Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HEMORRHAGE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1984

Delayed hemorrhagic infarction. A cause of late neonatal germinal matrix and intraventricular hemorrhage.

Although a single perinatal or postnatal event may be directly correlated to intraventricular hemorrhage (IVH) in some infants, in other infants IVH may be related to a series of insults. Asphyxia, hypotension, and a pressure-passive low cerebral blood flow (CBF) may lead to an infarction. Subsequent events known to cause sudden rises in the CBF may then produce a hemorrhage into damaged tissues. We report two cases of this proposed model for delayed hemorrhage into infarcted tissues, or late IVH. Both neonates were severely asphyxiated, and both experienced profound hypotension and a low CBF on the first postnatal day. Late IVH was found in both neonates; at 2 to 3 months of age, one neonate was found to have computed tomographic evidence for diffuse encephalomalacia, and the other neonate was noted to have an occipital porencephalic cyst.

Cerebral Hemorrhage↗
PubMed1995

Cocaine induced intracerebral hemorrhage: analysis of predisposing factors and mechanisms causing hemorrhagic strokes.

We analyzed 26 autopsy cases of cocaine induced intracerebral hemorrhage and compared those findings with those of 26 autopsy cases of cocaine induced cerebral aneurysm rupture. The incidence of hypertensive cardiovascular disease (HCVD) was significantly higher in persons with intracerebral hemorrhage than in those with aneurysm rupture. Our findings suggest that HCVD predisposes to cocaine induced intracerebral hemorrhage. We propose that the foregoing relationship results from a cocaine induced alteration of cerebral autoregulation in the context of increased cerebral blood flow.

Adult↗
PubMed2002

Middle cerebral artery dissecting aneurysm causing intracerebral hemorrhage 4 years after the non-hemorrhagic onset: a case report.

BACKGROUND: We report a case of dissecting middle cerebral artery (MCA) aneurysm causing intracerebral hemorrhage 4 years after the non-hemorrhagic onset. CASE DESCRIPTION: A 30-year-old male was diagnosed with an unruptured dissecting MCA aneurysm after a severe pulsating headache in August 1993. Angiography revealed dilatation of the distal portion of the temporo-occipital artery. During 2 years of follow-up, there were no significant changes on magnetic resonance imaging. In August 1997, he became comatose because of massive intracerebral hemorrhage caused by a dilated fusiform dissecting aneurysm. Emergency surgery and postoperative mild hypothermia resulted in full recovery. CONCLUSION: To date only 30 cases of dissecting MCA aneurysm have been reported and for unruptured aneurysms, surgical intervention was not chosen. However, the present case strongly suggests that long-term follow-up is necessary in patients with unruptured dissecting aneurysms of the anterior circulation, especially those with ectatic components.

Adult↗
PubMed2002

[Bilateral adrenal hemorrhage occurring two times in primary antiphospholipid syndrome (APS). Anticoagulation as treatment of hemorrhage].

HISTORY: A 56-year-old man was admitted for investigation of abdominal pain radiating to the back. The patient was known to suffer from APS and autoimmune thrombocytopenia, and was therefore treated with oral anticoagulants. The clinical examination was normal. INVESTIGATIONS: Ultrasound detected an area with low echogenicity in the region of the right adrenal gland. A CAT scan identified this mass as an adrenal hemorrhage. DIAGNOSIS AND TREATMENT: Anticoagulation treatment was discontinued because the bleeding and thrombocytopenia and the patient's pain subsided. A few days later, he experienced similar pain, this time radiating to the left side. A second hematoma was discovered in the left adrenal gland. The patient developed symptoms of acute adrenal insufficiency, which subsided after therapy. The bilateral adrenal hemorrhage was considered to be secondary bleeding following thromboses in the venous system of the adrenal gland. The thromboses were due to the underlying APS. Anticoagulation therapy was resumed, and the patient's condition stabilised without further complications. CONCLUSION: The cessation of anticoagulation therapy in this patient paradoxically led to hemorrhage, this time of the contralateral adrenal gland. Unilateral and, especially, bilateral adrenal bleeding should give rise to the suspicion of thrombophilic disorders such as APS or heparin-induced thrombocytopenia (HIT); for which careful anticoagulation is the treatment of choice.

Abdominal Pain↗
PubMed1987

Colonic hemorrhage produced in mice by a unique vero cell cytotoxin from an Escherichia coli strain that causes hemorrhagic colitis.

