Trends in bed occupancy for inpatients with diabetes before and after the introduction of a diabetes inpatient specialist nurse service.

AIMS: To compare diabetes bed occupancy and inpatient length of stay, before and after the introduction of a dedicated diabetes inpatient specialist nurse (DISN) service in a large UK Hospital. METHODS: We analysed bed occupancy data for medical or surgical inpatients for 6 years (1998-2004 inclusive), with a DISN service in the final 2 years. Excess bed days per diabetes patient were derived from age band, specialty, and seasonally matched data for all inpatients without diabetes. We also analysed the number of inpatients with known diabetes who did not have diabetes recorded as a discharge diagnosis. RESULTS: There were 14,722 patients with diabetes (9.7% of all inpatients) who accounted for 101 564 occupied bed days (12.4% of total). Of these, 18 161 days (17.8%) were excess compared with matched patients without diabetes, and were concentrated in those < 75 years old. Mean excess bed days per diabetes inpatient under 60 years of age was estimated to be 1.9 days before the DISN appointment, and this was reduced to 1.2 bed days after the appointment (P = 0.03). This is equivalent to 700 bed days saved per year per 1000 inpatients with diabetes under 60 years old, with an identical saving for those aged 61-75 years (P = 0.008), a saving of 1330 diabetes bed days per year by one DISN. Excess diabetes bed occupancy was 167 excess bed days per year per 1000 patients with diabetes in the local population after the DISN appointment. One quarter of the known Type 2 diabetes population were admitted annually, but one quarter of patients had no diagnostic code for diabetes. CONCLUSIONS: Diabetes excess bed occupancy was concentrated in patients < 75 years old, and this was reduced notably following the introduction of a DISN service.

A mobile screening programme for the cardiovascular and microvascular complications of Type 2 diabetes in primary care.

The Diabetes National Service framework (NSF), and the quality payments in the new contract for UK General Practitioners, promote regular screening for diabetes complications. The new contract also includes immediate incentives to meet screening and quality targets, but it will be difficult to meet these targets in primary care. We have developed a mobile 'annual review' programme for patients with Type 2 diabetes managed solely in primary care, that screens for cardiovascular disease, hypertension, retinopathy and neuropathy at the patient's general practice, and gives written foot care, dietary advice and level 1 smoking cessation advice to all patients.

An integrated mobile foot and retinal screening programme for people with Type 2 diabetes managed in primary care.

AIMS: To undertake a vascular and neurological assessment on the feet of all patients with Type 2 diabetes managed solely in local primary care. METHODS: A mobile screening podiatrist (working with an existing mobile retinal screening programme) screened a selected population of 4022 patients with Type 2 diabetes managed solely in 82 general practices. Doppler pressure assessments of peripheral vasculature, bioesthesiometer and monofilament assessment of peripheral neuropathy. RESULTS: This service was administratively simple to set up and integrated well with the retinal screening service and secondary care foot clinic, and was valued by the practices. Disease prevalences were 1.04% for foot ulceration, 19% for peripheral vascular disease and up to 29% for peripheral neuropathy. CONCLUSIONS: This programme screens all patients with known diabetes managed solely in primary care within a district and describes foot morbidity and allows risk stratification. This pattern of service could be a useful template for discussing the diabetes National Service Framework with primary care groups.

Impact of pregnancy on the progression of diabetic retinopathy in Type 1 diabetes.

AIMS: To evaluate the impact of pregnancy on the progression of diabetic retinopathy in women with Type 1 diabetes mellitus and to identify risk factors for the progression of retinopathy during pregnancy. METHODS: One hundred and seventy-nine pregnancies in 139 women with pregestational Type 1 diabetes were studied prospectively between January 1990 and December 1998. Dilated fundal examination was performed at booking, 24 weeks and 34 weeks or 4-6 weekly if retinopathy present at booking. Data were collected on glycaemic control (HbA(1c)) throughout pregnancy. RESULTS: Progression to proliferative retinopathy was seen in four (2.2%) pregnancies while moderate progression was seen in a further five (2.8%) pregnancies. Progression of retinopathy was significantly increased in women with duration of diabetes 10-19 years compared with duration < 10 years (10% vs. 0%; P = 0.007) and in women with moderate to severe background retinopathy at booking (30% vs. 3.7%; P = 0.01). Although HbA(1c) at booking was higher (7.5% vs. 6.6%; P = 0.08) and the fall in HbA(1c) between booking and 24 weeks was greater (1.6% vs. 1.2%; P = 0.2) in those women showing progression of retinopathy, these changes were not significant. CONCLUSIONS: Progression of retinopathy in pregnancy was uncommon (5.0% pregnancies) but was significantly more common in women with duration of diabetes > 10 years and in women with moderate to severe retinopathy at baseline. Laser therapy was needed in 2.2% pregnancies, which is much lower than that reported in earlier studies. Diabet. Med. 18, 573-577 (2001)

Prevalence of HFE (hemochromatosis gene) mutations in unselected male patients with type 2 diabetes.

