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Biomedical subjects

L Uccioli

Publications and source records attributed to L Uccioli.

At least 37 records · Page 2Linked to original sources
PubMed1995

Manufactured shoes in the prevention of diabetic foot ulcers.

OBJECTIVE: To evaluate the efficacy of manufactured shoes specially designed for diabetic patients (Podiabetes by Buratto Italy) to prevent relapses of foot ulcerations. RESEARCH DESIGN AND METHODS: A prospective multicenter randomized follow-up study of patients with previous foot ulcerations was conducted. Patients were alternatively assigned to wear either their own shoes (control group, C; n = 36) or therapeutic shoes (Podiabetes group, P; n = 33). The number of ulcer relapses was recorded during 1-year follow-up. RESULTS: Both C and P groups had similar risk factors for foot ulceration (i.e., previous foot ulceration, mean vibratory perception threshold > 25 mV). After 1 year, the foot ulcer relapses were significantly lower in P than in C (27.7 vs. 58.3%; P = 0.009; odds ratio 0.26 [0.2-1.54]). In a multiple regression analysis, the use of therapeutic shoes was negatively associated with foot ulcer relapses (coefficient of variation = -0.315; 95% confidence interval = -0.54 to -0.08; P = 0.009). CONCLUSIONS: The use of specially designed shoes is effective in preventing relapses in diabetic patients with previous ulceration.

Confidence Intervals↗
PubMed1995

Body sway in diabetic neuropathy.

OBJECTIVE: To evaluate the influence of peripheral neuropathy on body sway assessed by posturography. RESEARCH DESIGN AND METHODS: The age-matched study subjects included 10 insulin-dependent diabetes mellitus (IDDM) patients with peripheral neuropathy (DN), 23 IDDM patients without peripheral neuropathy (D) according to the San Antonio Consensus Conference guidelines, and 21 control subjects (C). All subjects with symptoms and/or clinical signs of postural instability were excluded from the study. RESULTS: The trace surface was significantly larger in the DN than in the C and D groups (P < 0.05), and the trace length was longer in the DN than in the C and D groups (P < 0.01). Mean velocity was faster in the DN than in the other two groups (P < 0.001). A direct relationship was found between the parameters of posturography and some parameters of the nerve conduction velocity. CONCLUSIONS: Diabetic patients with peripheral neuropathy demonstrate a relative deficit in their ability to maintain posture. Posturography allows an early disclosure of the failure of postural control.

Adult↗
PubMed1994

Visual evoked potentials after photostress in insulin-dependent diabetic patients with or without retinopathy.

Visual evoked potentials (VEPs) were assessed under basal conditions and after photostress in normal control subjects, in insulin-dependent diabetic patients with retinopathy (IDDPWR) and in insulin-dependent diabetic patients without retinopathy (IDDP). The VEPs recorded under basal conditions showed a P100 latency significantly higher in IDDP and IDDP-WR eyes than in control eyes and in IDDPWR than in IDDP eyes (P < 0.01). N75-P100 amplitude was significantly lower in IDDP and IDDPWR eyes than in control eyes (P < 0.01). No difference was recorded in the N75-P100 amplitudes between IDDP and IDDPWR eyes. In all eyes, the VEPs recorded after photostress showed an increase in latency and a decrease in amplitude. In both IDDPWR eyes and IDDP eyes VEPs recorded at 20, 40 and 60 s after photostress showed higher mean increments in P100 latency than in C control eyes, and IDDPWR eyes showed higher mean increments in P100 latency than IDDP eyes (IDDP vs control P < 0.01, IDDPWR vs control P < 0.01, IDDPWR vs IDDP P < 0.017). The mean reductions in amplitude observed at 20, 40 and 60 s after photostress in IDDP and IDDPWR eyes were lower than in control eyes (IDDP vs control P = 0.01, IDDPWR vs control P < 0.01, IDDPWR vs IDDP P < 0.01). VEPs were superimposable on the basal VEP (recovery time) at 73.9 s in control eyes, at 88.17 s in IDDP eyes and at 113.3 s in IDDPWR eyes. VEPs after photostress in IDDP patients with normal visual acuity and no fluorangiographic signs of retinopathy may show multiple modifications. This may indicate the presence of an early functional deficiency of the central retinal layers.

