High eradication rates of Helicobacter pylori with a new sequential treatment.

BACKGROUND: Eradication rates of Helicobacter pylori with standard triple therapy are disappointing, and studies from several countries confirm this poor performance. AIM: To assess the eradication rate of a new sequential treatment regimen compared with conventional triple therapy for the eradication of H. pylori infection. METHODS: One thousand and forty-nine dyspeptic patients were studied prospectively. H. pylori-infected patients were randomized to receive 10-day sequential therapy [rabeprazole (40 mg daily) plus amoxicillin (1 g twice daily) for the first 5 days, followed by rabeprazole (20 mg), clarithromycin (500 mg) and tinidazole (500 mg) twice daily for the remaining 5 days] or standard 7-day therapy [corrected] [rabeprazole (20 mg), clarithromycin (500 mg) and amoxicillin (1 g) twice daily]. H. pylori status was assessed by histology, rapid urease test and 13C-urea breath test at baseline and 6 weeks or more after completion of treatment. RESULTS: Higher eradication rates were found with the sequential regimen compared to the standard regimen (intention-to-treat: 92% vs. 74%, P < 0.0001; per protocol: 95% vs. 77%, P < 0.0001). Higher eradication rates were also seen in patients with peptic ulcer disease and non-ulcer dyspepsia. In both treatments, compliance was similar (> 90%), as was the rate of side-effects, which were mild. CONCLUSIONS: This 10-day sequential treatment regimen achieves high eradication rates in peptic ulcer disease and non-ulcer dyspepsia.

[Histiocytic necrotizing lymphadenitis or Kikuchi and Fujimoto's disease. A case report]. / Linfoadenite necrotizzante istiocitaria o malattia di Kikuchi e Fujimoto. Descrizione di un caso.

We describe a case of necrotizing histiocytic lymphadenitis or Kikuchi and Fujimoto disease, a rare lymphadenopathy of unknown etiology usually striking young women. It was formerly described in Japan, and subsequently in other countries and in Italy as an anatomo-clinical entity. The disease has a favourable prognosis, therefore it has to be considered differently from other lymphadenopathies with severe prognosis whose anatomo-pathological differential features were analyzed by the authors. The case here observed differs from other cases described in literature because of the presence of a perilymphadenitic component.

Accuracy of strain-gauge plethysmography as a diagnostic test in clinically suspected deep venous thrombosis.

Strain-gauge plethysmography (SGP) is currently employed in the diagnosis of deep venous thrombosis (DVT), but its accuracy has not been adequately tested. In this study we evaluated SGP against venography in 209 consecutive patients referred to us because of clinically suspected DVT of lower limbs. Venography was performed bilaterally if symptoms or signs suggesting DVT were present in both limbs. It was always performed after SGP and independently assessed. A total of 269 limbs could be evaluated with both SGP and venography, which disclosed DVT in 128 limbs of 110 patients. There were 109 proximal and 19 distal DVT. Out of the 128 limbs with DVT, SGP was positive in 114 (sensitivity = 89%) using Maximal Venous Outflow (MVO) as the diagnostic parameter, and positive in 116 (sensitivity = 91%) using an index obtained multiplying MVO for Venous Capacitance (VC). Out of the 141 venographically negative limbs, there were 6 false positive results using MVO and 9 using MVO X VC (specificity = 96% and 94% respectively). SGP sensitivity in acute proximal venous thrombosis was 97%, while it was about 60% in distal DVT. Most false positive results occurred in patients with edema of cardiac origin. SGP appears to be a useful diagnostic test in suspected DVT of lower limbs, particularly when both MVO and the index MVO X VC are used.

Correlation between changes induced by venous occlusion on factor VIII-von Willebrand factor components and fibrinolytic activity.

The effects of standardized venous occlusion (VO) on factor VIII-von Willebrand factor (F VIII-VWF) components (F VIII:C, F VIIIR:AG, F VIIIR:RCof) and on fibrinolytic activity were investigated in 45 healthy subjects, in 28 women on oral contraceptives, and in 78 patients with various chronic diseases (28 with peripheral arterial disease, 19 with liver cirrhosis, 13 with rheumatoid arthritis, and 18 with diabetes). All the three F VIII-VWF components showed highly significant increases, although not of the same magnitude, with consequent variations in the ratios between them. A significant activation of fibrinolysis was also demonstrated with both euglobulin lysis time (ELT) and diluted blood clot lysis time (DBCLT). A strong linear correlation between pre- and post-stasis values was recorded for all the F VIII-VWF components and for the two fibrinolysis tests. No significant relationship was, on the contrary, found between F VIII-VWF and fibrinolytic parameters.

Normal prostacyclinlike activity and response to plasma exchange in thrombotic thrombocytopenic purpura: report of 2 cases.

2 cases of acute idiopathic thrombotic thrombocytopenic purpura are reported. Both of them were treated with plasma exchange, antiplatelet drugs and prednisolone and both completely recovered. Plasma exchange appeared to be the critical treatment. In 1 of these cases the prostacyclinlike activity released from venous tissues and the ability of plasma to stimulate synthesis of prostacyclinlike activity from venous tissues exhausted after repeated washings were investigated. Both activities were detectable and comparable to those of a healthy control. These findings do not support the hypothesis of a major role played by the prostacyclin system in the pathogenesis of thrombotic thrombocytopenic purpura.

