2004-2015年湖北省阳新县预防控制血吸虫病效果分析

目的 评价2004-2015年阳新县预防控制血吸虫病的效果,为血吸虫病传播阻断和消除提供科学依据。方法 依据阳新县血吸虫病疫情层次和流行规律,采取综合治理的防治策略,持续实施卫生、水利、林业、农业等血防综合治理项目。分析比较2004-2015年该县血吸虫病疫情控制的效果。结果 阳新县实施血防综合治理整县推进后,全县推算病人数由2004年的22 240降至为2015年的1 471;人群感染率由2004年的8.57%降至2015年的0.16%;急性血吸虫感染（急感）病人由2004年的64例降至0,2009年以后未发生急感病例;耕牛感染率由2004年的8.87%降至0;钉螺面积和易感地带面积分别由2004年的3 446.21、1 111.59 hm2降至2015年的2 285.75、41.28 hm2;钉螺感染率由2004年的0.76%降至0。结论 自2004年实施血防综合治理整县推进的防治策略后,阳新县血吸虫病疫情显著下降,但要进一步巩固血防成果,仍需加大富河流域的治理力度,并强化家畜传染源的防控。     

Chronic pancreatitis in Japan: epidemiology,prognosis, diagnostic criteria,and future problems

Chronic pancreatitis is a chronic clinical disorder characterized by irreversible damage to the pancreas and the development of histologic evidence of inflammation and fibrosis, and eventually the destruction and permanent loss of exocrine and endocrine tissue. A nationwide survey in Japan revealed an increase in the total number of patients treated for chronic pancreatitis from 32 000 in 1994 to 42 000 in 1999. The overall prevalence and the incidence rate of chronic pancreatitis also increased, from 28.5 and 5.4, respectively, in 1994 to 32.91 and 5.77 per 100 000 population, respectively, in 1999. Diagnostic criteria for chronic pancreatitis in Japan were proposed by the Japan Pancreas Society in 1995 and revised in 2001. The criteria were established to rule out false-positive cases and to confidently diagnose definite and probable cases of chronic pancreatitis, and thus easily detect advanced chronic pancreatitis, but the criteria are unable to lead to the early diagnosis of chronic pancreatitis. Cancer is the major cause of death in patients with chronic pancreatitis in Japan (49.6% of all deaths in patients with chronic pancreatitis). Clarification of the mechanisms by which possible chronic pancreatitis progresses to probable or definite chronic pancreatitis, and to pancreatic cancer, is an important research goal. Because even chronic pancreatitis defined as irreversible appears to be reversible for some time in its clinical course, there is an urgent need to develop methods for diagnosing reversible chronic pancreatitis, and to prevent the transition from chronic pancreatitis to pancreatic cancer. Received: December 9, 2002 / Accepted December 20, 2002 Reprint requests to: M. Otsuki     

Hereditary disorders of platelet function

The most common hereditary disorders of platelet function are those in which there is decreased platelet aggregation in response to more than one of the commonly used aggregating agents, collagen, ADP, adrenaline and arachidonic acid. When measured, there is usually also a reduction in the extent of the platelet release reaction and often also thromboxane production. In a proportion of these cases it is possible to demonstrate that there is a decrease in or absence of the contents of the dense storage granules which accounts for the decrease in platelet responsiveness. In most other cases the primary cause of the decreased responsiveness has not been determined, although in some cases deficiency of cyclooxygenase or thromboxane synthetase has been demonstrated. Investigation of patients with these disorders is often difficult because the tests involved are difficult to subject to adequate quality control, their sensitivity and specificity has not been adequately defined, and lack of reproducibility renders it difficult in less severe cases to be certain of abnormality even after repeat tests. Much less common but of great interest are the disorders in which the primary abnormality is in one of the glycoproteins on the platelet surface. In Glanzmann's thrombasthenia glycoprotein IIb.IIIa is absent or greatly decreased leading to failure of activated platelets to bind fibrinogen to their surface. In contrast to the decrease in aggregation seen in the above disorders, the platelets do not aggregate at all in response to the usual aggregating agents. In Bernard-Soulier syndrome there are severe deficiencies of three glycoproteins, particularly lb, leading to inability to bind von Willebrand's factor and consequent inability of the platelets to aggregate in response to ristocetin. Study of the disorders of platelet function will continue to contribute to our ability to detect and treat these disorders and to our knowledge of platelet physiology and biochemistry.     

Do biochemical markers have a role in osteoarthritis diagnosis and treatment?

