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Biomedical subjects

G Ghirlanda

Publications and source records attributed to G Ghirlanda.

At least 163 records · Page 9Linked to original sources
PubMedDate not supplied

Blunted erythropoietin response to anemia in patients with Type 1 diabetes.

BACKGROUND: It is known that patients with renal failure have normochromic normocytic anemia due to impaired endogenous erythropoietin (EPO) synthesis. The aim of this work was to determine whether low serum erythropoietin (s-EPO) levels play a role in the pathogenesis of anemia in patients with Type 1 diabetes without overt nephropathy. METHODS: We included in the study 13 patients with Type 1 diabetes whose Hb levels were <11 g/dl. Blood cell count, s-EPO, urinary albumin excretion rate (AER), HbA(1c), glomerular filtration rate, serum iron, serum ferritin, the presence of neuropathy, retinopathy and nephropathy were determined. RESULTS: Ten out of 13 patients with anemia (77%) had a blunted EPO response to anemia. All ten patients with low EPO levels had autonomic neuropathy; five had clinical nephropathy but with serum creatinine<1.6 mg/dl. Three patients were treated with rHuEPO and showed an improvement in their anemia after treatment. CONCLUSION: The majority of patients with Type 1 diabetes who had anemia also had low EPO levels. The pathogenesis of this phenomenon is probably multifactorial. Autonomic neuropathy appears to play a role, but it is not sufficient, per se, to be the only cause. Dysautonomia might enhance the effect of renal damage.

Adult↗
PubMedDate not supplied

Effect of somatostatin (SRIF) on plasma glucose and insulin response to glucagon in liver cirrhosis.

The present study was performed in order to evaluate the plasma glucose pattern in cirrhotic patients who, in the course of a continuous somatostatin infusion (500 microgram/h), were given pulses of glucagon (1 mg i.v.). In normal as well as in cirrhotic subjects somatostatin infusion provoked a marked reduction of the IRI plasma level and this was uninfluenced by subsequent glucagon administration. The rise in plasma glucose level in response to i.v. glucagon administration during somatostatin infusion was less marked in cirrhotics compared to normal subjects. This can be attributed to a variety of factors such as reduced number of liver cells or quantitative or qualitative changes of the liver cell glucagon receptors. Glucagon does not seem to contribute to the pathogenesis of carbohydrate intolerance in liver cirrhosis.

Adult↗
PubMedDate not supplied

Decreased insulin binding to red blood cells in liver cirrhosis.

eleven male cirrhotic subjects, all with impaired glucose tolerance (IGT), were studied. Insulin binding to circulating erythrocytes was evaluated. The specific bound fraction was decreased compared to normals (5.95 +/-0.76 vs 7.08 +/- 0.84%; p less than 0.005). An negative correlation was found between fasting insulin and bound fraction (r = -0.68; p less than 0.05). We suggest that serum insulin may be chronically augmented as a consequence of liver damage. This induces a down-regulation of insulin receptors that is responsible for insulin resistance and at least in part for the impairment of glucose tolerance.

Erythrocytes↗
PubMedDate not supplied

Thromboxane production in diabetes mellitus.

A correlation between increased platelet adhesiveness and aggregation and the development of angiopathy in diabetes mellitus can be made. Thromboxane produced by platelets represents a potent platelet aggregation factor. We studied the platelet TXB2 production during blood coagulation in carefully selected patients with type II diabetes mellitus in good metabolic control and the results were correlated with the presence or absence of microangiopathy, fasting blood glucose levels, type of therapy, age, duration of diabetes and the most important hematochemical parameters. No statistically significant differences were found between serum TXB2 concentrations in diabetic patients and control subjects, in diabetics with or without microangiopathy and in diabetics on insulin therapy or on oral hypoglycemic agents. We did not observe any correlation between TXB2 production and age, duration of diabetes, sex, basal blood glucose levels, total and HDL-cholesterol, triglycerides, blood creatinine and blood electrolytes. The thromboxane production may be a not important factor for determining the increased platelet aggregation which is at the origin of the angiopathy in diabetes mellitus.

Adult↗
PubMedDate not supplied

Response of insulin receptors to oral glucose in normal subjects.

Insulin binding to circulating monocytes was studied in ten male volunteers before and 1, 2, and 5 hours after the oral intake of 100 g of glucose. Results indicate an increase in the specific cell binding fraction with a change in receptor affinity 5 hours after glucose. Since the same changes appear 3 hours after food intake they are probably not directly induced by insulinemia.

Adult↗
PubMedDate not supplied

The use of dynamic posturography to detect neurosensorial disorder in IDDM without clinical neuropathy.

The main aim was to evaluate the relative importance of sensory interactions for postural stability in 45 patients with insulin-dependent diabetes mellitus (IDDM) with and without peripheral neuropathy. All subjects had normal electronystagmography. Dynamic posturography provides functional, selective testing of three sensory modalities in maintenance of balance, i.e., vestibular, visual, and somatosensory. The Sensory Organization Test (SOT) includes six test conditions during which the subject tries to maintain an upright stance with as little sway as possible. The subject stands on a movable platform facing a square visual surrounding, which can be rotated independently. The test is performed first with the eyes open, then with the eyes closed. The second component of posturography testing consists of the Motor Control Test (MCT) concerning motor responses routinely used in balance maintenance. Compared to control subjects, IDDM patients with peripheral neuropathy but not patients without neuropathy showed lower scores for test conditions SOT 1 (analysis of variance, ANOVA F = 8.3; Scheffe test: p = 0.0007), SOT 2 (F = 6.6; p = 0.004), SOT 3 (F = 3.4; p = 0.04), and SOT 6 (F = 3.4; p = 0.04). The muscle response latencies in MCT were prolonged for small forward perturbations (F = 4.6; p = 0.02) in neuropathic patients (148.3+/-14.2 ms) with respect to control subjects, but not in non-neuropathic patients with respect to control subjects (135.2+/-13.3 ms). Sural (r = 0.2; p = 0.002) and peroneal (r = 0.12; p = 0.02) nerve conduction velocities showed significant correlations with muscle response latencies of MCT for small forward perturbations. Our results suggest a subclinical dysequilibrium in IDDM patients with peripheral neuropathy. The results of dynamic posturography may reflect the impairment of the somatosensory system, rather than a specific lesion of vestibular and/or visual modalities.