Adult↗
PubMed1994

Autonomic neuropathy and transcutaneous oxymetry in diabetic lower extremities.

Transcutaneous oxygen tension is a useful method with which to assess the functional status of skin blood flow. The reduced values observed in diabetic patients have been interpreted as a consequence of peripheral vascular disease. However, diabetic patients show lower transcutaneous oxygen tension values than control subjects with equivalent degrees of peripheral vascular disease, suggesting that additional factors are involved. Since the autonomic nervous system influences peripheral circulation, we studied the relationship between autonomic neuropathy and foot transcutaneous oxymetry in non-insulin-dependent diabetic (NIDDM) patients without peripheral vascular disease. The following age-matched patients were selected and evaluated: control subjects, C, (n = 20), NIDDM patients without autonomic neuropathy, D, (n = 16) and with autonomic neuropathy, DN, (n = 20). All diabetic patients showed lower transcutaneous oxygen tension values than control subjects, while no differences were observed between the diabetic patients with and without autonomic neuropathy. In addition the saturation index that increases in the presence of autonomic neuropathy does not correlate with foot TcPO2. In conclusion autonomic neuropathy does not influence foot TcPO2 and therefore it is unlikely that it contributes to development of foot lesions during induction of foot skin ischaemia.

Autonomic Nervous System↗
PubMed1994

Autonomic neuropathy influences great toe blood pressure.

OBJECTIVE: To assess the influence of autonomic neuropathy on toe blood pressure (TBP), a parameter used currently as an ischemic index. RESEARCH DESIGN AND METHODS: The age-matched study subjects included 20 non-insulin-dependent diabetes mellitus (NIDDM) patients with autonomic neuropathy (DN) and 10 NIDDM patients without autonomic neuropathy (D), assessed by standard cardiovascular tests and galvanic skin response, and 8 control subjects (C). None of the subjects had peripheral vascular disease (PVD) (ankle/brachial index 0.9-1.1. RESULTS: The TBP and toe/brachial index (TBI) were significantly lower in DN than in C and D (P < 0.01). The saturation index (SI), the ratio between foot venous and arterial partial pressure of oxygen (PO2), was significantly higher in DN than in C and D (P < 0.05). An inverse relationship was found between TBI and SI (r = 0.554, P = 0.001). CONCLUSIONS: The autonomic nervous system directly influences peripheral circulation. In diabetic patients without PVD, a failure of sympathetic fibers caused by autonomic neuropathy could lead to a reduction of TBP. Therefore, TBP cannot be used as an ischemic index in diabetic patients.

Analysis of Variance↗
PubMed1993

Evidence of plasma CoQ10-lowering effect by HMG-CoA reductase inhibitors: a double-blind, placebo-controlled study.

Inhibitors of HMG-CoA reductase are new safe and effective cholesterol-lowering agents. Elevation of alanine-amino transferase (ALT) and aspartate-amino transferase (AST) has been described in a few cases and a myopathy with elevation of creatinine kinase (CK) has been reported rarely. The inhibition of HMG-CoA reductase affects also the biosynthesis of ubiquinone (CoQ10). We studied two groups of five healthy volunteers treated with 20 mg/day of pravastatin (Squibb, Italy) or simvastatin (MSD) for a month. Then we treated 30 hypercholesterolemic patients in a double-blind controlled study with pravastatin, simvastatin (20 mg/day), or placebo for 3 months. At the beginning, and 3 months thereafter we measured plasma total cholesterol, CoQ10, ALT, AST, CK, and other parameters (urea, creatinine, uric acid, total bilirubin, gamma GT, total protein). Significant changes in the healthy volunteer group were detected for total cholesterol and CoQ10 levels, which underwent about a 40% reduction after the treatment. The same extent of reduction, compared with placebo was measured in hypercholesterolemic patients treated with pravastatin or simvastatin. Our data show that the treatment with HMG-CoA reductase inhibitors lowers both total cholesterol and CoQ10 plasma levels in normal volunteers and in hypercholesterolemic patients. CoQ10 is essential for the production of energy and also has antioxidative properties. A diminution of CoQ10 availability may be the cause of membrane alteration with consequent cellular damage.

