had higher concentrations-(194, 0-1086) than men (117, 0-779), P = 0.069. Lp(a) and insulin concentrations were significantly higher when the men and women were obese. In all subjects, there were significant correlations between Lp(a) and BMI (r = 0.23), total cholesterol (TC) (r = 0.17) and LDL (r = 0.20). Lp(a) correlated only with glucose in men (r = 0.28). In women it correlated with age (r = 0.20), BMI (r = 0.30), BP (r = 0.20), TC (r = 0.20) and LDL (r = 0.26). Multivariate analyses confirmed BMI and low-density lipoprotein (LDL) as the significant determinants of serum Lp(a). On apo (a) phenotyping, 114 (67%), 51 (30%) and 6 (4%) had single, double and null phenotypes respectively. The isoforms and their corresponding kringle IV repeat numbers were: F (14 repeats in 3%, mean Lp(a) 497 mg/l); S1 (19 repeats in 14%, mean 245 mg/l); S2 (23 repeats in 16%, mean 264 mg/l); S3 (27 repeats in 35%, mean 236 mg/l); and S4 (35 repeats in 28%, mean 235 mg/l). The results from the Kuwaiti population studied suggest that: (1) serum Lp(a) concentrations and distribution are similar to the pattern in Caucasians and Asians but not African-Americans or Africans; (2) serum Lp(a) is variably influenced by BMI and LDL--the impact of either factor differs between the sexes; (3) there is a high frequency of the single-banded phenotype; (4) contrary to reports in some Caucasian and Asian populations, there is no simple relationship between kringle IV repeat numbers and plasma Lp(a) concentrations.

Background/Aim: This study was performed to comparatively evaluate the results obtained for low-density lipoprotein (LDL) cholesterol concentrations by either a newly described direct method or the Friedewald equation in subjects with and without chronic renal disease. Methods: Fasting plasma was obtained from a total of 169 subjects, 105 with normal renal function (including 53 hyperlipidaemic) and 64 with chronic renal disease (nephrotic syndrome and/or chronic renal failure; including 40 hyperlipidaemic patients), and analyzed for LDL cholesterol using the Friedewald equation and a direct LDL assay method. Results: The Friedewald equation and the direct LDL cholesterol assay correlated well with each other (r = 0.79–0.90 in all subjects with plasma triglyceride, TG, levels greater than or less than 4.0 mmol/l and with and without chronic renal disease and/or hyperlipidaemia, all p < 0.0001). The values for LDL cholesterol, however, tended to be higher with the direct measurement. This mean difference was trivial in hyperlipidaemic subjects with (8.5%) and without (7.1%) normal renal function (both p < 0.05), but could be clinically significant in those with TG >4.0 mmol/l (mean difference 18%, p < 0.001). Indeed, bias plots confirmed this observation of wider negative bias for Friedewald estimation in these moderately hypertriglyceridaemic subjects. Conclusion: For most routine laboratories the options immediately available for assessment of lipid levels are the Friedewald equation or the direct measurement. The Friedewald equation and the direct assay method for LDL cholesterol are about equally good for assessment of the LDL status in patients with chronic renal disease and plasma TG 4.0 mmol/l or to patients who, for whatever reason, are unable to produce fasting samples.