It is possible to use biomarkers in cohort studies and in clinical trials to increase our understanding of disease, to elucidate disease mechanisms, and to bolster a clinical impression of the disease state of osteoarthritis. Whether it will be possible to utilize biomarkers meaningfully to characterize the disease state in an individual patient remains to be seen. Major concepts related to the use of biomarkers for research and clinical practice, and factors influencing biomarker concentrations, are described in this review in order to address the potential role of biomarkers in osteoarthritis diagnosis, prognosis, and treatment.     

Fiscal policy and tobacco control: a unique opportunity to benefit public health and the public treasury

Various studies and analyses show that an increase in tobacco prices through taxation is one of the most efficient tools in the application of integral policies in the fight against tobacco. Increases in taxes contribute to cessation, to reductions in consumption and in the number of deaths among addicts and to decrease the number of people who start to smoke. However, many governments hesitate to apply high taxes to tobacco for fear of possible negative economic results including loss of jobs and a decrease in fiscal revenue as a consequence of smuggling. Both literature and empirical experience indicate that these negative consequences do not occur or have been overestimated, often due to arguments promoted by the tobacco industry itself. Increases in tobacco taxes result in greater fiscal income, even in the presence of smuggling, which can be confronted without eroding tobacco control policies. Numerous countries, including Mexico, still have a wide margin for increasing tobacco taxes, and thereby to take advantage of an exceptional opportunity that benefits both the population's health and the public treasury. To do so, governments must stand up to the powerful tobacco industry, which is aware of the efficiency of taxes to combat tobacco use and therefore resorts to intense ad campaigns, political lobbying and negotiation of voluntary agreements for "self-regulation" in order to avoid stricter legislative or fiscal measures.     

Morphologic characterization of the pathway of transferrin endocytosis and recycling in human KB cells.

The pathway of transferrin uptake and recycling was investigated in KB cells to attempt to identify the organelles involved in the return of transferrin to the cell surface. Comparison was made with the pathway of internalization of epidermal growth factor (EGF), which has been shown to terminate in lysosomes. A horseradish peroxidase conjugate of transferrin (TF-HRP) was incubated with KB and at 4 degrees C and, at various times after warming to 37 degrees C, the location of TF-HRP was examined at the electron microscopic level. Transferrin, like EGF, was found to enter cells via coated pits and to move to the Golgi region in receptosomes (endosomes). Transferrin was located in the tubular elements of the transreticular portion of the Golgi but not in Golgi stacks. Interestingly, transferrin was not concentrated in the coated pits of the Golgi. In contrast, EGF was highly concentrated there. Transferrin was next detected in tubular elements (approximately equal to 600 A in width and up to 5,000 A in length) that were closely associated with microtubules and in dumbbell-shaped structures. In contrast, EGF was not detected in these structures. These results suggest that those organelles containing transferrin, but not EGF, participate in the return of receptor-bound transferrin to the cell surface.     

Idiopathic inflammatory myopathies: epidemiology,classification, and diagnostic criteria

Epidemiologic studies have helped to define the prevalence and incidence of PM, DM, and IBM and have highlighted differences in risk between men and women and in the age at onset for the different forms of myositis. Additionally, these studies have shown that there is a substantially higher risk of PM and DM in certain racial groups which is likely to be genetically determined. These differences are all likely to be fundamental in terms of the pathogenesis of these diseases but, as yet, their full significance remains uncertain. They do, however, suggest that the interplay between genetic and environmental initiating factors is different in the three disorders. Additional population-based studies in homogeneous racial groups, in parallel with studies of susceptibility genes for autoimmune disease, such as those encoding the MHC and inflammatory cytokines, are needed to throw further light on the role of genetic factors in the pathogenesis of the IIMs [47]. Because of the paucity of epidemiologic data on IBM, further studies are required to determine the degree of variation in prevalence in different populations and racial groups, as well as the consistency of the male association and age spectrum of manifestations of the disease. The particularly strong association with DR3 in this form of IIM [48] clearly points to the importance of genetic factors in pathogenesis, but further studies of DR3-associated genes in the MHC and of other candidate genes are needed to define more precisely the genes that convey susceptibility to the disease in different racial groups. Epidemiologic studies also have the potential to identify environmental factors that may play a part in disease initiation in genetically susceptible individuals. Seasonal patterns of disease onset have been reported, particularly in patients with DM [49-51] as well as seasonal variation in the frequency of relapses [52], pointing to the probable involvement of intercurrent infections, ultraviolet light exposure, or other environmental factors in disease initiation and reactivation. Further prospective studies are required to determine the contribution of environmental exposures and how they interact with genetic susceptibility factors to lead to myositis. One of the major limitations of a number of the previous epidemiologic studies is the lack of precision in the diagnostic criteria used and the classification of cases of IIM. The Bohan and Peter criteria [1] which were used in most studies after 1975, were introduced before IBM was recognized as an entity distinct from PM; most of the published incidence and prevalence figures for PM are therefore likely to be inaccurate. Multicentered, interdisciplinary, prospective studies, incorporating comprehensive clinical, laboratory, and pathologic information, are needed to develop and validate better diagnostic and classification criteria and to determine the true prevalence and incidence of the many forms of IIM.     

