Postoperative pain as complication of hernia surgical repair with mesh and plug

The authors assess the incidence of locoregional chronic pain after inguinal hernia repair. One hundred consecutive patients, with a mean age of 65.4 years, suffering from primary monolateral inguinal hernia, underwent suture-less mesh-plug hernioplasty. In all cases the inguinal nerves were identified. In the early postoperative period, a questionnaire was given to all patients in order to assess the frequency, type and intensity of postoperative locoregional pain and the impact of the pain on their quality of life. Sixty patients were available for follow-up with clinical examination and these were given the same questionnaire 2-4 years after hernioplasty. Pain intensity was scored by means of a visual-analogue scale (from 0 to 10). The incidence of locoregional pain after hernioplasty was 13.0% in the early postoperative period and 25.0% after a longer period of follow-up. None of the patients presented recurrent hernia. The symptomatic patients reported mild or moderate neurogenic pain. Severe pain was not reported. On the whole, the presence of mild-to-moderate chronic pain had no impact on the patients' quality of life. Our study confirms the high incidence of locoregional chronic pain even after sutureless mesh-plug hernioplasty, but that this has no serious effects on the patients' quality of life.     

Relaxin inhibits the activation of human neutrophils: involvement of the nitric oxide pathway

In animal models of inflammation, the pregnancy hormone relaxin was shown to reduce the recruitment of leukocytes, especially neutrophils, in inflamed tissues. The current study was designed to clarify whether relaxin could inhibit activation of isolated human neutrophils and, if so, whether the nitric oxide (NO) biosynthetic pathway was involved, as occurs in other relaxin targets. Human neutrophils were preincubated with 1, 10, and 100 nmol/liter porcine relaxin for 1 h before activation with N-formyl-Met-Leu-Phe (10 micromol/liter) or phorbol-12-myristate-13-acetate (0.1 micromol/liter). In selected experiments, the NO synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA, 100 micromol/liter) was added to the samples 30 min before relaxin. In other experiments, chemically inactivated relaxin (10 nmol/liter) was substituted for authentic relaxin. Untreated, nonactivated neutrophils were the controls. Relaxin reduced significantly and in a concentration-dependent fashion the expression of the surface activation marker CD11b, as well as the generation of superoxide anion, the rise of intracellular Ca(2+), the release of cytoplasmic granules, and the chemotactic migration. These effects of relaxin were blunted by N(G)-monomethyl-L-arginine and could not be reproduced by inactivated relaxin. Relaxin also increased neutrophil inducible NO synthase expression and NO generation. This study provides evidence that relaxin inhibits the activation of human neutrophils stimulated by different proinflammatory agents. This novel property of relaxin could be of relevance in toning down maternal neutrophil activation during pregnancy, thereby counteracting the occurrence of pregnancy-related disorders such as preeclampsia, which is regarded as an excess maternal inflammatory response to pregnancy.     

Effect of oral L-arginine on blood pressure and symptoms and endothelial function in patients with systemic hypertension, positive exercise tests, and normal coronary arteries

Thirteen hypertensive patients with microvascular angina were studied before and after receiving oral L-arginine (4 weeks, 2 g, 3 times daily). L-arginine significantly improved angina class, systolic blood pressure at rest, and quality of life. Maximal forearm blood flow, plasma L-arginine, L-arginine:asymmetric dimethyl arginine ratio, and cyclic guanylate monophosphate increased significantly after treatment. In medically treated hypertensive patients with micro-vascular angina, oral L-arginine may represent a useful therapeutic option.     

A pilot study of nurse-led, home-based telecardiology for patients with chronic heart failure

We assessed the feasibility of home-based telecardiology for patients with chronic heart failure (CHF). Seventy-four CHF patients were enrolled into a programme of telephone follow-up and single-lead electrocardiography (ECG) monitoring. The patients transmitted their ECG data by fixed telephone line to a receiving station, where a nurse was available for an interactive teleconsultation. Patients were followed up for a mean (SD) of 307 (108) days; 1467 calls were analysed (213 ad hoc consultations and 1254 scheduled consultations). A total of 124 cardiovascular events were recorded. Modifications to therapy were suggested in response to 119 calls; hospital admissions were suggested for 13 patients, further investigations for 7 and a consultation with the patient's general practitioner for 13. No action was taken after 1330 calls. Twenty-two ECG abnormalities were recorded. In 63 patients receiving the beta-blocker carvedilol, the mean dosage increased from 36 to 42 mg. In the previous year there were 1.8 hospitalizations per patient, while in the follow-up period there were 0.2 hospitalizations per patient. Following up CHF patients using a nurse-led telecardiology programme seems to be feasible and useful.     

