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A Meo

Publications and source records attributed to A Meo.

At least 19 recordsLinked to original sources
PubMed2005

The almond milk: a new approach to the management of cow-milk allergy/intolerance in infants.

AIM: Elimination of the offending food is imperative in the management of children with cow-milk allergy/intolerance (CMA/CMI). Herein we report the result of randomized clinical trial carried out to test the efficacy and safety of a new almond-based food (hereinafter named almond milk) in a group of infant with CMI/CMA. METHODS: A group of 52 infants aged 5 to 9 months and with documented CMI/CMA was enrolled and randomized to: almond milk (Group A, n=26); soy-based formula (Group B, n=13); protein hydrolysate-based formula (n=13). The main efficacy outcomes were the improvement in clinical symptoms and the decrease in serum levels of soluble CD30 (a potential marker for atopic disorders; sCD30). RESULTS: Elimination of the offending food and supplementation with a milk protein-free formula produced a considerable improvement of clinical manifestations within 5-12 days in all cases examined (at the onset of the study: 26.4+/-5.4 U/mL and 7.9+/-5.2 U/mL in IgE+ and IgE- infants respectively, after 6 months of supplementation: 16.6+/-4.8 U/mL and 7.1+/-4.5 U/mL in IgE+ and IgE- infants respectively). No difference in growth rate (increment of weight, length and head circumference) was found, during the entire study, between infants given the almond milk and babies given the soy-based formula or the protein hydrolysate-based formula. Supplementation with the soy-based and protein hydrolysate-based formulas caused the development, in some subjects, of a secondary sensitization (23% to soy-based and 15% protein hydrolysate-based formula), whereas supplementation with the almond milk did not. CONCLUSIONS: Though preliminary, the present findings seem to demonstrate that the almond milk may an efficacious substitute of cow milk in infants with CMA/CMI. One could speculate that some active principles contained in the almond milk could contribute to its beneficial effect observed in CMI/CMA-affected infants.

Animals↗
PubMed2002

Osteoporosis and beta-thalassemia major: role of the IGF-I/IGFBP-III axis.

Patients with beta-thalassaemia major are susceptible to osteopenia due to several factors which interfere with bone remodeling. It is known that bone metabolism and skeletal consolidation result from a complex sequence of hormonal changes, where the concerted actions of GH, IGF-I and sex hormones and their receptors, are responsible for the timing and attainment of skeletal consolidation. IGF-I and the corresponding binding protein (IGFBP-III), markers of bone metabolism and lumbar and femoral neck BMD were measured in 28 adult patients, undergoing hormonal replacement and chelation therapy and a hypertransfusion program, with beta-thalassaemia major (12 males with mean age 22.5+/-3.1 and 16 females with mean age 27.5+/-8.2), and in 28 healthy volunteers matched for age, anthropometric features and sex to the patients. BMD values, both at lumbar and femoral neck level were significantly lower (p<0.001 and p<0.05) by 18.7 and 4.2% respectively, in patients than in the controls. Markers of bone resorption [pyridinoline (Pyr) 78.1+/-15.7 vs 47.5+/-11.2 pmol/pmol urinary creatinine, p<0.001 and deoxypyridinoline (D-Pyr) 21.9+/-3.5 vs 14.5+/-5.4 pmol/ micromol urinary creatinine, p<0.001] were higher in patients than in controls, whereas the marker of bone formation was slightly lower [osteocalcin (BGP) 3.8+/-0.6 vs 4.6+/-1.7 pmol/ml, p<0.05]. Plasma levels of IGF-I (21.07+/-5.12 vs 35.25+/-8.33 nmol/ml, p<0.001) and IGF binding protein III (IGFBP-III) (1.9+/-0.4 vs 2.5+/-0.1 mg/ml, p<0.001) were lower in patients than in controls and positively correlated with BMD L2-L4 (r=0.57, p<0.05 and r=0.47, p<0.05 respectively), BMD neck (r=0.40, p<0.05 and r=0.34, p<0.05 respectively) and BGP (r=0.52, p<0.05 and r=0.34, p<0.05 respectively). Our beta-thalassaemic patients, in spite of normalizing hemoglobin levels, adequate hormone replacement and chelation therapies, showed osteopenia and an unbalanced bone turnover with an increased resorptive phase and a decreased formation phase probably correlated to low levels of IGF-I and IGFBP-III observed in our study.