Predictive value of preoperative in vitro and in vivo studies for correct individual heparinization in cardiac surgery.

Heparin administration for operations with extracorporeal circulation (ECC) usually is performed following prefixed, standardized protocols. These regimens secure an adequate level of anticoagulation, but they often involve prolonged periods of overheparinization associated with an undue risk of hemorrhage. The predictive value of preoperative studies in the anticoagulant effect of heparin was investigated in 10 patients. The study was performed both in vitro and in vivo using the Xa inhibitor assay as an index of the anticoagulation induced by heparin. Adding variable amounts of heparin in vitro to patient's plasma resulted in straight (at least up to 7 U. per milliliter) and parallel, but not coincident, dose/response curves, so confirming a different individual sensitivity to heparin. Disappearance curves of the anticoagulant effect in plasma following intravenous administration of a single standard dose of heparin in the same patients showed an even greater patient-to-patient variability, with "half-life" times ranging from 30 to 150 minutes. No relationship was found between the parameters (in vitro sensitivity to heparin and clearance rate from plasma in vivo). Moreover, neither of them could be correlated with the response to heparin, subsequently observed during ECC in the same patients. Preoperative investigations with the methods presently available are not adequate to choose individual heparin administration regimens for cardiac operations.

In vitro and in vivo effects of adrenaline and phentolamine on platelet function.

In vitro and in vivo effects of adrenaline (ADR) on platelet aggregation, on platelet factor 3 (PF3) availability and on platelet factor 4 (PF4) release were studied in man. Inhibitory action of an alpha-blocker, phentolamine (PHEN) was investigated in the same conditions. The threshold concentration (TC) of ADR inducing the typical two-phase response in aggregation tests when added to platelet-rich plasma (PRP) varied in different pools of plasma, but always induced an evident PF4 release and increased PF3 availability. A further increase in both parameters was obtained with higher concentrations but without any significant dose/response correlation. Adding PHEN alone to PRP did not induce platelet aggregation or modify PF4 release induced by stirring, but it reduced PF3 availability. On the other hand, PHEN prevented the effects of ADR in different platelet tests, at appropriate concentrations. Intravenous infusion of ADR lowered the TC, and increased PF3 availability and PF4 release. In vivo administration of PHEN, in contrast, increased TC and reduced PF3 availability, while PF4 remained unchanged.

Inherited platelet abnormalities associated with low factor VIII activity in the same family.

Six of eight examined members belonging to two generations of the same (NEG-TUR) family were shown to have functional changes in platelets and/or a moderate decrease of factor VIII activity (FVIII:C) in plasma, with normal values of factor VIII-related antigen (VIII R:AG). Platelet defects (mainly a reduced PF3 availability, present in five patients) and factor VIII decrease were combined differently in individual members. Only two male members with both the PF 3 and FVIII:C defects had moderate haemorrhagic symptoms following traumatic injuries. One of them had also an absent adhesiveness to glass, the other one an absent adhesiveness to collagen and a reduced platelet aggregation by ADP and by collagen. Bleeding time, platelet function tests (in the other members), and routine coagulation tests were within normal range; ristocetin aggregation was also normal in all members. We think that two inherited defects, a mild haemophilia A and a "sui generis" thrombocytopathy, co-exist in this family.

Impaired fibrin formation in advanced cirrhosis.

The process of fibrin formation was systematically in 25 patients with severe alcoholic cirrhosis. Results of functional tests are reported. A significant lengthening of the thrombin time was found which could not be completely attributed either to hypofibrinogenaemia or to an increase in physiological anticoagulants or to the presence of pathological antithrombins. A defect in fibrin polymerization was seen in the absence of significant levels of antipolymerizing agents. Indirect evidence pointed to an abnormal fibrinogen function. This was mainly suggested by the "polymerization curves" of mixtures of normal and pathological plasmas and the changes in physico-chemical properties of the clot (optical and elastic properties; tensile strength). Altered synthesis in hepatocytes may lead to an "acquired dysfibrinogenaemia" in the late stages of liver cirrhosis, although alteration of a normal fibrinogen molecule after secretion cannot be definitely excluded.

In vitro effects of bencyclan on coagulation, fibrinolysis and platelet function.

The in vitro effects of N-3-(1-benzyl-cycloheptyloxy)-propyl-N,N-dimethylammonium-hydrogenfumarate (bencyclan) on clotting, fibrinolytic and platelet function test were investigated by adding the drug to normal human plasma. An anticoagulant activity, mainly of an antithromboplastin nature (directed against later stages of intrinsic thromboplastin formation and against tissue thromboplastin), was observed, while thrombin phase was unaffected. No effect was found in the fibrinolytic system tested (euglobulin lysis, UK-activated fibrinolysis, "hanging clot" method). The drug, although capable of aggregating platelets by itself at very high concentrations, showed a striking inhibitory effect, over a wide range of concentrations, both on platelet aggregation induced by ADP, epinephrine or collagen and on platelet adhesiveness to glass or collagen. Clot retraction was also clearly inhibited. PF3 availability was influenced with a peculiar two-phase behaviour dose-dependently. High concentrations showed a promoting action, while the lower were obviously inhibitory. It is suggested that the effects on platelet function may be due to an influence of the drug on cell membrane.