Interplay between surface properties of standard, vitamin E blended and oxidised ultra high molecular weight polyethylene used in total joint replacement and adhesion of Staphylococcus aureus and Escherichia coli.

We have assessed the different adhesive properties of some of the most common bacteria associated with periprosthetic joint infection on various types of ultra high molecular Weight Polyethylene (UHMWPE). Quantitative in vitro analysis of the adhesion of biofilm producing strains of Staphylococcus aureus and Escherichia coli to physically and chemically characterised standard UHMWPE (PE), vitamin E blended UHMWPE (VE-PE) and oxidised UHMWPE (OX-PE) was performed using a sonication protocol. A significant decreased bacterial adhesion was registered for both strains on VE-PE, in comparison with that observed on PE, within 48 hours of observation (S. aureus p = 0.024 and E. coli p = 0.008). Since Vitamin E reduces bacterial adhesive ability, VE-stabilised UHMWPE could be valuable in joint replacement by presenting excellent mechanical properties, while reducing bacterial adhesiveness.

Four-year impact of a continuous quality improvement effort implemented by a network of diabetes outpatient clinics: the AMD-Annals initiative.

AIMS: We evaluated the impact of a continuous quality improvement effort implemented by a network of Italian diabetes clinics operating in the national healthcare system. METHODS: This was a controlled before-and-after study involving 95 centres, of which 67 joined the initiative since 2004 (group A) and 18 were first involved in 2007 (group B, control). All centres used electronic medical record systems. Information on quality indicators was extracted for the period 2004-2007. Data were centrally analysed anonymously and results were published annually. Each centre's performance was ranked against the 'best performers'. We compared quality indicators between the two groups of centres over 4 years. RESULTS: Over 100 000 Type 2 diabetes mellitus patients were evaluated annually. The proportion of patients with glycated haemoglobin levels < 7% increased by 6% in group A (2007-2004 difference) and by 1.3% in group B. The proportion of patients with low-density lipoprotein-cholesterol < 100 mg/dl improved by over 10% in both groups. The rate of patients with blood pressure values < or = 130/85 mmHg increased in group A (+6.4%), but not in group B (-1.4%). The use of insulin increased in group A only (+5.2%), while the use of statins increased by over 20% in both groups. CONCLUSIONS: A physician-led quality improvement effort, based on the systematic evaluation of routine data, is effective in improving the performance of a large number of diabetes clinics. The small percentage increase in the number of patients at target, if applied to large numbers of patients, would translate into a significant impact on public health.

The refusal of food in childhood: From our clinical experience to an evaluation of recent diagnostic classifications.

The aim of this study, which was carried out because of the importance of eating disorders (EDs) acquired by the young and the need to organise resources and interventions for patients and their families, was to quantify the increased incidence of EDs arising early in life in order to identify the nosographic classification that best reflects the complexity of the symptoms. Between 2003 and 2008, we assessed 128 subjects aged less than 14 years and observed a constant increase in ED-related problems. Our analysis shows the importance of representative classification criteria suitable for young patients in order to improve diagnosis and therapeutic planning. The need for a specific classification for early childhood is underlined by the fact that comorbidities and overlapping patterns often complicate adequate assessment.

Circulating adhesion molecules and carotid artery structural changes in patients with noninsulin-dependent diabetes mellitus.

Hypertension and non insulin-dependent diabetes mellitus (NIDDM) are well-known risk factors for atherosclerotic disease. Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) may exert a relevant role in the pathogenesis of atherosclerosis; their prognostic relevance has been recently demonstrated. The aim of the study was to investigate possible inter-relation between circulating adhesion molecule levels, carotid artery structure and endothelial function in 15 patients with NIDDM, as well as in 15 patients with both NIDDM and essential hypertension (NIDDM+EH) compared with 15 normal subjects (NS) and 15 euglycaemic patients with EH, matched for age, sex and body weight. All subjects were submitted to a biopsy of the gluteal subcutaneous fat. Small arteries were dissected and mounted on a micromyograph, and the media-to-lumen (M/L) ratio was then calculated. Carotid artery structure was investigated by Doppler ultrasound. Endothelial function was evaluated by investigation of the flow-mediated dilatation (FMD) of the brachial artery. ICAM-1 and VCAM-1 plasma levels were measured by ELISA. ICAM-1 and VCAM-1 plasma levels were significantly greater and FMD smaller in EH, NIDDM and NIDDM+EH than in NS, but no difference was observed among the three pathological groups. Carotid artery structural changes were more pronounced in NIDDM+EH. No significant difference was observed among NIDDM, EH and NS. The M/L ratio of subcutaneous small resistance arteries was significantly greater in NIDDM+EH than in NIDDM or EH. NS had a smaller M/L ratio than the other groups. Significant correlations were observed between ICAM-1 plasma levels and indices of carotid artery structure in diabetic patients. However, the relations were close only in NIDDM+EH. In conclusion, our data suggest that NIDDM+EH may present more pronounced vascular structural alterations than NIDDM, and that adhesion molecules plasma levels are closely inter-related with carotid artery structural alterations, at least in NIDDM+EH, but not with M/L ratio of small resistance arteries.