Adult↗
PubMed1993

Abnormal agonist-stimulated cardiac parasympathetic acetylcholine release in streptozocin-induced diabetes.

We examined the effect of three distinct depolarizing conditions on [3H]ACh release from cardiac postganglionic parasympathetic neurons in age-matched controls and insulin-treated STZ-induced diabetic rats to determine whether alterations in neurotransmitter release were present in the diabetic group. The effect of TTX, which exerts a use- and voltage-dependent block of sodium channels, was examined on the release of ACh stimulated by SRIF14 (preferentially acts at the cell body). We also studied the effect of STZ-induced diabetes on [3H]ACh release by the relatively site-specific depolarizing agent VT (preferentially acts at the axon) and high potassium (non-site-specific). Basal, SRIF14-(10(-7) M), VT-(10(-4) M), and K+ (100 mM)-stimulated [3H]ACh release was similar in control and STZ-induced diabetic animals. However, in STZ-induced diabetic but not control rats, SRIF14-induced [3H]ACh release was resistant to TTX (2 x 10(-7) M). In addition, the response to submaximal K+ (25 mM) stimulation was greater in STZ-induced diabetic compared with control animals. Treatment with insulin corrected these abnormalities. These data indicate that in the acute STZ-induced diabetic rat, SRIF14-, VT-, and high K(+)-evoked release of ACH is not impaired, which suggests that the mechanisms associated with ACh storage and release in postganglionic cardiac parasympathetic neurons are not affected in this model.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1992

Lower limb arterio-venous shunts, autonomic neuropathy and diabetic foot.

We have quantitatively assessed the percentage of lower limb arterio-venous (a-v) shunting using a radioisotopic technique and correlated it with autonomic neuropathy evaluated by cardiovascular tests. We have studied three groups of diabetic patients: Group A, 12 non-neuropathic subjects without foot lesions; Group B, 12 neuropathic subjects without foot lesions; Group C, 12 neuropathic subjects with recurrent foot ulcers. Shunting was higher in Group C (10.4 +/- 2.7%) than in Group B (6.8 +/- 2.3%, P less than 0.01) and Group A (3.8 +/- 1.2%, P less than 0.001). Shunts in Group B were higher than in Group A (P less than 0.05). All the tests exploring autonomic function were more impaired in Groups B and C than in Group A, with no difference between Groups B and C. A direct correlation was found between a-v shunting and the following cardiovascular tests: postural hypotension (PH) (r = 0.41, P less than 0.02), sustained handgrip (SH) (r = 0.56, P less than 0.001), deep breathing (DB) (r = 0.40, P less than 0.005) and lying to standing (LS) (r = 0.44, P less than 0.01). A positive correlation was also found between a-v shunts and duration of the disease (r = 0.62, P less than 0.001). Arterio-venous shunting was found to be directly related to autonomic neuropathy even if the higher shunting found in the patients with foot ulcers was not related to a higher degree of autonomic involvement; in addition, this group of patients was characterized by having a more advanced sensory and motor neuropathy. In conclusion, autonomic neuropathy, through its influence on a-v shunts, may play a role in the pathogenesis of diabetic foot, but peripheral neuropathy probably plays a key role in conditioning the development of the overt clinical manifestations of diabetic foot.