Adult↗
PubMed2002

Three-year prospective evaluation of glucose tolerance, beta-cell function and peripheral insulin sensitivity in non-diabetic patients with thalassemia major.

The aim of this prospective study was to evaluate the evolution of glucose tolerance (GT), insulin secretion and peripheral insulin sensitivity during a 3-yr follow-up in a homogenous population consisting of fourteen non-diabetic adults with thalassemia major (TM). All the patients underwent 2 OGTTs with a 3-yr interval and random measurements of fasting glycemia during the entire follow-up. At the time of both OGTTs, peripheral insulin sensitivity was assessed by both homeostatic model assessment (HOMA) index and a novel index derived from the OGTT. At the second OGTT patients exhibited both significantly higher fasting glucose concentrations and enhanced glycemic responses, with greater average glucose areas. GT deterioration over time was accompanied by a reduction of insulin sensitivity, with no concomitant change of insulin secretion. No patient developed diabetes mellitus (DM) during follow-up. To conclude, the natural history of glycometabolic status in TM adults seems to be characterized by a GT deterioration over time, which may probably reflect an increase of insulin resistance. GT deterioration is more evident in patients with the highest responses to the 1st OGTT and particularly in those with pre-existing impaired GT.

Adult↗
PubMed2002

Bisphosphonates in the treatment of thalassemia-induced osteoporosis.

The aim of our randomized, placebo-controlled study was to investigate the effects of 2 years' daily oral administration of alendronate or intramuscular administration of clodronate every 10 days, on bone remodeling parameters and bone mineral density (BMD), safety and tolerability in a group of osteoporotic thalassemic patients. Twenty-five young patients (mean age 26.6 +/- 7.1 years) with beta-thalassemia major were randomly divided to receive placebo or 100 mg of clodronate intramuscularly every 10 days or 10 mg of alendronate per os daily. All patients took 500 mg of elemental calcium and 400 IU cholecalciferol in the evening at meal time. After 2 years, pyridinium crosslinks, which are bone resorption markers, did not differ significantly from baseline values in the placebo group, whereas they had decreased significantly in the clodronate and alendronate groups. Osteocalcin, a bone formation marker, did not change significantly in the placebo group, whereas it decreased slightly, but not significantly, in the clodronate and alendronate groups after 12 and 24 months. At the end of the study, the lumbar spine BMD had decreased significantly in the placebo group; it did not change significantly in the clodronate group; in the alendronate group it had increased but not significantly, whereas the increase was significant with respect to the placebo group. Femoral neck BMD decreased significantly in the placebo group; it did not change significantly in the clodronate group, but increased significantly in the alendronate group. No relevant side effects were recorded during our study. In conclusion, in patients with thalassemia-induced osteoporosis, the daily administration of alendronate significantly increases BMD, the most important predictor of the risk of fracture at several sites. Clodronate treatment at our dosage is ineffective in this pathology in spite of the good compliance of patients.

Absorptiometry, Photon↗
PubMed2001

Molecular analysis of beta-thalassaemia patients in a high incidence area of southern Italy.

The prevalence of eight mutations in 84 patients with beta-thalassaemia major and in 16 subjects with thalassaemia intermedia was investigated. All of the patients were Italian, originating from Eastern Sicily (Messina area) and some Calabrian regions. Genomic DNA was amplified by polymerase chain reaction (PCR). DNA molecular investigations were performed by allele-specific oligonucleotide (ASO) hybridization, to identify the following beta-thalassaemia mutations: CD39 (C-T), IVS1-110 (G-A), IVS1-6 (T-C), IVS1-1 (G-A), IVS2-745 (C-G), IVS2-1 (G-A), -87 (C-G), CD6 A (-A). Our data underline that in thalassemia intermedia two mutations were statistically prevalent: IVS1-6 T-->C (P < 0.001) and CD 6-A (P < 0.05). CD 39 was statistically prevalent in beta-thalassaemia major patients (P < 0.01). The difference between the two groups was not statistically significant for all the other mutations. Five different genotypes were recorded among thalassaemia intermedia and 15 among beta-thalassaemia major patients. Twenty-five percent of the intermedia patients and 4.5% of the major patients had homozygosity for mild mutations (group I); 62.5% of the intermedia patients and 26.2% of the major patients had combinations of mild/severe mutations (group II). In addition, homozygosity or double heterozygosity for severe mutations (group III) was found in 12.5% of the intermedia patients and 69% of the major patients. Some genotypes were restricted to thalassaemia intermedia, including heterozygosity -87/IVS1-6 and IVS1-6/CD 6-A. It is essential to understand the distribution and frequency of the relevant mutations in each population where beta-thalassaemias exist. This is of particular importance for genotype-phenotype correlation and for carrier detection, genetic counselling and prenatal diagnosis.