Endothelial dysfunction in small resistance arteries of patients with non-insulin-dependent diabetes mellitus.

OBJECTIVE: Arterial hypertension is frequently associated with the presence of endothelial dysfunction in human subcutaneous small resistance arteries, as evaluated by responses to acetylcholine or bradykinin; however it is not known whether patients with diabetes mellitus show similar alterations. Therefore, we have investigated endothelial function in subcutaneous arteries of normotensive subjects (NT), of patients with essential hypertension (EH), of patients with non-insulin-dependent diabetes mellitus (NIDDM), as well as of patients with both essential hypertension and non-insulin-dependent diabetes mellitus (NIDDM+EH). PATIENTS AND METHODS: All subjects were submitted to a biopsy of the subcutaneous fat Small arteries were dissected and mounted on a micromyograph. The media to lumen ratio (M/L) was calculated. A concentration-response curve to acetylcholine, to bradykinin as well as to the endothelium-independent vasodilator sodium nitroprusside were performed. We also evaluated the contractile response to endothelin-1. Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) plasma levels were also measured. RESULTS: The vasodilatation to acetylcholine and bradykinin (but not to sodium nitroprusside) was significantly and similarly reduced in EH, in NIDDM, and in NIDDM+EH compared with NT. The contractile response to endothelin-1 was similarly reduced in EH, in NIDDM and in NIDDM+EH. Plasma ICAM-1 and VCAM-1 concentrations were higher in EH, NIDDM and NIDDM+EH than in NT. CONCLUSIONS: An evident endothelial dysfunction was detected in patients with NIDDM, and the simultaneous presence of EH did not seem to exert an additive effect. The contractile responses to endothelin-1 were reduced possibly as a consequence of ET(A) receptor down-regulation.

[Control of postoperative pain in heart surgery. Comparison of analgesics]. / Il controllo del dolore postoperatorio in cardiochirurgia. Analgesici a confronto.

BACKGROUND: Evaluation of the efficacy of three analgesic drugs (tramadol, ketorolac, and morphine) for the control of postoperative pain in cardiac surgery. DESIGN: prospective randomized study. SETTING: University Hospital, Postoperative intensive care unit. PARTICIPANTS AND INTERVENTION: sixty patients, who underwent cardiac surgery, were studied. They were randomly allocated in four groups, treated with a different postoperative analgesic therapy: A) tramadol in continuous infusion; B) ketorolac in continuous infusion; C) tramadol, in repeated boluses; D) morphine, in repeated boluses. MEASUREMENTS: the analgesic efficacy of each drug and administration protocol was evaluated by hemodynamic stability, arterial blood gases analysis, Visual Analogue Scale (VAS), resting and after cough, the VAS derivatives PID and SPID, the concentration of plasma epinephrine and norepinephrine, at eight postoperative times. Adverse effects were also registered. RESULTS: Only tramadol, in continuous i.v. infusion, achieves the required analgesic effect, significantly decreasing both VAS scores, at the end of the administration of the drug. This treatment reduced epinephrine plasma levels in the first postoperative day, when the residual analgesic effect of surgical anesthesia can be considered disappeared. CONCLUSIONS: Tramadol in continuous infusion (dose 12 mg/h) proved to be effective for the control of postoperative pain after cardiac surgery. The proposed dose represents a good compromise between analgesic efficacy and interference with the vital functions of operated patients.

Structural alterations in subcutaneous small arteries of normotensive and hypertensive patients with non-insulin-dependent diabetes mellitus.