Perinatal changes in bombesin-stimulated muscle contraction in rabbit stomach and colon

Bombesin and its mammalian homologue, gastrin-releasing peptide, stimulate smooth muscle contraction and may promote the growth of gastrointestinal tissues. Isometric contraction of strips from circular muscle of the gastric fundus and longitudinal muscle of the distal colon were used to compare changes in the response to bombesin in newborn and weanling rabbits. There was an age-related qualitative change in gastric muscle from biphasic contractions including phasic and tonic components in the newborn to phasic contractions alone in the weanling. The colon contractions were tonic at both ages. In both tissues there was an age-related fivefold increase in stress in response to maximally effective concentrations of bethanechol (P less than 0.05). In contrast, in the stomach age-related decreases in the response to maximally effective concentrations of bombesin were observed, from 2930 +/- 179 mN/cm2 (98% of the maximal response to bethanechol) in the newborn to 565 +/- 81 mN/cm2 (4% of the maximal response to bethanechol) in the weanling (P less than 0.005). In the colon, a twofold increase in response to bombesin was observed, from 446 +/- 59 mN/cm2 (82% of the response to bethanechol) in the newborn to 862 +/- 11 mN/cm2 (29% of the response to bethanechol) in the weanling (P less than 0.05). No age-related changes were observed in the potency of bombesin in either tissue. Neither atropine nor tetrodotoxin altered the contractions in either tissue, suggesting that bombesin interacted directly with myocytes. There was three times as much bombesinlike immunoreactivity in the stomach compared with the colon, but no age-related changes in either tissue. In summary, by the age of weanling the stomach lost the tonic component of contraction and 80% of the efficacy of bombesin-stimulated phasic contraction that had been present in the newborn. The loss of efficacy, absolute in the stomach and relative to bethanechol in the colon, suggest that bombesin may be most important in stimulating motility in the neonatal period.     

Immunologic response in an elderly population with a mean age of 85

Previous studies of changes in immune responses in the elderly have been limited in both number and age of elderly subjects and have produced conflicting results. Using 260 subjects, mean age 84.6, the present study conclusively demonstrates that T cell response is decreased in the elderly. Decreases in response to phytohemagglutinin and concanavalin A were demonstrated in groups aged 70 to 79, 80 to 84, and 85 to 89, although a group 90 to 106 years old showed a decreased response only to phytohemagglutinin. None of the groups had a decreased response to pokeweed mitogen. No response to all three mitogens was observed in 13 percent of the group aged 70 to 89, but in none of the group aged 90 to 106 or in the young groups. No differences in natural killer cell cytotoxicity were observed among the elderly groups. In contrast to previous studies, these results suggest that: the decreased immune response of the elderly is not directly related to age, over age 70; and there may be a selection process in which subjects who live to the age of 90 are those in whom the least decrease in immune response is demonstrated.     

Plasma aldosterone and corticosterone responses to adrenocorticotropin, angiotensin, potassium, and stress in spontaneously hypertensive rats

The responses of plasma aldosterone and corticosterone to ACTH, angiotensin II (AII), and potassium chloride (KCl) infusion and the aldosterone, corticosterone and PRA responses to immobilization stress were studied in 2-month-old spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) normotensive controls. Basal levels of plasma aldosterone and corticosterone were greater and PRA was less in the SHR than in the WKY. Aldosterone and corticosterone responses to graded AII were similar in both groups. Aldosterone and corticosterone responses to graded doses of KCl and ACTH, however, were significantly greater in SHR than in WKY normotensive rats. Plasma corticosterone, PRA, and aldosterone responses to immobilization stress were reduced in SHR compared to WKY. At 2 months of age, blood pressure was definitely elevated in SHR and was associated with low PRA and relatively high basal levels of aldosterone and corticosterone. Discordance between the renin-angiotensin system and mineralocorticoid secretion in the SHR may be due to enhanced adrenal sensitivity to factors such as ACTH and potassium. Suppressed PRA in SHR may be due, in part, to increased mineralocorticoid secretion, resulting in sodium retention and intravascular volume expansion.     

