Manchester et al from Denver reported a series of 257 pregnancies which were complicated by suspected fetal abnormality on ultrasonography.' Thirty seven per cent of the infants born had additional anomalies not detected by prenatal ultrasonography, and the authors concluded that prenatal diagnoses based on ultrasonography were remarkably accurate but were insensitive to associated anomalies in individual cases. Our study confirms this, a revised diagnosis being made in 53 (40%) of such cases.We believe that examination of midtrimester fetuses by a clinical geneticist is a worthwhile service and improves diagnosis, which in turn benefits the diagnostic teams and parental counselling. It is best carried out by a clinician experienced in dysmorphology, used to normal variations in the appearance of fetuses at various stages in gestation, and familiar with rare dysmorphic syndromes. The collaboration of cytogeneticists and paediatric pathologists is important in defining the full extent of the anomalies in order to arrive at the final post-termination diagnosis, on which the parents will base their future reproductive decisions.We thank Dr T Andrews, regional cytogenetic servicc, anXr his staff and Dr A J Barson, department of pacdiltric pathology, University of Manchester, and his staff for their skilled work and cooperation.

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Microalbuminuria is known to predict mortality in elderly, non-insulin dependent diabetic individuals. To test whether this is also so when studied prospectively and over a longer period, we followed 228 persons with known diabetes mellitus and an age and sex matched, non-diabetic cohort for eight to nine years. Both cohorts were found during a population screening in 1981-1982 of 5292 citizens aged 60 to 74 years. At ascertainment extensive clinical and biochemical examinations including determination of urinary albumin were carried out. At May 15, 1990 111 diabetic and 46 non-diabetics had died (P less than 0.0001). In the diabetic cohort the median value of urinary albumin excretion (UAE) was 17.40 micrograms/min. In the group with values at or above 17.40 micrograms/min 62 died, compared with 40 deaths in the group with values below (P = 0.003). In the non-diabetic cohort the median UAE value was 7.52 micrograms/min. In the upper group 26 died, in the lower 15 (P = 0.05). Cox regression analyses showed coefficients of regression for ln(UAE) of 0.333 (P less than 0.001) for the diabetic group and 0.236 (P = 0.048) for the non-diabetic group. In the Cox model for the diabetics, ischemic heart disease was also of independent significance to mortality. The final model for the non-diabetics included hypertension and sex as significant variables. It is concluded that in a prospective study of elderly diabetics urinary albumin excretion rate is the best prognostic factor for long-term mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

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Summary. Many patients with Type 2 (non-insulin-dependent) diabetes mellitus are treated with insulin in order to control hyperglycaemia. We studied fasting plasma C-peptide, glucagon stimulated plasma C-peptide, and 24 h urinary Cpeptide in relation to clinical type of diabetes in 132 insulin treated diabetic subjects. Patients were classified clinically as Type 1 (insulin-dependent) diabetic subjects in the presence of at least two of the following criteria: 1) significant ketonuria, 2)insulin treatment started within one year after diagnosis, 3) age of diagnosis < 40 years, and 4) weight below 110% of ideal weight of the same age and sex. Eighty patients were classified as Type 1 and 52 as Type 2 diabetic subjects. A second classification of patients into 6 C-peptide classes was then performed. Class I consisted of patients without islet Bcell function. Class II-VI had preserved islet B-cell function and were separated according to the 20%, 40%, 60% and 80% C-peptide percentiles. The two classifications of patients were compared by calculating the prevalence of clinical Type I and Type 2 diabetes in each of the C-peptide classes. This analysis showed that patients with a fasting plasma C-peptide value < 0.20 nmol/1, a glucagon stimulated plasma C-peptide value < 0.32 nmol/1, and a urinary C-peptide value < 3.1 nmol/1, or < 0.54 nmol/mmol creatinine/24 h, or < 5.4 nmol/24 h mainly were Type I diabetic patients; while patients with Cpeptide levels above these values mainly were Type 2. At these limits the percentage, predictive value of positive tests as indicators of Type 2 diabetes were as follows: fasting C-peptide 83%, stimulated C-peptide 86%, and urinary C-peptide expressed as nmol/1 76%, as nmol/mmol creatinine/24 h 79%, and as nmol/24 h 78%. Similarly, the percentage predictive value of negative tests as indicators of Type 1 diabetes were as follows: fasting C-peptide 86%, stimulated C-peptide 88%, and urinary C-peptide expressed as nmol/1 79%, as nmol. mmol creatinine-24 h 81%, and as nmol/24 h 80%. If patients without detectable C-peptide were excluded, the predictive value of negative tests were as follows: fasting C-peptide 81%, stimulated C-peptide 88%, urinary C-peptide expressed as nmol/161%, as nmol/mmol creatinine/24h 69%, and as nmol/24 h 64%. In conclusion, post glucagon C-peptide gives a good distinction between Type 1 and Type 2 diabetes mellitus in insulin treated diabetes while 24 h urinary C-peptide gives a less sensitive distinction between the clinical types of diabetes.