BACKGROUND: It is not presently known whether non-insulin-dependent diabetes mellitus (NIDDM) is associated with the presence of structural alterations in small arteries or whether the combination of hypertension and NIDDM may have an additive effect on endothelial dysfunction. Therefore, we investigated subcutaneous small arteries in 12 normotensive subjects (NT group), 18 patients with essential hypertension (EH group), 13 patients with NIDDM, and 11 patients with NIDDM and EH (NIDDM+EH group). METHODS AND RESULTS: Subcutaneous small arteries were evaluated by a micromyographic technique. The internal diameter, the media-to-lumen ratio, remodeling and growth indices, and the collagen-to-elastin ratio were calculated. Concentration-response curves to acetylcholine, bradykinin, the endothelium-independent vasodilator sodium nitroprusside, and endothelin-1 were performed. The media-to-lumen ratio was higher in the EH, NIDDM, and NIDDM+EH groups compared with the NT group. EH patients showed the presence of eutrophic remodeling, whereas NIDDM and NIDDM+EH patients showed 40% to 46% cell growth. The collagen-to-elastin ratio was significantly increased in the EH and NIDDM+EH groups compared with the NT group. The vasodilatation to acetylcholine and bradykinin was similarly reduced in EH, NIDDM, and NIDDM+EH groups compared with the NT group. The contractile responses to endothelin-1 were similarly reduced in EH, NIDDM, and NIDDM+EH patients. CONCLUSIONS: Our data suggest that the effects of NIDDM and EH on small artery morphology are quantitatively similar but qualitatively different and that the presence of hypertension in diabetic patients has little additive effect on small artery morphology and none on endothelial dysfunction.

Myxedema coma of both primary and secondary origin, with non-classic presentation and extremely elevated creatine kinase.

Myxedema coma is a rare, often fatal endocrine emergency that concerns elderly patients with long-standing primary hypothyroidism; myxedema coma of central origin is exceedingly rare. Here, we report a 37-year-old woman in whom classical symptoms of hypothyroidism had been absent. Six years earlier, she had severe obstetric hemorrhage and, shortly after, two subsequent episodes of pericardial effusion. On the day of admission, pericardiocentesis was performed for the third episode of pericardial effusion. Because of the subsequent grave arrhythmias and unconsciousness, she was transferred to our ICU. Prior to the endocrine consultation, a silent myocardial infarction had been suspected, based on the extremely high serum levels of creatine kinase (CK) and isoenzyme CK-MB. However, based on thyroid sonography, pituitary computed tomography, elevated titers of antithyroid antibodies and pituitary stimulation tests, the final diagnosis was myxedema coma of dual origin: an atrophic variant of Hashimoto's thyroiditis and post-necrotic pituitary atrophy (Sheehan syndrome). Substitutive therapy caused a prompt clinical amelioration and normalization of CK levels. Our patient is the first case of myxedema coma of double etiology, and illustrates how its presentation deviates markedly from the one endocrinologists and physicians at ICU are prepared to encounter. In addition, cardiac problems as those of our patient should not discourage from substitutive treatment (using L-thyroxine and the gastrointestinal route of absorption), if the age is relatively low.

Nonenzymic glycation of apolipoprotein B in patients with insulin- and noninsulin-dependent diabetes mellitus.

OBJECTIVE: To evaluate the level of nonenzymatic glycation of apolipoprotein B in patients with insulin and noninsulin dependent diabetes mellitus. METHODS: Using a method based on a combination of affinity chromatography and immunonephelometry, we measured the concentration of glycated apolipoprotein B (apo B) in serum of 140 diabetic patients, 43 insulin-dependent (IDDM), and 97 noninsulin-dependent (NIDDM), and 45 nondiabetic control subjects. RESULTS: Although total apo B concentration in serum was significantly increased only in NIDDM patients, both groups of diabetics showed higher percentages of glycated apo B (IDDM, 4.84 +/- 0.8%; NIDDM, 5.61 +/- 1.1%) than did control subjects (4.28 +/- 1.0%), the greatest percentage (5.80%) being found in patients with diabetic nephropathy. No significant correlations were found between glycated apo B and the traditional parameters of glycemic control, such as glycated hemoglobin and fructosamines, and direct influence by sudden plasma glucose fluctuations on apo B glycation was not shown either, perhaps for a low inherent glycability of this apolipoprotein. CONCLUSIONS: It is unclear if these low proportions of glycated apo B in vivo may significantly affect lipoprotein metabolism assuming a pathophysiological role in atherogenesis.