Changes in the contractile response of arteires and veins from hypertensive rabbits to sympathetic nerve activity: assessment of some postsynaptic influences.

Contractile responses to field stimulation of intramural nerves of arteries and veins taken from rabbits made hypertensive by partial constriction of the abdominal aorta have been related to the carotid artery pressure. The increase in contraction of cephalic and short saphenous veins with rise in carotid artery pressure can be accounted for by an increase in sensitivity of the alpha-adrenergic receptor. The neurogenic contraction of the ear artery increased with carotid artery pressure rise. Changes in some of the extraneuronal factors that influence transmitter distribution and disposition in the tunica media were examined. In hypertensive animals, the percentage of released adrenergic transmitter entering the vessel wall might be expected to decrease due to an increase in medial thickness. However, this percentage was not significantly altered in the ear artery probably due, in part, to a concomitant increase in medial permeability to the transmitter. Extraneuronal transmitter disposition factors, i.e. extraneuronal uptake, monoamine oxidase, and catechol-O-methyltransferase activity are directly related to the wet weight of the vessel wall. Thus, their contribution to transmitter disposition would be expected to increase with increase in vessel wall thickness and tend to reduce the response to sympathetic activity. As the contractile response increased in the hypertensive vessels despite such changes, the increase in effector cell mass and density of neuronal terminal plexus, shown previously to increase with hypertension, are more important than these other considerations.     

Sex-specific increase in the prevalence of atrial fibrillation (The Copenhagen City Heart Study)

Atrial fibrillation (AF) is the most frequently encountered cardiac arrhythmia. It is a risk factor for stroke and premature death. We studied the temporal changes in the prevalence of AF from 1976 to 1994 in a random population aged 50 to 89 years. The prevalence of AF, diagnosed from electrocardiograms (ECGs), was determined in 8,606 patients examined in 1976 to 1978, in 8,943 patients examined in 1981 to 1983, and in 6,733 subjecs examined in 1991 to 1994. Changes in prevalence of AF were estimated by logistic regression analysis. In men, the age-standardized prevalence of AF increased from 1.4% in 1976 to 1978 (odds ratio [OR] 1.0, reference) to 1.9% in 1981 to 1983 (OR 1.6, 95% confidence interval [CI] 1.1 to 2.1), and to 3.3% in 1991 to 1994 (OR 2.3, 95% CI 1.6 to 3.4, p <0.001, adjusted for age). In women, the prevalence of AF decreased from 1.5% in 1976 to 1978 (OR 1.0, reference) to 1.0% in 1981 to 1983 (OR 0.7, 95% CI 0.5 to 1.0), and to 1.1% in 1991 to 1994 (OR 0.7, 95% CI 0.5 to 1.0), although the overall decrease was not significant (p = 0.11, adjusted for age). After adjusting for changes in comorbidity, body weight, and height, the increase in the prevalence of AF in men from 1976 to 1978 and from 1991 to 1994 remained significant (OR 1.9, 95% CI 1.3 to 2.8, P = 0.002). Although unchanged in women, the prevalence of AF in men more than doubled from the 1970s to the 1990s. The factors responsible for this gender-specific increase in the prevalence of this common arrhythmia have yet to be identified.     

Vectorcardiographic study on left ventricular hypertrophy in spontaneously hypertensive rats.

To observe cardiac changes in spontaneously hypertensive rats (SHR) functionally, the vectrocardiographic approach was tried, applying the Takayasu lead system to rats. This vectrocardiogram (VCG) was shown to be sufficiently good to detect left ventricular hypertrophy (LVH) in SHR. VCG in SHR showed specific features, some of which were left upward deviation of the maximum QRS vector in the frontal plane, an increased magnitude of the maximum spatial QRS vector, and prolongations of such indices as the QRS duration, time to the maximum spatial QRS vector and QT interval with abnormal ST-T changes. The P wave of SHR in the X scalar electrocardiogram, lower and wider than that of Wistar-Kyoto rats may also be a significant feature of LVH in SHR. The angle of the maximum QRS vector in the horizontal plane was not proven to be a suitable index of LVH in SHR. Most of the histometrical findings were closely correlated to blood pressure. Some of the vectrocardiographic findings were significantly correlated both to blood pressure and to some of the characteristic findings of LVH, such as the weights of the heart and the left ventricle and so forth. This experiment also indicated that LVH in SHR was not limited only to quantitative myocardial hypertrophy. It also seemed to be related to reversible or irreversible qualitative changes of coronary arteries or myocardium, such as myocardial fibrosis. This vectrocardiographic method was shown to be useful in obtaining various information about the cardiovascular system in rats, especially in SHR, and it seemed to be helpful for further understanding hypertensive cardiac diseases in humans.     