Adolescent↗
PubMed2000

Two rare lumbar tumours with unusual MRI characteristics.

We present two rare lumbar lesions with similar MRI features: high signal on T1-weighted and proton density images and low signal on T2-weighted images; a melanotic schwannoma, and a giant-cell tumour-like lesion. Melanin in the first case and haemosiderin and metahaemoglobin in the second were responsible for the MRI characteristics.

Aged↗
PubMed1998

Short stature and body proportion in thalassaemia.

Short stature and short trunk have been reported in thalassaemic patients. We report a study on stature and body proportions in 476 patients (2-36 years old) with beta-thalassaemia major, followed in 12 Italian centres. Auxological data (standing height, sitting height, subischial leg length, target height), haematological data (age at first transfusion, age at start of desferrioxamine [DFX] chelation, mean dose of DFX, ferritin values) and information regarding the presence of endocrine disorders and of bone lesions, were collected and analysed according to the age of the patients, in order to investigate the natural history of the disproportion and the role of siderosis, DFX toxicity and endocrine disorders. Our data indicate that about 18% of thalassaemic patients exhibit short stature; disproportion between the upper and lower body segments is present in 14%; however, a short trunk despite normal stature is present in another 40% of patients. This is due to a spinal growth impairment which starts in infancy and progressively aggravates. We think that a short trunk is peculiar to the disease itself; however, other factors such as hypogonadism, siderosis, or DFX-induced bone dysplasia are probably involved in aggravating the body disproportion in these patients.

Adolescent↗
PubMed1998

Glucose tolerance, insulin secretion and peripheral sensitivity in thalassaemia major.

Glyco-metabolic status was evaluated in 29 pubertal homozygous thalassaemics aged from 17 to 42 years and in 12 age-matched healthy subjects. Diagnosis of diabetes mellitus was assessed in 4 patients (13.8%), who became diabetic after the age of 18 years. With respect to controls non-diabetic patients exhibited significantly higher fasting plasma glucose levels and more sustained glycemic responses to oral glucose tolerance test, whereas their overall insulin output was significantly lower. Moreover non-diabetic thalassaemic patients showed a clear reduction of both beta-cell function and insulin resistance indices (HOMA model). In conclusion our data show a high prevalence of diabetes but do not support the existence of an insulin resistant status in thalassaemia major, at least in adulthood.

Adolescent↗
PubMed1998

[Tryptase levels are elevated during spontaneous ischemic episodes in unstable angina but not after the ergonovine test in variant angina].

Activated mast cells are present in human coronary atheromas, as well as in the adventitia of patients with variant angina, and may play an important role in plaque rupture and coronary vasomotion. To assess whether or not activation of mast cells is a primary event, we measured serum levels of tryptase, a specific marker of mast cell activation, in 8 patients with unstable angina during a spontaneous ischemic episode (Group 1) and in 5 patients with variant angina (Group 2) during ergonovine-induced coronary spasm. Blood samples were collected as soon as possible after the onset of pain and ECG changes (0 min), and after 5, 15 and 60 min. Tryptase levels in Group 1 were 0.13 U/l (range 0.017-0.44) at the onset of pain and significantly raised to 0.75 U/l (range 0.05-2.49) at 5 min, decreasing to 0.076 U/l (range 0.018-0.16) at 15 min and to 0.085 U/l (range 0.01-0.25) at 60 min (p = 0.035). Conversely, tryptase levels in Group 2 were 0.09 U/l (range 0.07-0.13) at 0 min, 0.11 U/l (range 0.07-0.22) at 5 min, 0.10 U/l (range 0.07-0.18) at 15 min, 0.11 U/l (range 0.07-0.17) at 60 min (NS). In conclusion, tryptase levels raise during spontaneous ischemic episodes in unstable angina, but not after ergonovine-provoked ischemia in variant angina, suggesting that a primary, yet unknown stimulus, may activate mast cells during some ischemic episodes in unstable angina.