To assess the prevalence of mutations in the HFE (hemochromatosis) gene in unselected male patients with type 2 diabetes, we examined 220 white men without known diabetes and 220 age-matched white men with type 2 diabetes for mutations in the HFE gene. Nucleotide 845 (C282Y) and 187(H63D) alleles were amplified by polymerase chain reaction (PCR) with lymphocyte DNA. The PCR products were analyzed by restriction enzyme digestion. One of the 220 patients (0.45%) with diabetes was homozygous for the HFE 845A (C282Y) mutation and 25 (11.3%) were heterozygous for the same mutation, of whom 3 (1.3%) were compound heterozygotes also carrying the HFE 187G (H63D) mutation. These frequencies did not differ significantly from the control population without diabetes. There is no evidence that HFE mutations are found in excess in unselected male patients with type 2 diabetes, and there is no indication for a population-based search for an excess of these alleles in type 2 diabetes.

Pharmacokinetics of subcutaneously administered human, porcine and bovine neutral soluble insulin to normal man.

Highly purified neutral soluble human, porcine and bovine insulin (0.075 U/kg body weight) were administered randomly by subcutaneous injection to six normal men. Somatostatin by continuous intravenous infusion (100 micrograms/h) was used to suppress endogenous insulin secretion. The effects of the three species of insulins on plasma glucose, immunoreactive insulin (IRI), C-peptide and intermediary metabolite concentrations were essentially similar. The onset of hypoglycaemic action of bovine insulin was delayed compared to human and porcine insulin due possibly to a lower receptor binding of the bovine insulin. No local or systemic adverse reactions to the insulins were observed.

The effects of long term growth hormone releasing factor (GRF 1-40) administration on growth hormone secretion and synthesis in vitro.

The ability of human pancreatic GH releasing factor 1-40 (hpGRF 1-40) to release GH has been studied in rat anterior pituitary cells in primary culture. Over 24 hours hpGRF (1-40) increased total (cell content and secretion) production 2-fold with an ED50 of 20 pM. Subsequent hpGRF (1-40) stimulation of GH release was not affected by pretreatment when the fall in stored GH was taken into account. In contrast LH responses to gonadotrophin releasing hormone (GnRH) were markedly desensitized after 24 hours GnRH pretreatment in the same experimental system and using the same analysis. hpGRF (1-40) responses were not desensitized when pretreatment was for 3, 12 or 24 hours. The data show that hpGRF (1-40) responses do not desensitize in our experimental conditions under which GnRH responses show marked desensitization.

Vitamin D metabolites in post-menopausal women and their relationship to the myopathic electromyogram.

Proximal muscular weakness is a feature of many metabolic bone diseases but is not well recognized in spinal osteoporosis. Thirty-six post-menopausal women presenting with back pain, with or without osteoporosis, were therefore studied in order to define the relationship between abnormal electromyographic findings and disturbed vitamin D metabolism, as both low plasma 1,25 dihydroxy vitamin D concentrations and malabsorption of calcium have been reported in osteoporosis. Patients with abnormal electromyograms had lower concentrations of plasma 1,25 dihydroxy vitamin D (mean 78.3 pmol/l, SD 20.5, n = 15) than normal subjects of similar age (mean 110.4 pmol/l, SD 39.4, n = 21; P less than 0.01), but electromyographic abnormality was not associated with changes in radiocalcium absorption, plasma 25 hydroxy vitamin D, plasma calcium or phosphate or urinary calcium or hydroxy-proline excretion or impaired renal function. There was no relationship between abnormal electromyography and osteoporosis assessed by spinal radiographs and iliac crest biopsy. These findings are consistent with our previous suggestion that muscle weakness in many unrelated bone disorders is related to low plasma 1,25 dihydroxy vitamin D concentrations, but suggest that there is no relationship between proximal myopathy and spinal osteoporosis in post-menopausal women.

Parathyroid function during acute pancreatitis.