A novel PTPN11 gene mutation bridges Noonan syndrome, multiple lentigines/LEOPARD syndrome and Noonan-like/multiple giant cell lesion syndrome

Noonan (NS) and multiple lentigines/LEOPARD syndromes (LS) have proved to be associated with distinct PTPN11 mutations. Noonan-like/multiple giant cell lesion syndrome (NLS) is a rare disease, characterised by short stature, facial dysmorphisms, congenital heart defect (CHD) and central giant cell lesions. PTPN11 gene mutations have been reported in a single NLS family and two sporadic patients. Here we report a patient with a complex phenotype progressing throughout the years from NS at birth towards LS and NLS. PTPN11 gene analysis disclosed a novel missense mutation (Ala461Thr) in exon 12, affecting the consensus sequence of the SHP2-active site. This observation joins together NS and LS to NLS into a unique genetic defect, broadening the clinical and molecular spectrum of PTPN11-related disorders.     

NK cells: innate immunity against hematological malignancies?

Recent advances in the treatment of malignant haemopathies enable increased remission and cure rates, however, many patients relapse and finally die. Although specific immunity mediated by cytolytic T-lymphocytes might have an anti-cancer role, tumours escape from T-cell-based immune surveillance using various mechanisms, such as downregulation, mutation or loss of HLA class I molecules. As a consequence, these transformed cells could become targets for natural killer (NK) cells, whose cytotoxic capabilities are not blocked by HLA class I molecule engagement by specific inhibitory receptors. Novel developments in NK-cell research, particularly the identification of the role of non-HLA-restricted activating receptors (and in some cases of their ligands), have recently enabled us to reconsider NK-cell interactions with haematological malignant cells.     

Proteinuria as a predictor of disease progression in children with hypodysplastic nephropathy

