Biomedical subjects
Publications and source records attributed to M Alberetto.
Chronic obstructive pulmonary disease (COPD) can be accompanied by compensatory secondary erythrocytosis. However, the exact prevalence of secondary erythrocytosis in COPD is unknown. Although diagnostic criteria for polycythemia vera versus secondary erythrocytosis are mutually exclusive, we describe here the coexistence of polycythemia vera and COPD in the same patient.
The treatment of the diabetic foot is a common and sometimes difficult problem. The treatment of the characteristic lesions of the diabetic foot involves many forms of therapy: these include contact dressings and topical treatments. The different therapies that have been applied do not often give satisfactory results. Therefore, for this purpose, we have studied the effect of biostimulation of wound-healing by utilising the CO2 laser together with the action of the KTP laser on 25 patients (11 females and 14 males), all suffering from diabetes mellitus with polyneuropathic ulcers of the foot. Low out-put laser irradiation may stimulate granulation tissue and collagen production in fibroblasts. Many studies observed a regeneration of microcirculation in the ulcer and a regeneration of lymphatic circulation. The laser irradiation method produces a sterilizing effect from bacteria that over-infect the diabetic ulcer too. Each patient underwent a surgical treatment of the edges of the ulcers with CO2 and KTP laser (wavelength 532 nm) focused, and a combined phototherapy (CO2 laser and afterwards KTP laser, defocused). The irradiation was carried out through laser beam (by optic fiber for KTP) manually directed, until all of the ulcer surface became irradiated. On the skin around the ulcer, an omental derived cream (fractionated porcine omental lipid extracts) was daily applied, independently from the laser treatment, to evaluate the angiogenic effect of this substance.(ABSTRACT TRUNCATED AT 250 WORDS)
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It has been shown that human calcitonin (hCT) is absorbed through the nasal mucosa when administered together with promoters like sodium glycocholate (SGC) or dihydrofusinate. The aim of this study was to compare the clinical and metabolic effect of intranasal (in) and intramuscular (im) hCT in patients with osteoporosis or with Paget's disease of bones. Fifteen women with postmenopausal or with senile osteoporosis entered a randomized six months trial with in hCT (plus SGC) or with im hCT 100 U on alternate days. Six women in each group were treated for 2 months, and only four women in each group continued treatment for an additional 4 months period. In hCT, but not im hCT, reduced subjective pain, while urinary cAMP increased to a similar extent in the 2 groups. Other metabolic indexes and bone mineral content (BMC) were unchanged, no new fractures took place, and side effects were fewer with in than with im hCT. To confirm the analgesic effect of in hCT, twelve patients with Paget's disease of bone were randomly treated for 20 days with in or im hCT 100 U/day: during the short period of treatment, pain was reduced by in, not by im hCT, and urinary cAMP excretion similarly increased in the two groups of patients.
Occurrence of hypoglycemia during a prolonged fasting, accompanied by inappropriately high serum insulin levels, is considered a reliable index of the presence of insulinoma. Previous in vitro studies on insulin receptors, and in vivo hyperinsulinemic clamps have shown that patients with insulinoma are insulin resistant. In the present study 10 patients with insulinoma, 6 patients with nontumoral (also called functional or reactive hypoglycemia) hypoglycemia and 6 normal subjects were fasted for 24 h and their blood glucose levels were maintained constant by means of a programmed glucose infusion (isoglycemic glucose clamp) delivered by an artificial pancreas (Biostator). Blood glucose levels were monitored in continum, glucose infused (M) and glucose clearance (MCR) were evaluated at hourly intervals, and serum insulin (IRI) levels were evaluated every 6 h. Blood glucose levels were higher in controls than in patients with insulinoma and in patients with non tumoral hypoglycemia; M, MCR and IRI were progressively higher in controls, in patients with nontumoral hypoglycemia and in patients with insulinoma. The M/I index (M divided by IRI levels, an index of insulin sensitivity) was lower in patients with insulinoma than in other subjects and patients, indicating the existence of insulin resistance. These data indicate that: i) patients with insulinoma require large amounts of glucose to remain isoglycemic during a prolonged fast; ii) insulin resistance is a common feature of insulinoma and can be shown even under near physiologic conditions such as a 24-h fasting. The present study does not clarify whether insulin resistance occurs at the hepatic level or at other, peripheral levels.
The systemic availability of glucagon and human calcitonin given intranasally to healthy volunteers as spray solutions or powders has been examined. Glucagon was absorbed only when surfactants were used, and 9-lauryl ether (as a spray) and sodium glycocholate (as spray or powder) were equally active. Calcitonin was poorly absorbed when given alone but the surfactants dihydrofusinate (as spray or powder) and glycocholate (as a spray) were equally active in promoting absorption. Thus, enhancers are required to obtain significant nasal absorption of glucagon and calcitonin and powders and spray solutions did not differ in terms of systemic availability.
Intranasal glucagon can raise blood glucose levels in healthy subjects. The aims of this study were to 1) compare the hyperglycemic effect of intranasal and intramuscular glucagon in healthy subjects and type I (insulin-dependent) diabetes patients during euglycemic conditions and 2) test the efficacy of intranasal and intramuscular glucagon in counteracting hypoglycemic episodes in insulin-treated diabetic patients. Intranasal glucagon raised blood glucose levels in both healthy subjects and type I diabetic patients, the effect of intramuscular glucagon being similar for the first 30 min and higher thereafter. Intranasal glucagon was also quicker acting than oral glucose in healthy subjects. Intranasal glucagon raised blood glucose levels in patients with hypoglycemic episodes, although less effectively than intramuscular glucagon. These data indicate intranasal glucagon as a possible emergency remedy for self-medication in insulin-treated patients prone to hypoglycemic episodes.
Glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured by constant inulin and PAH infusion during euglycemia and intravenous dextrose-induced moderate hyperglycemia in seven insulin-dependent diabetics with persistently elevated GFR, seven diabetics with normal GFR, and in six normal control subjects. In euglycemia, RPF was higher and calculated renal vascular resistance (RVR) lower in the hyperfiltering than the normofiltering group (P less than 0.05 for both variables), but filtration fraction (FF) was similar in all groups. During hyperglycemia, mean GFR rose significantly from 157 +/- 20 to 174 +/- 30 ml/min/1.73 m2 (11.9%; P less than 0.05) in the hyperfiltering group only. There was no statistically significant change in mean GFR in the normofiltering diabetic (116 +/- 6 vs. 114 +/- 13 ml/min/1.73 m2) and the normal control groups (117 +/- 15 vs. 113 +/- 14 ml/min/1.73 m2). RPF and FF rose by 5.8% and 9.2%, respectively, in the hyperfiltering group only, with no change in the normofiltering or normal control groups. No change in RVR was found in any group. Total tubular sodium reabsorption was higher during euglycemia in the hyperfiltering diabetics (P less than 0.01), and rose significantly during hyperglycemia (P less than 0.05) in this group only. Overnight euglycemia did not remove the increased glomerular filtration and flow of hyperfiltering diabetics. Hyperglycemia further accentuated hyperfiltration by elevating renal plasma flow and filtration fraction.
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Indirect evidence suggests that sulfonylureas, in addition to stimulating insulin release, exert additional effects at extrapancreatic levels which are of value in the management of type 2 diabetes. In order to characterize in vivo some of these effects, insulin sensitivity was studied in 9 type 1 diabetics with no residual insulin secretory activity, during treatment with chlorpropamide (250 mg b.i.d. for 8 days) and with glipizide (5 mg t.i.d. for 8 days). Employing the glucose clamp technique with the aid of an artificial pancreas (Biostator), glucose disposal during insulin infusion (0.1 U/kg in 60 min) was calculated by the amount of glucose required to keep the blood glucose at preinfusion levels. Chlorpropamide and glipizide administration was accompanied by a significant increase of the amount of glucose required to clamp blood glucose levels, while serum (free) insulin levels were superimposable during the different clamping studies. In the absence of endogenous insulin release, these data strongly suggest that the two sulfonylureas employed enhance in vivo the peripheral sensitivity to insulin. Further studies are required to indicate a preferential site of action (liver, muscle, adipose tissue) of sulfonylureas.
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Using the artificial pancreas, blood glucose levels were maintained at 80 mg/dl in nine hypoglycemic patients (four with histologically proven insulinomas and five with nontumoral hypoglycemia) and in four normal subjects during a 24-h fast. The amount of glucose used, serum insulin levels, and glucose clearance were higher in patients with nontumoral hypoglycemia than in normal subjects and highest in the patients with an insulinoma. Surgical or pharmacological treatment resulted in normalization of all parameters. In contrast to the 72-h fast, the 24-h glucose clamp technique allowed the study of hypoglycemic patients without inducing hazardous hypoglycemia.
Regular or crystalline insulin with sodium glycocholate as surfactant administered intranasally to normal volunteers induced hypoglycaemia and an increase in serum immunoreactive insulin concentrations. Serum C-peptide concentrations decreased or remained unchanged. Insulin administered intravenously to three of these subjects yielded a potency ratio of 1:8 for intranasal and intravenous insulin. In four insulin-dependent diabetics a cross-over study was performed on different days, insulin being administered once intranasally and once subcutaneously in a ratio of 1:9. In these patients the intranasal insulin was more effective than the subcutaneous insulin in preventing hyperglycaemia after breakfast. In four other insulin-dependent diabetics 11-hours monitoring was performed twice on two different days, insulin being administered in divided dosage sufficient to achieve a reasonable glycaemic profile. The administration during the morning, whereas subcutaneous insulin was more effective than intranasal during the afternoon.
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The present experiments were performed to investigate the possible role of histamine and its receptors, H1 and H2, in the control of PRL and LH release in normal adult humans of both sexes. Histamine infusion (200 microgram, iv, in 15 min) induced PRL and LH release in men; in women, histamine inhibited LH release without affecting PRL release. Two H1 antagonists, dexchlorpheniramine (10 mg, iv) and promethazine (50 mg, im), reduced PRL release in both sexes, stimulated LH release in men, and inhibited LH release in women. Cimetidine, an H2 antagonist (400 mg, iv), elicited PRL release in both sexes, more consistently in females than in males, and was without effect on LH release in either sex. These data suggest that in humans, the effect of histamine on PRL release is linked to H1 and H2 receptors, which respectively stimulate and inhibit PRL release independently of sex. The effect of histamine on LH release appears to depend on sex and to be mediated only by H1 receptors. To rule out the possibility that the effects of histamine are merely due to a nonspecific stress reaction, we have evaluated PRL and LH release in otherwise normal men and women undergoing surgery for gallstones. Surgery was accompanied by PRL release in both sexes, more evident in women, and by LH release only in men. These results indicate that the effect of histamine on PRL and LH release in humans is linked to sex and H1 and H2 receptors and is not due to stress; further studies are required to clarify the possible mechanism and site of action of histamine in modifying PRL and LH release in humans.
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