A Vero cell cytotoxin that produces colonic lesions and subsequent colonic hemorrhage in mice has been purified from a strain of Escherichia coli O157:H7 that causes hemorrhagic colitis in humans. This toxin is different in physicochemical properties from the Shiga-like toxin previously associated with this organism and may be responsible for the unique diffuse mucosal hemorrhage in the colon of individuals with E. coli O157:H7 infections.

Animals↗
PubMed1997

Improvement of survival from hemorrhagic shock by enterectomy in rats: finding to implicate the role of the gut for irreversibility of hemorrhagic shock.

OBJECTIVE: This study used a Wiggers shock model to investigate the effect of the removal of the intestines on the outcome of hemorrhagic shock. METHODS: Rats were subjected to laparotomy for the removal of the entire small and large intestines (experimental group) or a sham operation (control group) before bloodshedding. During the period of shock, animals were maintained at 30-35 mm Hg arterial pressure for 2 hours. After reinfusion of the shed blood, rats were observed for over 3 hours for survival. The average volumes (mean +/- SEM) of shed blood were 6.84 +/- 0.23 mL (experimental group) and 6.49 +/- 0.39 mL (control group), with no significant difference between the two (p > 0.05). RESULTS: This protocol resulted in a 42% mortality (11 of 26) in the control group and 0% mortality (0 of 25) in the experimental group (p < 0.005, chi2). Moreover, in the survivors, the mean arterial pressure was significantly lower in the control (65.7 +/- 4.3 mm Hg) than in the experimental group (78.2 +/- 3.5 mm Hg) at the end of the experiment (p < 0.05). Comparing volume status, neither serial hematocrit values nor body weight changes through the experiment had a significant difference between the two groups (p's > 0.05). Serial quantitation of blood levels of tumor necrosis factor-alpha (TNF-alpha) revealed that systemic TNF-alpha concentrations peaked at 4 hours after shock in both groups. TNF-alpha levels were not reduced by enterectomy. Instead, the peak concentrations were significantly higher in the enterectomized (387.5 +/- 36.5 pg/mL, n = 13) than in the sham-enterectomized group (175.7 +/- 35.9 pg/mL, n = 12,p < 0.001). Limulus assay, used to detect endotoxins in the blood at 2 hours after restoration of blood volume, showed no endotoxemia in any specimen from either group. Four hours after hemorrhagic shock, blood levels of platelet-activating factor, quantitated by the radioimmunoassay method, were 2.88 +/- 0.18 ng/mL (experimental group, n = 8) and 2.32 +/- 0.32 ng/mL (control group, n = 6). The difference between these two means was not significant (p > 0.05). Measurement of hepatic adenosine triphosphate (ATP) by the luminometric method showed that hepatic ATP contents were significantly reduced in both groups after shock (p's < 0.05). However, a higher magnitude of hepatic ATP depletion occurred in the control group; significantly lower amounts of ATP in the liver tissues of the sham-enterectomized group (367 +/- 95 nmol/g, n = 7) than in that of the enterectomized group (870 +/- 100 nmol/g, n = 13) were observed at 5 hours after shock (p < 0.05). CONCLUSIONS: These experimental findings show that, in the absence of the intestines, hemorrhagic shock is associated with both an improved outcome and higher hepatic ATP levels in rats, suggesting the importance of intestinal participation in the process leading to hepatic ATP depletion as well as irreversibility in shock.

Adenosine Triphosphate↗
PubMed2006

Intracerebral hemorrhage due to hemorrhagic disease of the newborn and failure to administer vitamin K at birth.

In infants, intracerebral hemorrhage (ICH) is most likely the result of trauma or disturbances of coagulation function. Routine and standard care of the newborn includes the administration of vitamin K to prevent hemorrhagic disease of the newborn. We present two infants, the products of home deliveries, who did not receive vitamin K at birth. Both infants developed ICH at 5 weeks of age and presented with signs and symptoms of increased IC pressure. In both cases, recombinant factor VIIa was administered to correct coagulation function and allow immediate surgical intervention which included craniotomy and hematoma evacuation in one patient and placement of a ventriculostomy in the other to treat increased IC pressure. Despite this therapy, both infants were left with severe neurologic sequelae. These two cases illustrate that hemorrhagic disease of the newborn can occur when prophylactic vitamin K is not administered and that it can have devastating consequences. Given these issues, the routine administration of vitamin K to all infants is mandatory and should not be considered optional.

Antifibrinolytic Agents↗
PubMed2005

Comparison of hemorrhage control agents applied to lethal extremity arterial hemorrhages in swine.