Little is known about the role of proteinuria in the progression of childhood renal diseases. We analyzed the decline in creatinine clearance (C _Cr) and kidney survival in 225 children (185 males) with chronic renal failure (CRF) due to isolated hypodysplasia or hypodysplasia associated with urological abnormalities. The data were based on the information available in the Italian Pediatric Registry of CRF (ItalKid Project), which includes patients from all of Italy aged <20 years with C _Cr levels of <75 ml/min per 1.73 m². Patients aged <2 years and those with C _Cr levels of <20 ml/min per 1.73 m² or a follow-up of <1 year were excluded from the analysis, as were those receiving angiotensin-converting enzyme inhibitors. At baseline, the patients had a mean age of 7.8±4.2 years, a mean C _Cr of 50±16.3 ml/min per 1.73 m², a median urinary protein/urinary creatinine (uPr/uCr) ratio of 0.38 (range 0.02–7.21), and a mean duration of follow-up of 3.5±1.1 years. The patients were divided into three groups on the basis of their baseline proteinuria levels: group A normal (uPr/uCr <0.2) n=83; group B low (uPr/uCr 0.2–0.9) n=71; and group C mild (uPr/uCr >0.9) n=71. Patients in groups A and B showed a significantly slower decline in C _Cr than those in group C (slope +0.16±3.64 and –0.54±3.67 vs. –3.61±5.47, P<0.0001) and a higher rate of kidney survival after 5 years (96.7% and 94.1% vs. 44.9%, P<0.01). By multivariate analysis, the baseline uPr/uCr ratio (P<0.01) and age (P<0.0001) correlated with a faster decline in C _Cr irrespective of baseline C _Cr. There was no correlation with mean arterial blood pressure. We conclude that proteinuria is an independent predictor of progression to end-stage renal failure also in children whose renal impairment is due to congenital hypodysplasia.This paper was written on behalf of all the members of the ItalKid Project whose contribution has been essential. Members of the ItalKid Project:G. Aceto (Bari), G. Airoldi (Borgomanero), G. Amici (Ancona), A. Ammenti (Parma), B. Andretta (Padova), G. Ardissino (Milano), F. Ardito (Bologna), B. Assael (Verona), L. Avolio (Pavia), S. Bassi (Montichiari), F. Battaglino (Vicenza), R. Bellantuono (Bari), A. Bettinelli (Merate), C. Bigi (Lecco), S. Binda (Varese), C. Bini (Como), D. Bissi (Gallarate), R. Boero (Torino), R. Bonaudo (Torino), A. Bordugo (Pordenone), M. Borzani (Milano), M. Bosio (Milano), A. Bottelli (Varese), G. Bovio (Pavia), A. Bracone (Bra), G. Capasso (Napoli), M. Capizzi (Milano), D. Caringella (Bari), I. Carnera (Siracusa), M.R. Caruso (Bergamo), D. Cattarelli (Brescia), V. Cecchetti (Milano), M. Cecconi (Ancona), V. Cecinati (Bari), A. Ciofani (Pescara), A. Claris-Appiani (Milano), R. Coppo (Torino), F. Corona (Milano), A. Corsini (Bentivoglio), R. Costanzo (Ragusa), P. Cussino (Savigliano), M. DAgostino (Bergamo), V. Daccò (Milano), G. Daidone (Siracusa), R. DallAmico (Thiene), L. Dardanelli (Cuneo), R. De Castro (Bologna), V. De Cristofaro (Sondrio), M. De Gennaro (Roma), S. De Pascale (Bergamo), N. De Santo (Napoli), D. Delfino (R. Calabria), C.A. DellAgnola (Milano), L. Dello Strologo (Roma), L. Dertenois (Genova), A. Dessanti (Sassari), A. Di Benedetto (Catania), A. Di Leone (Cosenza), F. Di Lorenzo (Bologna), P. Di Turi (Bologna), A. Edefonti (Milano), W. Erckert (Silandro), A. Fabris (Verona), V. Fanos (Verona), C. Fede (Messina), A. Fella (Napoli), R. Ferraro (Scorrano), M.T. Ferrazzano (Anzio), R. Ferré (Breno), A. Ferretti (Napoli), B. Fogazzi (Brescia), P. Formentin (Cittadella), C. Fortini (Ferrara), E. Fossali (Milano), G. Fossati Bellani (Milano), M. Gaido (Torino), R. Galato (Milano), G. Gargano (Modena), V. Georgacopulo (Ferrara), L. Ghio (Milano), R. Giachino (Ivrea), M. Giani (Milano), S. Gianni (Siracusa), B. Gianoglio (Torino), M. Girodano (Bari), V. Goj (Milano), F. Grancini (Milano), G. Grott (Chieri), S. Guez (Milano), R. Gusmano (Genova), A. Iovino (Napoli), C. Isimbaldi (Lecco), A. La Manna (Napoli), G. Lama (Napoli), R. Landoni (Cinisello B.), S. Li Volti (Catania), A. Liardo (Caltagirone), V. Lotti (Cesena), R. Lubrano (Roma), I. Luongo (Napoli), E. Mancini (Bologna), N. Manganaro (Messina), M. Marangella (Torino), C. Marchesoni (Trento), K. Marenzi (Segrate), S. Maringhini (Palermo), G. Marra (Milano), E. Marras (Torino), V. Mei (Bologna), F. Menni (Milano), N. Miglietti (Brescia), R. Mignani (Rimini), P. Minelli (Bologna), R. Moioli (Milano), P. Molinari (Bologna), G. Montini (Padova), M. Montis (Cagliari), G. Mosiello (Roma), L. Murer (Padova), G. Nebbia (Milano), M. Neunhauserer (Brunico), P. Nitsch (Parma), M. Noto (Palermo), C. Oppezzo (Milano), F. Paolillo (Lodi), T. Papalia (Cosenza), R. Parini (Milano), L. Parola (Magenta), F. Passione (Foggia), L. Pavanello (CastelfrancoV.), C. Pecoraro (Napoli), M. Pedron (Bolzano), I. Pela (Firenze), A. Pellegatta (Busto Arsizio), P. Pelliccia (Chieti), M. Pennesi (Trieste), C. Pennetta (Manduria), R. Penza (Bari), L. Peratoner (Pordenone), F. Perfumo (Genova), G. Perino (Torino), C. Pesce (Vicenza), L. Pisanello (Padova), M. Pitter (Mirano), L. Pontesilli (Roma), M. Porcellini (Torino), A. Pota (Napoli), R. Prandini (Bologna), F. Puteo (Bari), I. Ratsch (Ancona), E. Ravaioli (Rimini), G. Remuzzi (Bergamo), G. Riccipetitoni (Cosenza), G. Ripanti (Pesaro), G. Rizzoni (Roma), N. Roberto (Milano), A. Rosini (Ancona), M. Rossi Doria (Bologna), S. Rota (Bergamo), M. Ruzza (Milano), D. Scorrano (Belluno), A. Selicorni (Milano), G. Selvaggio (Milano), F. Sereni (Milano), O. Sernia (Savigliano), C. Setzu (Cagliari), C. Sforzini (Milano), L. Stallone (S. Giovanni Rotondo), M. Tagliaferri (Treviglio), L. Tampieri (Lugo), A. Testagrossa (Messina), A. Turrisi (Trapani), G. Vallini (Cinisello Balsamo), E. Verrina (Genova), S. Viola (Pavia), G. Visconti (Palermo), A. Voghenzi (Ferrara), G. Zacchello (Padova)