Matrix Metalloproteinases in the Pathogenesis of Asthma and COPD

While asthma is an inflammatory disorder of the airways involving mediators released from mast cells and eosinophils, inflammation alone is insufficient to explain the chronic nature of the disease. Recent progress in the understanding of disease pathogenesis has revealed that airway remodeling, which is at least in part due to an excess of extracellular matrix (ECM) deposition in the airway wall, plays a significant role in airflow obstruction. Matrix metalloproteinases (MMPs) have been suggested to be the major proteolytic enzymes to induce airway remodeling in asthma and COPD. It has been widely accepted that different inflammatory processes are involved in asthma and COPD with different inflammatory cells, mediators, and responses to treatments. Despite these different processes, airflow obstruction and airway remodeling characterize these two diseases. MMP-2 and -9 have been reported to be involved in the pathogenesis of airway remodeling in both diseases and MMP-12, in addition to these MMPs, in the pathogenesis of COPD. In this review, we discuss the current views on the role of MMPs in the pathogenesis of bronchial asthma and COPD. Anti-MMP therapy could theoretically be useful to prevent airway remodeling in asthma and COPD. However, to date no clinical data are available regarding the efficacy of anti-MMP therapies in the treatment of patients with asthma and COPD.     

A central nervous system defect in biosynthesis of corticotropin-releasing hormone is associated with susceptibility to streptococcal cell wall-induced arthritis in Lewis rats.

We have recently found that susceptibility to streptococcal cell wall (SCW)-induced arthritis in Lewis (LEW/N) rats is due, in part, to defective inflammatory and stress mediator-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis. Conversely, the relative arthritis resistance of histocompatible Fischer (F344/N) rats is related to their intact responses to the same stimuli. Specifically, LEW/N rats, in contrast to F344/N rats, have markedly impaired plasma corticotropin and corticosterone responses to SCW, recombinant human interleukin 1 alpha, the serotonin agonist quipazine, or synthetic rat/human corticotropin-releasing hormone (CRH). To explore the mechanism of this defect, we examined the functional integrity of the hypothalamic CRH neuron in LEW/N rats compared to F344/N rats. LEW/N rats, in contrast to F344/N rats, showed profoundly deficient paraventricular nucleus CRH mRNA levels and hypothalamic CRH content in response to SCW. Compared to F344/N rats, there was no increase in LEW/N hypothalamic CRH content or CRH release from explanted LEW/N hypothalami in organ culture in response to recombinant interleukin 1 alpha. These data provide strong evidence that the defective LEW/N corticotropin and corticosterone responses to inflammatory and other stress mediators, and the LEW/N susceptibility to experimental arthritis, are due in part to a hypothalamic defect in the synthesis and secretion of CRH. The additional finding of deficient expression in LEW/N rats of the hypothalamic enkephalin gene, which is coordinately regulated with the CRH gene in response to stress, suggests that the primary defect is not in the CRH gene but is instead related to its inappropriate regulation.     

Plasma prolactin concentrations in parental male and female rats: effects of exposure to rat young

The effects of pup presentation on the PRL responses in parental male rats were measured and compared with those in parental virgin and lactating female rats. Blood samples were collected from rats through indwelling intraatrial cannulas after a suckling challenge, i.e. presentation of rat young. Lactating rats showed full parental behavior and characteristic large surges in plasma PRL levels within the first 5-10 min on each day that rat young were presented (days 4, 8, and 12 of lactation). When pups were not presented, PRL rises did not occur. In contrast to the pattern of PRL responses shown by lactating mothers, parental ovariectomized nulliparous female and parental intact male rats failed to show specific increases in PRL in response to pup presentation. Plasma PRL levels in these groups, as in nonparental female and male rats, occasionally rose in response to blood collection rather than to pup presentation alone. Treatment of nulliparous female as well as male rats with estradiol and progesterone Silastic implants for 21 days before the initiation of behavioral testing significantly reduced the latencies of both nulliparous females and males to respond to foster young from about 5 to 2 days. The PRL responses of these steroid-primed groups were quite different. The steroid-primed females exhibited a pattern of PRL responses to pups identical to that found in lactating rats. The steroid-primed parental males, in contrast, failed to show specific increases in plasma PRL levels in response to young. These data demonstrate a sex difference in the hormonal, but not behavioral, responses of male and female rats to young and are suggestive of possible sex differences in the hypothalamic and/or peripheral regulation of pup-induced PRL secretion.     