BACKGROUND: QuikClot powder (QC), chitosan dressing (CD), and fibrin sealant dressing (FSD) are new hemostatic products touted to be more effective in controlling severe extremity bleeding than the current standard gauze dressing. All have been utilized in the global war on terrorism. Our objective was to evaluate the hemostatic efficacy of these three products in a model of severe extremity arterial hemorrhage that could not be stopped by standard gauze treatment. METHODS: A model of severe extremity arterial hemorrhage was developed in swine that was 100% fatal with standard gauze application and manual compression. The Army Field Bandage (AFB) was the standard gauze control. Anesthetized animals (n = 60, 15/group, 37.7 +/- 2.5 kg) were splenectomized and instrumented. A reproducible femoral artery injury was created using a 6 mm aortic punch, and free bleeding was allowed for 45 seconds. Each hemostatic agent was applied twice with three-minute compressions. All products were applied on actively bleeding wounds through a pool of blood. Fluid resuscitation was started with the first compression and titrated to a mean pressure of 65 mm Hg. Animals were observed for 180 minutes or until death. Endpoints were percent survival, survival time, blood loss, resuscitation volume, wound temperatures and tissue histology. Data are expressed as mean +/- SD and analyzed by Fisher's exact, logrank, and nonparametric ANOVA tests. RESULTS: Baseline physiologic parameters were similar among groups. AFB did not produce hemostasis. QC also showed no hemostatic benefit, and QC treatment markedly increased maximum wound temperatures to an average of 70.8 +/- 4.2 degrees C (p < 0.001). CD stopped bleeding temporarily in only one animal. There were no survivors in the AFB, QC, or CD groups. CD numerically prolonged survival time (58.9 +/- 21.1 minute) compared with the control (38.4 +/- 24.7 minutes, p = 0.045) but the difference was not significant. FSD reduced bleeding (p < 0.05) and prevented exsanguination in 10/15 (2/3) animals, and resulted in a significantly longer average survival time (p < 0.0001). CONCLUSION: FSD was superior to other currently utilized hemostatic products in controlling lethal arterial hemorrhage in this model of a fatal extremity wound. CD showed some hemostatic benefit. The exothermic reaction of QC was significant and resulted in gross and histologic tissue changes of unknown clinical significance. Controlled human studies with the promising products are required.

Animals↗
PubMed1999

The informed consent process and the use of the exception to informed consent in the clinical trial of diaspirin cross-linked hemoglobin (DCLHb) in severe traumatic hemorrhagic shock. DCLHb Traumatic Hemorrhagic Shock study group.

UNLABELLED: In the clinical trial of diaspirin cross-linked hemoglobin (DCLHb), optimal therapy required the immediate enrollment of patients with severe, uncompensated, traumatic hemorrhagic shock. When it was not feasible to obtain prospective consent, an exception to informed consent was used according to FDA regulation 21 CFR 50.24. OBJECTIVES: To examine the informed consent process and the use of the consent exception and consent to continue (CTC), and to describe the patients for whom this process was used. METHODS: This was a multicenter, randomized, controlled, single-blinded efficacy trial of DCLHb as an adjunct to standard therapy in the treatment of severe, traumatic hemorrhagic shock. Patients with unstable vital signs or a critical base deficit were treated, with a primary study endpoint of 28-day mortality. RESULTS: During the 11-month study period, 112 patients were randomized in 18 U.S. trauma centers, and data from 98 of the infused patients were analyzed. Prospective consent was obtained from two patients, three family members, and one legally authorized representative (LAR) (6%). Consent to continue was requested for 89 patients (89%), and full participation was granted for 87 of these patients (98%). Consent to continue was provided by 54 (98%) of the 55 patients approached. The mean number of days for family/LAR CTC was 1.1 +/-3.8 days, and 50% of the time it was obtained on the day of study enrollment. Patient CTC was obtained in an average of 13 +/- 23 days, with a median of four days. Patients treated in this protocol were more likely to have sustained penetrating trauma than the overall trauma patient population treated in these trauma centers (44% vs 21%, p = 0.002). CONCLUSIONS: Informed consent in this study of an emergent therapy most often involved the use of the consent exception and consent to continue, the latter of which occurred in a timely manner. Nearly all of those who were approached for CTC approved full participation in the study, suggesting acceptance of the process outlined in the new regulations. Patients treated in a hemorrhagic shock clinical trial may differ from the general trauma patient population.