Adult↗
PubMedDate not supplied

Nicotinamide increases C-peptide secretion in patients with recent onset type 1 diabetes.

Nicotinamide, a poly-(ADP-ribose) synthetase inhibitor, has been shown in animal models to induce islet B-cell regeneration. An open controlled trial was therefore carried out for 1 year in 36 patients with recent onset (less than 4 weeks symptoms) Type 1 diabetes. Twenty-three patients were treated with nicotinamide (200 mg daily) in addition to insulin, and 13 control patients were treated with insulin alone. Metabolic and immunological variables at entry were similar in the two groups. A significant increase of stimulated plasma C-peptide levels compared to diagnosis was observed only in the nicotinamide treated group (1.4 +/- 0.3 (+/- SE) micrograms l-1 at diagnosis vs 2.4 +/- 0.4 at 6 months, p less than 0.04; and 3.0 +/- 0.5 at 1 year, p less than 0.01). Patients receiving nicotinamide had lower glycosylated haemoglobin levels at 6 months and 1 year compared to the control group (p less than 0.04 and p less than 0.03, respectively) although insulin dose was lower. Small doses of nicotinamide may be successful in improving metabolic control in recent onset Type 1 diabetes, probably by increasing residual islet B-cell function.

Adolescent↗
PubMedDate not supplied

Acetylcholine release in experimental autonomic neuropathy.

Autonomic neuropathy is a common complication of diabetes. In this study we evaluated autonomic neuropathy by determining somatostatin (S-14)-evoked acetylcholine (Ach) release from postsynaptic parasympathetic fibers in the atria of controls (C) and streptozotocin diabetic rats (STZ-D), with and without tetrodotoxin (TTX). The release induced by S-14 did not differ in C and STZ-D. TTX blocked S-14 induced Ach in C but failed in STZ-D. TTX resistance in STZ-D may be explained by variations of membrane potential in nerve fibers.

Acetylcholine↗
PubMedDate not supplied

Association of ankylosing spondylitis and monoclonal gammopathy: clinical case report and pathogenetic considerations.

Monoclonal gammopathy has rarely been reported in ankylosing spondylitis. We observed a patient with ankylosing spondylitis and monoclonal gammopathy with no signs of malignancy, chronic infections or amyloidosis. This association may show some possible pathogenetic mechanisms involved in these two different diseases of still uncertain etiology.

HLA Antigens↗
PubMedDate not supplied

Charcot's foot.

Diabetic osteoarthropathy is a chronic progressive arthropathy involving the bones and joints being constantly associated to somatic and autonomic peripheral neuropathy. The pathogenesis is related to sensory and motor neuropathy with morphologic foot alterations, relaxation and abnormal position on walking till complete collapse of the foot shown by the depressed longitudinal medial arch. Bone reabsorption due to osteoclasis and increased blood flow until osteomalacia appears, is characteristic of this arthropathy. The clinical features vary according to the location and severity of articular impairment and the stage of identification. The metatarsophalangeal or tarsometatarsal joint may be involved. The typical manifestation of Charcot's foot is plantar ulcer of variable location according to the weight-bearing area. Treatment tends to reduce the abnormal stress predisposing to ulceration with tailored footwear and orthoses.

Adult↗
PubMedDate not supplied

Lower limb ischemia.

Diabetes mellitus is the major cause of nontraumatic amputations in the industrialized countries. In 1980 the scientific societies of diabetology and the patients' associations subscribed at St. Vincent a declaration together with the WHO, where a 50% decrease in amputations was among the primary objectives of clinical diabetology. The main cause of amputations is foot ischemia related to obliterating peripheral arterial disease, more diffuse and severe in diabetics, typically affecting the infrapopliteal vessels. Clinical patterns of foot ischemia include superficial necrotic areas and gangrene involving the entire foot with necrosis of all anatomic planes. Infection is a common complication with a negative impact on prognosis. Definitive treatment of ischemia is achieved with revascularization which at present due to the advances in diagnostic procedures can be performed in diabetics with the same effectiveness observed in non diabetics.

Amputation, Surgical↗
PubMedDate not supplied

Perioperative treatment of the diabetic patient.

The diabetic patient is frequently undergoing surgery for the underlying disease and its complications. Before referring the patient to surgery the diabetologist should carefully evaluate the presence of complications, cardiovascular, renal and neurologic disorders in particular. Generally no problems are posed by patients with NIDDM undergoing elective surgery. For more demanding patients and for those with IDDM the most effective and ready treatment is the continuous intravenous infusion of glucose, insulin and potassium. With this regimen, it is possible to perform major surgery in diabetics with a lower risk.

Amputation, Surgical↗