Deaths from diabetes are under-reported in national mortality statistics.

Subjects with diabetes who attended rural surveys in Western Australia from 1978 to 1982 were followed up to ascertain death rates and the causes of death recorded on death certificates. Cardiovascular disease was assigned as the direct cause of death in 63% of deaths, with equal rates in male and female subjects, and renal disease in 8% of deaths with the proportion in women (12%) being greater than that in men (4%). The diagnosis of diabetes was stated on only 65% of the death certificates, and in only 24% was diabetes recorded as a direct or antecedent cause. In the same cohort the Australian Bureau of Statistics coded diabetes as the underlying cause of death in 24%, while attributing deaths to cardiovascular disease in 50% of the cases. This study suggests that diabetes is considerably underreported both on doctors' death certificates and in the mortality figures of the Australian Bureau of Statistics.

Prostaglandin E1 therapy for impotence, comparison with papaverine.

The efficacy of prostaglandin E1 as a pharmacological treatment of erectile dysfunction (impotence) was compared with the standard treatment, papaverine, in a single blind, crossover trial. A total of 129 impotent men received intracavernous injections of either prostaglandin E1 (5 micrograms) or papaverine (18 mg.) 1 month apart. Observations by 1 observer recorded 10 to 20 minutes after injection demonstrated that prostaglandin E1 generated a better erection in 72 men (55.8%) compared to papaverine. Papaverine was more effective than prostaglandin E1 in 23 men (17.8%, chi-square 6.26, p less than 0.025). Subjective assessment by the patients who detected a difference showed that 71 (55%) preferred prostaglandin E1 and 35 (27%) preferred papaverine (chi-square 11.56, p less than 0.001). A total of 34 men achieved full erections with prostaglandin E1 compared to 17 who used papaverine.

An estimate of diabetes prevalence from a national population sample: a male excess.

We report the prevalence of diabetes in a population sample of 10,083 persons who were aged 25 to 64 years in eight city centres. One hundred and sixty-nine persons were known to have diabetes and 48 persons were newly-discovered to have diabetes on the basis of fasting hyperglycaemia (plasma glucose level, equal to or greater than 7.8 mmol/L). Type-1 diabetes was identified by clinical criteria and accounted for 19% of cases of known diabetes, but this proportion ranged from 67% of persons with known diabetes in the age-group of 25-29 years, to between 9% and 15% in the age-groups of persons who were 50 years of age and over. For both known and newly-discovered cases, persons with type-2 diabetes showed a significant male preponderance, which suggests that an environmental factor is operating preferentially on male subjects to cause this form of diabetes. The results of the present study, when taken with those of other recent prevalence studies, enable an approximate estimate of numbers of persons with diabetes in Australia. Approximately 250,000 persons have diagnosed diabetes, of whom 40,000 persons have type-1 diabetes, including 7000 persons who are less than 25 years of age. The number of persons with undiagnosed diabetes who could be identified on the basis of fasting hyperglycaemia is estimated to be 75,000; an additional 150,000 persons would be diagnosed to have diabetes if they were to undergo glucose tolerance tests. This study gave prevalence rates for known diabetes in Australia in 1984 of 1.6% at all ages and 2.4% for adults who were 21 years of age and older; additionally, the estimated prevalence rates for undiagnosed diabetes were 1.4% for all ages and 2.2% for adults.

Diabetes in Western Australian children: descriptive epidemiology.

The prevalence and incidence of diabetes mellitus in the age group zero to 14 years in Western Australia were determined from a survey by means of Schools Health Services. Additional information from the State's computer-linked hospital records system, the State's only children's hospital, diabetic clinics and physicians enabled virtually complete ascertainment of cases of childhood diabetes. Only 60% of school-age diabetic children were known to school nurses before the survey, but the nurses were able to identify two-thirds of the remainder during the survey. Among non-Aboriginal children, the prevalence of diabetes in the age group zero to 14 years was 0.59 per 1000 children and the incidence was 12.3 per 100,000 children per year. These rates are somewhat lower than those that have been reported from the United Kingdom and North America, and substantially lower than the rates that were reported from Scandinavia. All but one of the diabetic children who were identified required insulin and were assumed to be insulin-dependent. An excess of boys was found. None of 8715 Aboriginal or part-Aboriginal children had insulin-dependent diabetes mellitus, which indicates that this racial group has a low prevalence of this condition. In case--control studies, which used questionnaires for parents, no significant trends were found in relation to the history of immunizations or of specific viral illnesses except for a past history of varicella which was less frequent in diabetic children. A past history of established breast-feeding (of more than one week) was less frequent in diabetic children, as was the ingestion of vitamin C supplements before the onset of diabetes. Some evidence for a seasonality of onset was obtained. The diabetic children were absent from school for more days and had more admissions to hospital than did non-diabetic children. The majority of diabetic children were prescribed insulin twice a day or more often (84%); performed home blood-glucose monitoring (74%); and attended hospital diabetic clinics (91%).