The renal handling of calcium and phosphate, which normally reflects parathyroid hormone (PTH) activity, was studied during the first 5 days after admission to hospital in 18 patients with acute pancreatitis. The ionized calcium level in plasma was calculated from the total calcium, albumin, total protein and pH. Hypocalcaemia (Ca less than 1.08) was found in 6 patients and was associated with low urine calcium concentrations, hypophosphataemia and lower renal tubular reabsorption of phosphate. Although these changes were all consistent with an appropriate renal response to increased PTH production in the hypocalcaemic patients, measured levels of PTH were very variable. In one patient who developed tetany, calcium infusion resulted in a rise in plasma calcium and a reversal of renal changes, but had little influence upon PTH levels. We found no evidence that hypomagnesaemia or proteolytic degradation of PTH were factors in the aetiology of hypocalcaemia. The discrepancy between evidence of PTH activity from renal function and immunoassayable levels of PTH in plasma might indicate that the parathyroid response, although present, was inadequate to mobilize enough skeletal calcium to prevent hypocalcaemia; it underlines the need for caution in the interpretation of data fom radioimmunoassay techniques when taken in isolation in situations where they have not been fully evaluated.

Phosphate treatment of recurrent calcium stone disease.

A group of 38 male recurrent idiopathic calcium stone formers were treated with oral supplements of orthophosphate (1 g phosphorus extra in the diet per day) and followed at intervals up to 4 years. The urinary excretion of calcium decreased (p less than 0.001) and that of inorganic phosphate increased (p less than 0.001) during treatment. These changes resulted in a small decrease in the supersaturation of urine with respect to calcium oxalate, sufficient to reduce the percentage of urines which exceeded the upper limit of solubility of that salt, and a small increase in the supersaturation of urine with respect to calcium phosphate. The stone episode rate on treatment fell in 35 of the 38 patients from a mean pretreatment value of 0.66 episodes/year to 0.22 episodes/year. The 3 initially most prolific stone formers increased their rate of stone formation during treatment. Plasma biochemistry showed no evidence of parathyroid stimulation.

Relative importance of renal failure and increased bone resorption in the hypercalcaemia of myelomatosis.

In order to define the relative importance of renal failure and increased bone resorption in the hypercalcaemia of myelomatosis 22 untreated patients were studied, of whom 12 were hypercalcaemic. Most patients had malabsorption of radiocalcium from the gastrointestinal tract and evidence of increased bone resorption as assessed by fasting urinary hydroxyproline/creatinine ratio. The mean OHPr/Cr ratio, however, was similar in patients with and without hypercalcaemia. Renal failure and Bence Jones proteinuria occurred more frequently in the hypercalcaemic patients. In four patients with hypercalcaemia there was an increase in OHPr/Cr after saline infusion accompanied by an improvement in renal function and hypercalcaemia. Mithramycin given to the same patients further reduced hypercalcaemia, presumably by inhibiting bone resorption. It was concluded that the hypercalcaemia of myelomatosis is due to the combination of renal failure and increased bone resorption, but that the OHPr/Cr ratio in the untreated state is a poor indicator of the degree of bone resorption in hypercalcaemic patients.

Clinical and metabolic aspects of urinary stone disease in Leeds.

In summary, the persistent passage of urine excessively supersaturated with calcium oxalate and/or calcium phosphate in conjunction with a low level of inhibitory activity increases the risk of abnormal crystalluria and stones in a given individual. Treatment of the disorder must be aimed at correcting the abnormal risk factor(s) in that individual.

Should recurrent calcium oxalate stone formers become vegetarians?

The hypothesis that the incidence of calcium stone disease is related to the consumption of animal protein has been examined. Within the male population, recurrent idiopathic stone formers consumed more animal protein than did normal subjects. Single stone formers had animal protein intakes intermediate between those of normal men and those of recurrent stone formers. A high animal protein intake caused a significant increase in the urinary excretion of calcium, oxalate and uric acid, 3 of the 6 main urinary risk factors for calcium stone formation. The overall relative probability of forming stones, calculated from the combination of the 6 main urinary risk factors, was markedly increased by a high animal protein diet. Conversely, a low animal protein intake, such as taken by vegetarians, was associated with a low excretion of calcium, oxalate and uric acid and a low relative probability of forming stones.

The effect of high animal protein intake on the risk of calcium stone-formation in the urinary tract.

1. Studies were carried out on six normal male subjects to determine the short-term effect of increasing the dietary consumption of animal protein on the urinary risk factors for stone-formation, namely, volume, pH, calcium oxalate, uric acid and glycosaminoglycans. 2. An increase of 34 g/day of animal protein in the diet significantly increased urinary calcium (23%) and oxalate (24%). Total urinary nitrogen increased by an average of 368 mmol/day. The accompanying increase in dietary purine (11 mmol of purine nitrogen/day) caused a 48% increase in the excretion of uric acid. 3. The overall relative probability of forming stones, calculated from a combination of the risk factors, was markedly increased (250%) throughout the period of high animal protein ingestion.