Serum lipoprotein(a) is not increased in NIDDM patients with microalbuminuria.
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Biomedical subjects
Publications and source records attributed to L Rocca.
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Orthotics, the Cinderella of the NHS, needs a radical restructuring if it is to give patients the best serviice, argue Peter Bowker and colleagues.
In order to evaluate if the assessment of the paradoxical GH responses to TRH in diabetic subjects could be altered by the presence of spontaneous fluctuations in plasma GH levels, we compared GH responses to TRH and to saline injection in 19 insulin-dependent diabetic patients. We observed significant increments (greater than 5 ng/ml) in plasma GH levels after TRH iv administration in 5 of 19 patients (26%); on the other hand, a significant increase was also observed in 6 patients (31%) after saline. We conclude that, at least in some diabetics, spontaneous GH pulses might be misinterpreted as paradoxical GH responses after a nonspecific stimulus administration. Moreover, the real existence of the paradoxical GH response to TRH has to be assessed using the following strict criteria: a sufficient magnitude in GH increment (greater than 5 ng/ml), the comparison of the kinetics of GH secretion after TRH and saline in the same patient, the presence of a significant GH rise above basal levels within the first 30 min after TRH injection.
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The design of a hoist modification is described which allows a heavy tetraplegic patient to be put into a swivel walker and then lifted to the upright position with the end aid of one person.
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The aim of our study was to evaluate the acute effect of nifedipine, a calcium channel blocker, on exercise-induced microalbuminuria in normotensive and normoalbuminuric type 1 diabetic patients. Fifteen normotensive diabetic patients who were normoalbuminuric at rest (8 males and 7 females; age 16-35 years) and 10 normal subjects (6 males and 4 females; age 18-40 years) performed 4 submaximal cycloergometric exercises (90% of theoretical maximum heart rate); the first two exercises were performed in basal condition and the other 2 after 24 h of therapy with nifedipine AR (20 mg/b.i.d.) or placebo (2 cps/die). One hour after exercise in basal condition the microalbuminuria was 78 +/- 17 micrograms/min in diabetic patients vs 16 +/- 4 micrograms/min in normal subjects (p less than 0.001). After placebo no significant changes with respect to basal levels were observed 1 hour after exercise in either diabetic patients (82 +/- 16 microgram/min) or normal subjects (20 +/- 5 micrograms/min). In diabetic patients after nifedipine, systolic blood pressure was reduced both at rest and after exercise (p less than 0.05) with respect to basal condition or placebo. The urinary albumin excretion rate at rest was not modified, but it was significantly reduced 1 hour after exercise: 58 +/- 15 micrograms/min (p less than 0.01 vs placebo). This reduction correlated well with the reduction of exercise blood pressure in diabetic patients (r = 0.91, p less than 0.001). Our results indicate that acute administration of nifedipine reduced exercise-induced microalbuminuria in normotensive diabetic patients, probably by means of a reduction in exercise blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
Systemic and local reactions to insulins in patients affected by insulin-dependent diabetes are uncommon but may be life threatening. Both systemic and local adverse reactions to therapy may be managed by different therapeutic schemes. The availability of human (DNA recombinant) insulin raised hopes that this be the choice treatment for allergic complications. However, controlled studies showed that reaginic (IgE) antibodies are directed to common insulin determinants and not to heterologus protein contaminants. Therefore we investigated in 62 patients undergoing insulin therapy, prevalence and clinical significance of the detection of specific IgE to insulin. Furthermore, we searched for a relationship between atopic status and the presence of antiinsulin IgE. In our study prevalence of specific IgE to insulin was 16.1%. We showed a correlation between clinical symptoms and the presence of specific IgE to insulin, when these antibodies are of an elevated class (R.A.S.T. class 2 or more). When specific IgE were present we detected antibodies to all insulines (bovine, porcine and human) thus confirming that specific IgE are directed to a common antigenic determinant. Finally, we couldn't find a relationship between atopic status and the presence of reaginic antibodies to insulin.