Albuminuria↗
PubMed1989

Somatostatin stimulates acetylcholine release in the canine heart.

Previous reports of somatostatin's atropine-sensitive negative inotropic effect on cardiac function prompted the present studies to characterize the molecular forms and actions of somatostatin in the canine heart. Radioimmunoassay of cardiac extracts revealed concentrations of somatostatin-like immunoreactivity ranging from 0.50 +/- 0.13 pmol/g tissue (means +/- SE, n = 6) in the pulmonary artery to 0.78 +/- 0.23 pmol/g tissue in the right ventricle. On gel filtration of the extracts, two major molecular forms of somatostatin-like immunoreactivity were elicited, the predominant one coeluting with somatostatin-14 and a minor peak corresponding to somatostatin-28. Experiments performed with slices of atrial septum indicated that somatostatin-14 (10(-10) to 10(-7) M) stimulated the release of acetylcholine in a dose-dependent manner. This action of somatostatin-14 was additive with K+-evoked acetylcholine release, unaffected by hexamethonium, and blocked by tetrodotoxin, suggesting mediation via a nonnicotinic postganglionic neural pathway. Our studies lead us to conclude that somatostatin may function as a neurotransmitter in the heart, which exerts its negative inotropic action by promoting the release of acetylcholine.

Acetylcholine↗
PubMed1988

Glucagon and glucose tolerance in liver cirrhosis.

The present study was undertaken in order to establish the significance of glucagon in glucose intolerance in liver cirrhosis. The plasma glucose response to an oral glucose load (75 g) was determined in 10 control subjects and in 10 cirrhotic patients, after infusions of: glucagon (3 ng.kg-1.min-1) or saline (154 mmol/l); somatostatin (SRIH) (500 micrograms/h); and SRIH plus glucagon (3 ng.kg-1.min-1). Glucagon infusion did not impair glucose tolerance, neither in normal subjects nor in patients with cirrhosis. On the other hand, in both groups glucose tolerance was impaired by SRIH infusion, presumably owing to an absolute insulin deficiency. Both in normal subjects and in cirrhotic patients, SRIH plus glucagon infusion further impaired glucose tolerance, presumably as a result of excess glucagon and concomitant insulin deficiency. In conclusion, our data show that hyperglucagonemia is not an important factor in the development of the glucose intolerance in patients with hepatic cirrhosis.

Adult↗
PubMed1988

Treatment of severe psoriasis with somatostatin: four years of experience.

Over a period of 4 years, 20 patients suffering from severe forms of psoriasis (erythrodermic, sub-erythrodermic, resistant generalized forms and/or forms associated with acute arthropathy) were treated with 96 h of continuous i.v. infusion of somatostatin (Stilamin, Serono) diluted in D5W at 250 micrograms/h. In addition to the usual blood chemistry parameters, circadian levels of growth hormone (GH) and epidermal growth factor (EGF) were measured before, during, and after therapy. Approximately 2-3 weeks after termination of therapy, erythrodermic and suberythrodermic symptoms had disappeared. In some patients, a few lesions of psoriasis vulgaris remained, although they were much less severe. Remission of acute arthropathy was impressive. Blood chemistry parameters were unchanged after therapy. Circadian levels of GH and EGF, normal before therapy, were significantly decreased after therapy. The infusion was well-tolerated. Infusion rates of greater than 250 micrograms/h caused only some complaints of abdominal pain, nausea, and vomiting. During the 4 years, erythrodermic symptoms reappeared only in seven patients, three of whom were also arthropathic. After 6-8 months, they underwent a second course of somatostatin therapy with good results. The other patients are still able to control their disease with tar-based products alone or with low-dose 8-methoxypsoralen + UVA (PUVA) or UV therapy. The arthropathic patients control their symptoms with periodic low-dose nonsteroidal antiinflammatory drug therapy.

Epidermal Growth Factor↗
PubMed1986

Electrophysiologic effects of somatostatin in man.