[Brain stem auditory evoked potentials in obstructive sleep apnea syndrome]. / I potenziali evocati uditivi del tronco cerebrale nella sindrome dell'apnea ostruttiva nel sonno.

To evaluate a possible brainstem role in pathogenesis of obstructive sleep apnea syndrome, a study on brainstem auditory evoked potentials (BAEP), has been conducted. 15 OSAS patients, medium and severe form, with organic pathologies of the upper respiratory tract have been evaluated. 15 normal subjects were compared as control. All the patients were subjected to audiometry, including total liminal audiometry, timpanometry, acustic reflex, and BAEP study. BAEP evoked with trains of cliks at 11 and 51 periods/sec., showed morphological alterations and a longer central conductance of time interval (I-V interval) in only four patients. BAEP alterations noted in the OSAS-affected patients are neither constant nor specific. Therefore, the observed BAEP alterations might be due to apneas, as a consequence of the chronic hypoxic- hypercapnic status occurring in the brain-stem.

[Morphologic and ultrastructural changes of soft palate in patients who underwent palatopharyngoplasty]. / Rilievi istopatologici ed ultrastrutturali del palato molle in pazienti sottoposti ad intervento di palatofaringoplastica (PPP).

In order to clarify pathogenesis of Obstructive Sleep Apnea Syndrome (OSAS) in patients with anatomic abnormalities of upper airways, we studied soft palate and uvula of OSAS patients by means of histological and ultrastructural techniques. 38 OSAS patients, severe and moderately severe form, underwent modified Palatopharingoplasty. We evaluated only 16 OSAS patients' soft palate and uvula and observed histological changes in all of them: submucosal edema and minor salivary glandes ipertrophy and iperplasy are present. On the contrary, ultramicroscope showed normal muscle fibers. Strie Z alterations and sarcomeres disorganization, although present, have no statistical value. Very probably, ronflement and apneas determined the observed alterations through trauma on pharingeal wall. Therefore, they are not OSAS primary cause.

[The surgical treatment of obstructive sleep apnea syndrome]. / La terapia chirurgica nella sindrome dell'apnea ostruttiva nel sonno (OSAS).

Studies concerning the anatomical abnormalities of upper airways in patients affected by Obstructive Sleep Apnea Syndrome (OSAS) allowed the corrective surgical treatments in this syndrome. To provide an improvement or a definitive recovery of OSAS, various surgical treatments, i.e. functional nasal surgery, palatal surgery [Partial resection of palate (RPP), Uvulopalatopharingoplasty (UPPP), Palatopharingoplasty (PPP), modified Palatopharingoplasty (modified PPP)], mandibular and base tongue surgery, have been performed in order to obtain an enlargement of upper airways. It has been reported that in RPP, UPPP, PPP and modified PPP partial or total uvula and soft palate resection is conduct; in our research we performed modified PPP. 44 OSAS patients, severe or moderately severe form (polisomnographic diagnosis), underwent surgical treatment: 5 patients underwent functional nasal surgery; 9 patients underwent modified PPP; 29 patients underwent nasal and palatal surgery; only 1 patient underwent base tongue surgery. 32 patients underwent polisomnographic records after surgery (two months later) and we evaluated Apnea Index (I.A.) and a SaO2 low (nadir) with statistic tests. The results have been positive. Therefore, we have now 7 normal, 2 mild form, 7 moderate form, 3 moderately severe form and 13 severe form OSAS patients. If, on the one hand, all these surgical treatments can be considered a good way of therapy, on the other, only tracheostomy represents today the unfailing surgical therapy.

[The treatment of ENT phlogosis: seaprose S vs. nimesulide]. / Il trattamento delle flogosi in ORL-seaprose s vs nimesulide.