Adult↗
PubMed2005

Hemorrhagic shock-activated neutrophils augment TLR4 signaling-induced TLR2 upregulation in alveolar macrophages: role in hemorrhage-primed lung inflammation.

Hemorrhagic shock renders patients susceptible to the development of acute lung injury in response to a second inflammatory stimulus by as yet unclear mechanisms. We investigated the role of neutrophils (PMN) in alveolar macrophage (AMphi) priming, specifically, the role in mediating Toll-like receptor (TLR)4 and TLR2 cross talk in AMphi. Using a mouse model of hemorrhagic shock followed by intratracheal administration of LPS, we explored a novel function of shock-activated PMN in the mechanism of TLR2 upregulation induced by LPS-TLR4 signaling in AMphi. We showed that antecedent hemorrhagic shock enhanced LPS-induced TLR2 upregulation in AMphi. In neutropenic mice subjected to shock, the LPS-induced TLR2 expression was significantly reduced, and the response was restored upon repletion with PMN obtained from shock-resuscitated mice but not by PMN from sham-operated mice. These findings were recapitulated in mouse AMphi cocultured with PMN. The enhanced TLR2 upregulation in AMphi augmented the expression of macrophage inflammatory protein-2, TNF-alpha, and macrophage migration inhibitory factor in the AMphi in response to sequential challenges of LPS and peptidoglycan, a prototypical TLR2 ligand, which physiologically associated with amplified AMphi-induced PMN migration into air pouch and lung alveoli. Thus TLR2 expression in AMphi, signaled by TLR4 and regulated by shock-activated PMN, is an important positive-feedback mechanism responsible for shock-primed PMN infiltration into the lung after primary PMN sequestration.

Animals↗
PubMed2007

Hemodynamic responses and c-Fos changes associated with hypotensive hemorrhage: standardizing a protocol for severe hemorrhage in conscious rats.

The central mechanisms underlying the transition from compensation to decompensation during severe hemorrhage (HEM) are poorly understood. Furthermore, a lack of consistency in HEM protocols exists in the current literature. This study assessed the cardiovascular response and Fos-like immunoreactivity (FLI) in specific brain regions following severe HEM at three rates (2, 1, or 0.5 ml.kg(-1).min(-1)) in conscious rats. Heart rate (HR) and arterial pressure were recorded during the withdrawal of 30% of total blood volume (TBV). Data from animals hemorrhaged at the fast (F-HEM, n = 6), intermediate (I-HEM, n = 7), or slow (S-HEM, n = 7) rates were compared with saline (SAL, n = 5) and hypotensive (hydrazaline-induced, HYDRAZ, n = 5) controls. All HEM rates produced similar degrees of hypotension at the time of 30% TBV withdrawal. All HEM rates also produced bradycardia, but the change in HR was only significant in the F-HEM and I-HEM groups. Associated with I-HEM and F-HEM, but not HYDRAZ treatment were significant increases in FLI in the caudal ventrolateral periaqueductal gray (PAG), the central lateral nucleus of the rostral parabrachial nucleus, and locus coeruleus compared with SAL treatment. I-HEM also induced significant increases in FLI in the dorsomedial PAG, A7 region, and the cuneiform nucleus compared with SAL. S-HEM did not induce any significant change in FLI. Our results suggest that HEM at a rate of 1 ml.kg(-1).min(-1) may be most useful for investigating the potential role of the rostral brainstem regions in mediating hemorrhagic decompensation in conscious rats.

Animals↗
PubMed1996

De novo familial cavernous malformation presenting with hemorrhage 12.5 years after the initial hemorrhagic Ictus: natural history of an infantile form.

Cerebral cavernous malformations are congenital, non-neoplastic lesions, but they are known for their potential for growth. De novo lesion genesis is exceptional and occurs more commonly with the familial form of the disease. We report the case of a 13-year-old Caucasian boy with a positive family history, who underwent surgery for a left parietal hemorrhage during the 1st year of life and who recently presented with a new hemorrhage in the left temporal lobe quite distant from the previous hematoma bed. Both hemorrhages were caused by cavernous malformations. Sequential magnetic resonance scans prior to the recent presentation failed to disclose the growth of the new lesion. We reviewed the literature for mechanisms of new lesion formation.

Adolescent↗
PubMed1996

Will increased awareness among physicians of the significance of sudden agonizing headache affect the outcome of subarachnoid hemorrhage? Coventry and Warwickshire Study: audit of subarachnoid hemorrhage (establishing historical controls), hypothesis, campaign layout, and cost estimation.