Improving the time to thrombolytic therapy for myocardial infarction by using a quality assurance audit.

STUDY OBJECTIVE: To evaluate a program designed to improve the speed of delivery of thrombolytic therapy for myocardial infarction in an emergency department. DESIGN: Time to administer thrombolytic therapy was evaluated retrospectively in 1988. Then after physician and nurse education, time to therapy was audited in 1989 and 1990, with feedback to physicians. SETTING: A community hospital ED. PARTICIPANTS: Eight board-certified emergency physicians were monitored in their treatment of 58 patients. INTERVENTIONS: After the 1988 audit, the results for each physician were made known. Physician and nurse education was undertaken, and it was agreed to continue the audit. Nurses were encouraged to order ECGs rapidly, physicians were encouraged to make the treatment decision before consulting private physicians, and a goal of therapy in less than one hour was established. Further feedback on times was given to the physicians in 1989. MEASUREMENTS AND MAIN RESULTS: Mean time from ED arrival to thrombolytic therapy was 63 minutes in 1988, 47 minutes in 1989, and 38 minutes in 1990. This fall in time was significant (P = .0002). The number of patients treated within one hour rose from 45% in 1988 to 67% in 1989 and to 96% in 1990. CONCLUSION: Auditing time to thrombolytic therapy, combined with physician and nurse education and increased experience, can significantly improve the time to administration of thrombolytic therapy.     

Respiratory patterns after cholecystectomy. Effects of posture and CO2 stimulation

A marked reduction in the ratio of abdominal to rib cage motion has been observed after upper abdominal surgery. This study seeks to determine the effects on respiratory pattern of stimulation with CO2 and a change in posture from supine to semirecumbent posture (hips flexed, head of bed elevated at 30 degrees to the horizontal) in patients having undergone cholecystectomy. Canopy spirometry and respiratory inductive plethysmography were used to measure minute ventilation, tidal volume, and rib cage and abdominal motion in 14 otherwise healthy women, prior to elective cholecystectomy and on the first and third postoperative days. Preoperatively, the relative contribution of the chest wall compartment to tidal volume (Vc/VT) was increased both by moving from the supine to the semirecumbent posture and by stimulation with 4 percent inhaled CO2. On the first postoperative day, there was a reduction in abdominal motion. In contrast to what happened in the preoperative period, there was no change in the relative contribution of the rib cage and abdomen when the patients moved from the supine to semirecumbent position. With CO2 stimulation, there was a further increase in the already increased absolute tidal volume of the chest. On the third postoperative day, there was an increase in abdominal motion in the supine and sitting position and during 4 percent CO2 stimulation. These results demonstrate that the response to a change in posture and to 4 percent CO2 stimulation are markedly altered in the postoperative period by the reduction in abdominal motion.     

Markers of potential esophageal variceal rebleeding in cirrhotic patients undergoing endoscopic injection sclerotherapy

Endoscopic injection sclerotherapy has proven to be effective in reducing the severity of bleeding from esophageal varices in cirrhotic patients. However, rebleeding occurs in certain patients, and this can affect their long-term survival. Therefore, to evaluate varices that were likely to rebleed, the relationship between esophageal variceal re-bleeding and endoscopic variceal findings at the time of the initial injection scierotherapy were investigated, in cirrhotic patients. Sixty-three patients were investigated; they were assigned to three groups according to their Child's classification: A, B, and C. After the initial scierotherapy, rebleeding occurred in 14 patients (22%), specifically in 5% of those in group A, in 16% of those in group B, and in 47% of those in group C. The endoscopie findings at the time of the initial scierotherapy revealed that redness of the varices was most intense in the group C patients. Patients in whom the varices were intensely red and/or were located up to the level of the tracheal bifurcation were found to be the most likely to rebleed. Therefore, to prevent rebleeding in patients manifesting these signs, careful monitoring and repeated endoscopie injection scierotherapy is recommended.