Experimental and clinical studies suggest that somatostatin, a regulatory peptide widely distributed in human tissues may have electrophysiologic effects. We studied a group of 14 patients who underwent a complete electrophysiologic study for different rhythm disturbances. Somatostatin significantly increased the spontaneous cycle length, the atrial and atrioventricular nodal effective refractory periods, and the Wenckebach cycle length. The AH and HV intervals during sinus rhythm remained unchanged. The effectiveness of somatostatin to interrupt paroxysmal supraventricular tachycardias was assessed in 18 patients. Termination was obtained in 15 (82.5%). Our results show that somatostatin has a significant electrophysiologic effect on the human heart, and confirm its clinical effectiveness in some arrhythmias.

Arrhythmias, Cardiac↗
PubMed1986

Somatostatin response to a mixed meal in normals and in type I diabetics.

Somatostatin has been proposed as a regulatory peptide of nutrient entry and fuel homeostasis because of its ability to inhibit the release of substances involved in food digestion and metabolism. The aim of the study was to evaluate the somatostatin response to a test meal in type I diabetics at the clinical onset of the disease and after two months of intensive insulin therapy. Normal subjects and diabetics in good metabolic control showed a characteristic biphasic somatostatin rise after a test meal; this response was lacking in diabetics at the onset of the disease. The response of somatostatin to a mixed meal in normals confirms its involvement in nutrient digestion and metabolism. The lacking somatostatin response in newly diagnosed type I diabetics might be related to deficient GIP response to the test meal or to other factors such as the insulinopenia or metabolic derangement characteristic of the clinical onset of the disease.

Adult↗
PubMed1986

Somatostatin plasma levels and biological effects following subcutaneous administration of somatostatin in man.

The rate at which somatostatin appears in the circulation after subcutaneous bolus injection and continuous administration by pump was determined in normal subjects by serial radioimmunoassays of immunoreactive somatostatin. Following a single subcutaneous injection of 250 micrograms, the somatostatin peak in plasma appeared after 5 min and had only a transient effect on insulin levels. During continuous administration, somatostatin reached levels able to reduce significantly insulin and glucagon. Somatostatin plasma levels exerting biological effects were observed during the subcutaneous administration of the peptide.

Adult↗
PubMed1985

[Blood catecholamines in liver cirrhosis].

Haematic concentrations of catecholamines were found to be higher in cirrhotic patients with ascites, than cirrhotic patients without ascites and controls. In compensated and decompensated cirrhosis, different forms of sympathetic nervous activity were observed. The high catecholamine values in cirrhotic patients and the activation of the renin angiotensin-aldosterone system suggest the use of beta-blockers to reduce sodium-water retention.

Adrenergic beta-Antagonists↗
PubMed1985

[Somatostatin and the cardiovascular system: experiences and prospective use].

The recent demonstration that intravenous administration of somatostatin, an ubiquitous peptide-like substance, may interrupt paroxysmal supraventricular tachycardia in man has disclosed new perspectives in the assessment of the mechanisms of neuro-humoral cardiac regulation in normal and pathologic conditions. Prospective studies on normal subjects and diabetics with and without autonomic cardiac neuropathy, helped in giving an outlook on the mechanism by which somatostatin acts on the human heart. This substance exerts in vivo a powerful chronotropic and dromotropic influence on sinoatrial and A-V node cells both in normals and diabetics with and without autonomic cardiac neuropathy. This influence is blocked by preventive administration of atropine or atropine plus metoprolol (intrinsic heart rate). Since somatostatin-like-substances have been found in cholinergic postganglionic neurons of the cardiac vagus of some animals, the demonstrated "vagomimetic" action of somatostatin on human cardiac cells seems to support the hypothesis that also the human heart may contain vagal somatostatinergic neurons with modulatory function on the heart rate and rhythm. Present observations disclose new perspectives in the pathophysiology and therapy of cardiac arrhythmias.

Adult↗