BACKGROUND AND PURPOSE: The most common symptom associated with aneurysmal minor bleed ("warning leak") is a sudden agonizing headache. Early screening of these patients may improve the outcome of subarachnoid hemorrhage and may be highly cost-effective. METHODS: We conducted an extensive retrospective audit of subarachnoid hemorrhage over the last 10 years in the region of Coventry and Warwickshire, England, and initiated a continuous campaign among all physicians in the region for early neurosurgical referral of patients with sudden agonizing headache. RESULTS: Over the last 10 years the incidence of subarachnoid hemorrhage in the region was 8.7/100 000 per year. Surgical activity was 34% and early mortality 45.2%. Functional outcome, both overall and by grade on admission, was within internationally accepted levels. Warning leak symptoms before admission were experienced by 20% of patients. These patients sought medical advice but were not referred immediately to the neurosurgical unit. CONCLUSIONS: We have established our population as valid historical controls and outlined our campaign strategy. Lowering the clinical threshold at which patients with sudden agonizing headache are screened for aneurysms or arteriovenous malformations will undoubtedly increase diagnostic costs. However, for reasons given in the text, we estimated the cost per quality-adjusted life year gain to be 1000 pounds ($1500).

England↗
PubMed2004

White matter lesions, cognition, and recurrent hemorrhage in lobar intracerebral hemorrhage.

BACKGROUND: Accumulating evidence suggests that white matter lesions are associated with vascular cognitive impairment. The authors investigated the relationships between white matter lesions, cognitive impairment, and risk of recurrent hemorrhage in a prospectively identified cohort of patients with lobar intracerebral hemorrhage (ICH). METHODS: The authors collected clinical and genetic information on 182 consecutive patients age > or = 55 who had CT scan at admission for lobar ICH. White matter disease was graded on CT in all subjects and on MRI in a subset of 82 patients. All scans were interpreted blinded to clinical information. Survivors were followed for recurrent ICH by telephone interview. RESULTS: White matter damage was common (present on CT in 77%) and severe (advanced CT grade in 32%). White matter damage was correlated with the total number of hemorrhages on gradient-echo MRI and with risk of recurrent ICH. Subjects with cognitive impairment prior to their index ICH were more likely to have severe white matter damage on CT (OR 3.6, 95% CI 1.6 to 8.1, p = 0.003) and more likely to have advanced periventricular hyperintensities on MRI. The relationships between white matter damage and cognitive impairment were similar in the subset of 88 subjects meeting criteria for probable or definite cerebral amyloid angiopathy and remained independent after adjustment for age, cortical atrophy, and APOE genotype. CONCLUSIONS: White matter damage in lobar ICH is common and is associated with cognitive impairment. These data support the possibility that an underlying vasculopathy in lobar ICH patients, possibly cerebral amyloid angiopathy, can cause clinically important vascular dysfunction.

Cerebral Amyloid Angiopathy↗
PubMed1996

Petechial hemorrhages accompanying lobar hemorrhage: detection by gradient-echo MRI.

Based on the pathologic observation that severe cerebral amyloid angiopathy is often accompanied by multiple petechial hemorrhages, we prospectively obtained gradient-echo MRI on 15 elderly patients with lobar hemorrhage on CT. Nine of the 15 demonstrated accompanying petechial hemorrhages restricted to the cortical or corticosubcortical regions. No similar lesions were present on gradient-echo MRI in 10 elderly control patients. These findings suggest that cerebral amyloid angiopathy might be neuroradiologically diagnosed and staged during life.

Aged↗
PubMed1995

Simultaneous occurrence of aneurysmal subarachnoid hemorrhage and remote intracerebral hemorrhage--case report.

A 77-year-old female presented with a rare aneurysmal subarachnoid hemorrhage accompanied by a remote hypertensive intracerebral hemorrhage. With a past history of hypertension, she suddenly developed right hemiparesis followed by delayed loss of consciousness. Left carotid angiography demonstrated a left internal carotid-posterior communicating artery aneurysm. The intracerebral hematoma was located in the posterior limb of the internal capsule ipsilateral to the ruptured aneurysm. The aneurysm was clipped with a fenestrated clip 3 weeks after the onset. The rise in blood pressure at the onset of intracerebral hemorrhage probably caused the rupture of the internal carotid-posterior communicating artery aneurysm.