In the present multicentre study, the antiphlogistic activity of seaprose S was assessed according to an experimental design of the controlled type versus nimesulide in patients with phlogistic pathology of ENT relevance and in patients undergoing otoiatric surgical operations. One hundred and sixty patients (87 M, 73 F) were treated with seaprose S in 30 mg tablets (3tab/day) while 160 patients (95 M, 65 F) were treated with nimesulide in 100 mg (2 tab/day). The treatment lasted 7 days. At the beginning of the study, on the 3rd, 7th and 14th day (follow-up) the most significant signs and symptoms present in the pathological forms under consideration were evaluated. Common haematological and haematochemical laboratory parameters were also evaluated and any side effects occurring during the treatment were recorded. Considering the efficacy demonstrated, it was shown how the two drugs used possess an analogous action (NS) and are always able to exert positive control over the symptoms under examination. Administering seaprose S there were 9 cases of unexpected events (5.6%) while with nimesulide 26 patients (16.3%) showed problems of intolerance, with a highly significant statistical difference (p < 0.01) between the two groups. The analysis of the data obtained allows us thus to support the therapeutic use of seaprose S in the treatment of phlogosis of ENT relevance, since it has shown efficacy comparable to that of a NSAID such as nimesulide, but with greater safety.

Picotamide, a dual TXB synthetase inhibitor and TXB receptor antagonist, reduces exercise-induced albuminuria in microalbuminuric patients with NIDDM.

We investigated the short-term effect of the TXB inhibitor picotamide on albuminuria induced by exercise in 15 microalbuminuric (i.e., with UAE at rest between 20 and 200 micrograms/min) type II diabetic patients (12 men and 3 women, age 56 +/- 2, BMI 28 +/- 1 kg/m2) and in six normal age-matched control subjects. The diabetic subjects performed five submaximal exercise tests (90% of theoretical heart rate) on a cycle ergometer: the first two under basal conditions; the third and fifth after subjects had received picotamide (900 mg/day) or placebo (3 tablets/day) for 10 days; the fourth exercise always was performed after 10 days of wash-out. Control subjects performed two exercises: the first in baseline conditions and the second after 10 days of picotamide administration (900 mg/day). When diabetic patients were untreated, a significant (P < 0.05) increase in UAE with respect to baseline levels was observed immediately after and 1 h after the exercise test. After picotamide administration, UAE significantly decreased (P < 0.05) immediately after and 1 h after exercise, as compared with diabetic patients given a placebo. In normal subjects, exercise was followed by a slight increase in UAE, which was not significantly affected by picotamide administration. Our results show that short-term administration of picotamide is associated with a reduction in UAE after exercise in type II diabetes patients with microalbuminuria while at rest. Picotamide, a TXB synthetase and receptor inhibitor, may decrease exercise-induced albuminuria in diabetic patients through a reduction in circulating TXB levels and inhibition of TXB action, which in turn may act by lowering glomerular capillary hydraulic pressure.

High-dose folinic acid and 5-fluorouracil plus cisplatin on a weekly schedule in the treatment of advanced cancer of the head and neck.

A group of 60 patients with advanced head/neck cancer were treated with high-dose folinic acid (500 mg/m-2/week-1) plus 5-fluorouracil (400 mg/m-2/week-1 on day 1, and cisplatin (20 mg/m-2/week-1) 24 h after folinic acid infusion was completed. Out of 55 evaluable patients, 10 patients (18%) experienced a complete response with a mean duration of 11.4+ months, 25 patients had a partial response (45%) of 6.7+ months, 6 patients (11%) showed a stabilization of 4.8+ months, and 14 (25%) progressed. The overall response rate was 63.6% (95% confidence limits 56.5%-69.5%). Patients pretreated with radiotherapy had a 67% overall response rate, while those pretreated with chemotherapy showed a 54% overall response rate. All patients with cancer of the oropharynx had a major response, while patients with cancer of the oral cavity had the lowest response rate. The mean survival of patients who attained a complete response was 14.5+ months. Partial responders had a mean survival of 10.6+ months, while patients who progresses survived a mean of 3.6+ months. The treatment has been very well tolerated with few cases of grade 3 gastrointestinal toxicity. Grade 1-2 leukopenia was recorded in 64% of cases, grade 1-2 nausea/vomiting in 85%. In one case therapy was stopped because of persistent diarrhoea.

Effects of exogenous growth hormone pretreatment on the pituitary growth hormone response to growth hormone-releasing hormone alone or in combination with pyridostigmine in type I diabetic patients.