Diabetes and impaired glucose tolerance. A prevalence estimate based on the Busselton 1981 survey.

We have estimated the prevalence of diabetes and impaired glucose tolerance from the Busselton 1981 Population Survey using the 1980 World Health Organization (WHO) criteria. Standardized to the Australian non-Aboriginal population aged 25 years and over, the prevalence rates in this white community were 2.5% for known diabetes; 0.9% for newly discovered diabetes; 2.9% for impaired glucose tolerance; and 6.3% for all categories of abnormal glucose tolerance. There appears to have been a real increase in the frequency of diabetes since 1966. Using fasting serum C-peptide values and clinical criteria, 14% of all diabetic subjects were insulin-dependent. The male:female ratio for all categories of abnormal glucose tolerance was 1.4:1. Data from the United States indicate spectacularly higher rates for diabetes and impaired glucose tolerance in the white population. A national study of the prevalence of diabetes and impaired glucose tolerance in Australia is recommended. For epidemiological purposes, a single blood glucose value two hours after a 75 g oral glucose tolerance test is sufficient to categorize glucose tolerance as defined by WHO.

Treatment of cryptorchidism with pulsatile luteinizing hormone-releasing hormone (LH-RH).

This preliminary report describes a new method of treating bilateral cryptorchidism that may modify the need for surgical intervention. Four of five boys (3 1/2, 3 1/2, 7, 11 and 12 1/2 years of age) given hourly subcutaneous pulses of luteinizing hormone-releasing hormone (LH-RH, 10 to 100 micrograms/day, given in a 3-min pulse every hour) showed evidence of testicular descent after 3 to 19 weeks. The battery-operated, programmable syringe driver was well tolerated by the boys, and the daily insertion of the scalp-vein needles was managed at home by their parents.

Residual pancreatic function in insulin dependent diabetics.

The relative contributions of alpha and residual beta cell function and the presence of insulin binding antibodies to indices of glucose control have been assessed in a group of 44 patients with insulin dependent disease of variable duration. Residual beta cell secretion was detected in 18 patients (40%) but no patient receiving insulin for more than five years showed evidence of residual function. Indices of glucose control were significantly better (p less than 0.001) in patients demonstrating residual secretion. In contrast, no relation was found between glucose control and either fasting of post prandial plasma glucagon concentrations. Insulin binding antibodies were detected in all but two patients but did not correlate with either daily insulin dose or glucose control. These results are consistent with the view that residual beta cell function contributes to improved glucose control in the yearly years of insulin dependency but alpha cell function and insulin antibodies do not.

Pituitary function in normoprolactinaemic infertile men receiving bromocriptine.

A double blind trial of bromocriptine 7.5 mg daily versus placebo was carried out in ten infertile men. Pretreatment basal plasma prolactin, thyroid stimulating hormone (TSH) testosterone and luteinizing hormone (LH) concentrations were normal, but plasma follicle-stimulating-hormone (FSH) was raised in four individuals. After 4 months treatment with bromocriptine a significant fall in plasma prolactin was observed (P less than 0.01), both under basal conditions and following thyroid stimulating hormone releasing hormone (TRH). Basal plasma gonadotrophin, testosterone and thyroid stimulating hormone (TSH) concentrations did not alter. No change in sperm density, volume or motility was noted. However an apparent fall in the peak plasma LH (but not FSH) response to gonadotrophin releasing hormone (LHRH) was observed in patients receiving bromocriptine. This reduction in plasma LH responsiveness was significant when compared with the baseline response (P less than 0.05) but failed to reach significance when compared with the placebo response. It is concluded that prolonged bromocriptine therapy in normoprolactinaemic men does not suppress FSH secretion, and any reduction in plasma LH responsiveness to LHRH is not accompanied by a significant fall in plasma testosterone.

1,25-dihydroxy-vitamin D3: a new treatment for hypoparathyroidism.

Eleven subjects aged four to 76 years with primary hypoparathyroidism have been treated with 1,25-dihydroxycholecalciferol (1,25-D3). Five subjects were not on vitamin D analogues before starting this drug. 1,25-D3 was found to be an effective treatment and a rapid biochemical response to dose adjustments was observed. In two subjects hypercalcaemia and reversible renal failure occurred. Thiazide-type diuretics necessitated dose reductions in a further two subjects. A scheme for starting hypoparathyroid subjects on this treatment is suggested. The need for regular biochemical assessment and awareness of possible drug interactions is emphasised. It is felt that 1,25-vitamin D3 has practical advantages over traditional forms of vitamin D in the treatment of hypoparathyroidism.