Aged↗
PubMed1999

Results of early surgical evacuation of packed intraventricular hemorrhage from aneurysm rupture in patients with poor-grade subarachnoid hemorrhage.

OBJECT: The goal of this study was to evaluate the results of early surgical evacuation of "packed" intraventricular hemorrhage (IVH) in patients with poor-grade subarachnoid hemorrhage (SAH). METHODS: The authors performed surgery within 24 hours after onset of SAH, identified on neuroimaging as a cast distending the ventricular system, in 74 patients with poor-grade SAH (World Federation of Neurosurgical Societies Grades IV and V) without intracerebral hemorrhage. Eighteen of these patients had packed IVH; in these patients the intraventricular clots were extensively evacuated via frontal corticotomy performed under microscopic view. CONCLUSIONS: Overall, 42% of the 74 patients undergoing craniotomy in the acute stage had favorable outcomes, whereas 30% died. Using multivariate analysis, variables significantly associated with favorable outcome in patients with poor-grade SAH included absence of a packed intraventricular clot on computerized tomography scanning; absence of a history of cardiac disease; and a Glasgow Coma Scale score of 11 or 12. None of the 18 patients who had packed IVH had favorable outcomes and seven of these died. In six recently treated patients with packed IVH, which was examined using fluid-attenuated inversion recovery imaging, extensive periventricular brain damage was found both immediately after surgery and during the chronic stage. Accordingly, the authors believe that irreversible periventricular brain damage is already complete immediately after packed IVH occurs.

Adult↗
PubMed1999

[Helicobacter pylori and digestive hemorrhage due to duodenal ulcer: the prevalence of the infection, the efficacy of 3 triple therapies and the role of eradication in preventing a hemorrhagic recurrence].

BACKGROUND: To report the prevalence of Helicobacter pylori in patients with bleeding duodenal ulcer and to verify the effect of eradication on hemorrhage recurrence. To evaluate the efficacy on H. pylori eradication and on ulcer healing of three one-week triple therapies and to compare their efficacy with that of a dual therapy. PATIENTS AND METHODS: One-hundred and eleven patients with bleeding duodenal ulcer not taking gastroerosive drugs were prospectively studied. At endoscopy, biopsies from gastric antrum and body were obtained (haematoxylin-eosin), and a 13C-urea breath test was also performed. Both diagnostic methods were repeated one month after completing one of the following treatments (randomized study): omeprazole (20 mg/12 h), amoxycillin (1 g/12 h) and clarithromycin (500 mg/12 h) (OAC, n = 27); omeprazole (20 mg/12 h), clarithromycin (500 mg/12 h) and metronidazole (500 mg/12 h) (OCM, n = 27); lansoprazole (30 mg/12 h), amoxycillin (1 g/12 h) and clarithromycin (500 mg/12 h) (LAC, n = 27); and lansoprazole (30 mg/12 h) and clarithromycin (500 mg/8 h) (LC, n = 27). The first three therapies were administered for one week, and LC for two weeks. Once eradication was confirmed no antisecretory therapy was administered. A breath test was performed in the follow-up at 6 months and at one year. RESULTS: The prevalence of H. pylori infection was 97.3% (95% CI: 92-99%). Five patients were lost from the study during follow-up. The eradication efficacy (intention-to-treat) was: OAC, 89% (72-96%); OCM: 93% (77-98%); LAC, 93% (77-98%), and LC, 70% (51-84%). Overall triple therapy efficacy was higher than that of dual therapy (91% vs 70%; p < 0.05). Thirteen patients needed a 2nd or 3rd therapy, and eradication success was finally achieved in all cases. The type of therapy was the only variable which influenced on H. pylori eradication (OR: 4.5; 95% CI: 1.4-14%; p < 0.01) and H. pylori eradication was the only variable which influenced on ulcer healing (OR: 4.7; 95% CI: 1.2-19%; p < 0.05). The yearly reinfection rate was 2.8% (0.9-7.8%). No hemorrhage recurrences occurred during the one year follow-up period. CONCLUSIONS: H. pylori prevalence in bleeding doudenal ulcer is almost 100%. These patients will be spared of hemorrhage recurrence at least for one year if infection is eradicated. Therefore, eradication therapy is the therapy of choice, and maintenance therapy with antisecretory drugs is no longer needed. One-week triple therapies with a proton pump inhibitor and two antibiotics (clarithromycin plus amoxycillin or metronidazole) have a high efficacy in patients with bleeding duodenal ulcer.

Anti-Bacterial Agents↗