We evaluated the effects of iv pretreatment with exogenous GH on the GH response to GHRH either alone or in combination with pyridostigmine in 14 Type I diabetic patients and 6 normal subjects. All the subjects received an iv bolus injection of biosynthetic human GH, 2 IU; 2 h later they received either a. pyridostigmine, 120 mg orally, or b. placebo, 2 tablets orally, followed 1 h later by iv injection of GHRH(1-29) NH2, 100 micrograms. In normal subjects the median GH peak after GH+ GHRH was 1.8, range 1.2-6.9 micrograms/l. Pyridostigmine enhanced the GH response to GHRH in all subjects. The median GH peak after pyridostigmine + GH + GHRH was 32.7, range 19.8-42.1 micrograms/l (p less than 0.001 vs GHRH alone). Seven diabetic subjects had median GH peaks after GH + GHRH greater than 6.9 micrograms/l (the maximum GH peak after GH + GHRH in normal subjects) (group A: median GH peak 35.7, range 21.7-55 micrograms/l). The other diabetic subjects had GH peak lower than 6.9 micrograms/l (group B: median GH peak 4.4, range 2.1-6.5 micrograms/l). Pyridostigmine significantly increased the GH response to GHRH in group B patients (median GH peak 29.3, range 15.7-93.4 micrograms/l, p less than 0.001 vs GH + GHRH alone), but not in group A patients (median GH peak 39.9, range 21.9-64.9 micrograms/l). Group A diabetic patients were younger and had higher HbA1c and blood glucose levels than group B patients. In those diabetic patients with an exaggerated GH response to GH + GHRH, pyridostigmine failed to cause the increase in GH secretion observed in diabetic and control subjects with no responses to GH + GHRH.(ABSTRACT TRUNCATED AT 250 WORDS)

Low-dose octreotide is able to cause a maximal inhibition of the glycemic responses to a mixed meal in obese type 2 diabetic patients treated with insulin.

Short-term studies have shown that octreotide, a long-acting somatostatin analog, blunts postprandial glycemic responses and reduces insulin requirement in insulin treated diabetic patients. The aim of our study was to investigate the effects of three single, different doses of octreotide on the glycemic response to a mixed meal in eight insulin treated type 2 diabetic patients after secondary failure with hypoglycemic agents. Previous treatments were substituted by regular insulin, 0.5 U/kg/day divided into three sc injections, for at least seven days. All patients received: (a) regular insulin (0.1 U/kg, sc) at 7.30 am; (b) octreotide 25 micrograms sc or (c) 50 micrograms sc or (d) 100 micrograms sc simultaneously with insulin but injected at different sites. From 8.00 to 8.15 the patients consumed a preconstituted fluid mixed meal of 250 ml. Following insulin alone a significant increase in blood glucose levels was observed after the meal. Abolished and not significantly different blood glucose responses to the meal after each of the three doses of octreotide were observed. Our findings suggest that with a low dose of octreotide (25 micrograms) it is possible to abolish the postprandial glycemic peak in type 2 diabetic patients treated with insulin.

Impaired growth hormone (GH) response to pyridostigmine in type 1 diabetic patients with exaggerated GH-releasing hormone-stimulated GH secretion.

In the present study we investigated the effects of the acetylcholinesterase inhibitor pyridostigmine (PD), which is hypothesized to decrease hypothalamic somatostatin tone, alone and in association with GH-releasing hormone (GHRH) on GH secretion in 18 type 1 diabetic patients and 12 normal subjects using a randomized double blind placebo-controlled protocol. All subjects received either 120 mg oral PD or placebo 60 min before iv injection of either human GHRH-(1-29) NH2 (100 micrograms) or sterile water (2 mL). In normal subjects both PD alone and GHRH alone caused a significant increase in GH. PD and GHRH acted in a synergistic fashion when combined. In diabetic patients the GH response to GHRH was variable. To segregate the responses, the ratio between the GH increase after GHRH plus PD and after GHRH alone was calculated for each subject. In 10 diabetic patients (group A) the ratio was lower than 2 SD (P less than 0.05) from the mean response of normal subjects. These patients showed an exaggerated GH increase after GHRH and a lower GH increase after PD with respect to normal subjects. Eight diabetic patients (group B) showed a ratio similar to that in normal subjects and similar GH responses to the stimuli. No significant differences were found between groups A and B with respect to age, body mass index, and blood glucose levels. Duration of diabetes was longer and basal GH levels were higher in group A. Hemoglobin-A1c was higher in group A, but of only borderline statistical significance (P = 0.052). Our data demonstrate that in diabetic patients with exaggerated GH responses to GHRH an increase in cholinergic tone does not affect GH secretion. These data suggest that in some type 1 diabetic patients an altered somatostatinergic control of GH secretion may contribute to their abnormal GH response to GHRH.