Aged↗
PubMed1998

[Clinical presentation of unstable angina may influence the formation of thrombin during spontaneous episodes of ischemia].

In order to evaluate whether different clinical presentations of unstable angina are associated with a different degree or pattern of activation of the hemostatic, fibrinolytic and inflammatory systems, we measured plasma levels of thrombin-antithrombin III, plasmin-alpha2- antiplasmin complexes and C-reactive protein, as markers of activation of coagulation, fibrinolysis and inflammation respectively, in two groups of patients: 7 patients with de novo unstable angina (Group 1) and 7 patients with destabilizing unstable angina (Group 2). Blood samples were taken on admission for measuring levels of C-reactive protein and during ischemic episodes at the onset of ECG changes and pain (0 min) and after 5, 15 and 60 min in order to assess the peak values of thrombin-antithrombin III and plasmin-alpha2-antiplasmin during the episode. Thrombin-antithrombin III levels in Group 1 were 1.8 microgram/l (0.3-4.15) at 0 min and increased to 17 micrograms/l (2.8-60) after 5 to 15 min (p = 0.013); conversely thrombin-antithrombin III levels in Group 2 were 2.15 microgram/l (1.4-3.8) at 0 min and raised to 4 micrograms/l (2-43) after 5 to 15 min (NS). No significant differences in both groups were observed in plasmin-alpha2-antiplasmin levels (Group 1:650 micrograms/l, ranged 492-956, at 0 min vs 670 microgram/l, range 415-977, at peak; Group 2: 480 micrograms/l, range 274-955, at 0 min vs 502 micrograms/l, range 304-1027, at peak; NS). Inversely, C-reactive protein levels on admission were 4 mg/dl (range 2-27) in Group 1, and 1 mg/dl (range 0.6-4) in Group 2 (p = 0.006). In conclusion, patients with de novo unstable angina have significantly enhanced thrombin (but not plasmin) production during spontaneous ischemic episodes than patients with destabilizing unstable angina. Furthermore, patients with de novo unstable angina have enhanced acute phase responses than patients with destabilizing unstable angina. Our data suggest that different pathogenetic mechanisms may be responsible for acute ischemic episodes in unstable angina and may explain different response to antithrombotic therapy in unstable angina patients.

Aged↗
PubMed1988

A case of intraneural cyst of the common peroneal nerve.

Intraneural cysts of the common peroneal nerve, as of other peripheral nerves, are rare. Their etiopathogenesis is unknown, though theories involving a tumor of synovial origin, mucoid degeneration or injury have all been proposed. An ex-amateur footballer with paralysis of the left CPN but unaffected peroneus longus proved, on surgical exploration of the CPN at the level of the head of the fibula, to have an intraneural cyst, which was removed. As it was a true intraneural cyst with no cleavage plane, no endothelial lining and no articular peduncle, and given the footballing history, the pathogenesis was considered to be traumatic. A year after cysts removal, the patient has fully regained the strength of the left foot.

Cysts↗
PubMedDate not supplied

Arthroscopic treatment of lateral meniscal cysts using an outside-in technique.

This paper describes 19 cases of lateral meniscal cysts treated arthroscopically using an outside-in technique. In all patients, a horizontal or radial lesion (or both) of the meniscus was present. After the meniscal lesion was arthroscopically removed, the cyst was decompressed both from inside and percutaneously from outside with a motorized instrument introduced through a transmeniscal approach. The follow-up ranged from 2 to 5 years with an average of 3.3 years. On the basis of the evaluation scale developed by Cerullo et al. (1991), the results were rated excellent or good in 17 patients and fair in 2. No patient had cyst recurrence. The computed tomography follow-up examination, done in 10 of the 19 patients after an average of 3 years, showed a good remodeling of the meniscus. One of the two patients with a fair result had hypermobility of the posterior horn of the lateral meniscus due to the resection of the meniscal tissue overlying the popliteus tendon, whereas the other had pain and patellar crepitation owing to a preexisting patellofemoral abnormality.

Adult↗