First Report of a New Subgroup 16Sr II-M 'Candidatus Phytoplasma aurantifolia' Associated with Witches'-Broom Disease of Tephrosia purpurea in India.

Wild indigo (Tephrosia purpurea (L.) Pers.) grows as a common weed throughout the Indian subcontinent. The plant has pinnate leaves, white or purplish flowers, and flat hairy pods, and is cultivated as a green manure crop. The plant extracts contain compounds such as tephrosin, an aromatic ester, prenylated flavonoid, and sesquiterpene (2) that have medicinal properties. The newly recognized disease, Tephrosia purpurea witches' broom (TPWB), was characterized by chlorosis, stunting, and proliferative branching, which were suggestive of phytoplasma infection during a field survey conducted in November 2013. To determine the presence of phytoplasma, 2 g of compound leaves from three symptomatic and asymptomatic plants were used for total DNA extraction using the CTAB method. The phytoplasma 16S rRNA gene was detected in all three symptomatic plants using nested PCR with universal phytoplasma primer pairs, P1/P7 followed by R16F2n/R16R2 (4). No amplification was observed in DNA isolated from asymptomatic plants. PCR fragments (1,246 bp in length) generated from symptomatic T. purpurea plants were sequenced directly using five different primers viz. 343R, 536F, 704F, 907R, and 1103F. TPWB phytoplasma 16S rRNA gene sequence (GenBank Accession No. HG792252) showed 99.12% homology with a 'Candidatus Phytoplasma aurantifolia' strain WBDL (U15442) when compared using the EzTaxon 16S rRNA database (3). Virtual restriction fragment length polymorphism (RFLP) analysis was carried out on the obtained sequence using iPhyClassifier (5). The virtual RFLP pattern derived from the HG792252 sequence was different to the reference patterns of previously established 16Sr groups and subgroups. The reference pattern of the 16Sr group II, subgroup C (AJ293216) was most similar with a similarity coefficient of 0.92, which placed it in a new subgroup, 16Sr II-M (1). Furthermore, virtual RFLP results were confirmed by digesting R16F2n/R16R2 amplicon with BstUI, DraI, HinfI, HpaI, and MseI restriction enzymes according to manufacturer's instructions. To our knowledge, this is the first report of a 'Ca. P. aurantifolia'-related strain associated with witches'-broom disease of T. purpurea in India. References: (1) H. Cai et al. Int. J. Syst. Evol. Microbiol. 58:1448, 2008. (2) A. K. Khalafalah et al. Pharmacognosy Res. 2:72, 2010. (3) O.-S. Kim et al. Int. J. Syst. Evol. Microbiol. 62:716, 2012. (4) C. Smart et al. Appl. Environ. Microbiol. 62:2988, 1996. (5) Y. Zhao et al. Int. J. Syst. Evol. Microbiol. 59:2582, 2009.

Randomised clinical trial: the efficacy and safety of pancreatin enteric-coated minimicrospheres (Creon 40000 MMS) in patients with pancreatic exocrine insufficiency due to chronic pancreatitis--a double-blind, placebo-controlled study.

BACKGROUND: Pancreatic exocrine insufficiency (PEI) results in maldigestion, leading to abdominal pain, steatorrhoea, malnutrition and weight loss. AIM: To assess the efficacy and safety of pancreatin (Creon 40000 MMS) in treating PEI due to chronic pancreatitis (CP). METHODS: This was a 1-week, double-blind, randomised, placebo-controlled, parallel-group, multicentre study in India. Men and women ≥18 years of age with proven CP and PEI [defined as a coefficient of fat absorption (CFA) ≤80% during run-in phase] were randomised 1:1 to pancreatin or placebo (two capsules orally per main meal, one with snacks). The primary outcome measure was change in CFA from baseline to end of double-blind treatment (analysis of covariance). RESULTS: Of 62 patients randomised (34 pancreatin, 28 placebo), 61 completed treatment; one patient in the placebo arm withdrew consent before completion. Patient characteristics were similar in both groups except for the proportion of men (pancreatin 82% vs. placebo 68%). Patients receiving pancreatin had a statistically significant greater improvement in fat absorption from baseline to the end of double-blind treatment compared with those receiving placebo, with a least squares mean change (95% CI) in CFA of 18.5% (15.8-21.2) vs. 4.1% (1.0-7.2), respectively. This resulted in a treatment difference of 14.4% (10.3-18.5); P = 0.001. Patients receiving pancreatin also had a statistically significant greater improvement in nitrogen absorption and greater reductions in mean stool fat, stool frequency and stool weight compared with those receiving placebo. Treatment-emergent adverse events occurred in 12 patients on pancreatin and in seven on placebo; none led to study discontinuation. CONCLUSIONS: The results provide evidence for the efficacy of pancreatin (Creon 40000 MMS) in patients with pancreatic exocrine insufficiency due to chronic pancreatitis, and confirm that this formulation is well tolerated, with a good safety profile, at the dose administered.

Dose-dependent response of central dopaminergic systems to buspirone in mice.

Buspirone, a partial agonist of 5-hydroxytryptaminelA autoreceptors, preferentially blocks the presynaptic rather than the postsynaptic D2 dopamine (DA) receptors. Behavioural effects of a wide dose range of buspirone were therefore studied in mice. Buspirone at 0.625 to 5 mg/kg ip induced stereotyped cage climbing behaviour which was antagonized by pretreatment with haloperidol, alpha-methyl-p-tyrosine and small doses of apomorphine. Buspirone at 10, 20 and 40 mg/kg ip induced catalepsy and antagonized oral stereotypies induced by high doses of apomorphine and methamphetamine and apomorphine-induced cage climbing behaviour. The findings indicate that buspirone at 0.625 to 5 mg/kg selectively blocks the presynaptic mesolimbic D2 DA autoreceptors and releases DA which stimulates the postsynaptic mesolimbic D2 and D1 DA receptors and induces cage climbing behaviour. Buspirone, at 10, 20 and 40 mg/kg blocks the postsynaptic striatal and mesolimbic D2 and D1 DA receptors. Pretreatment with 1-tryptophan, dexfenfluramine and fluoxetine antagonized buspirone induced cage climbing behaviour and potentiated buspirone induced catalepsy. Pretreatment with trazodone, mianserin and p-chlorophenylalanine potentiated buspirone induced cage climbing behaviour and antagonized buspirone induced catalepsy. The results indicate that drugs which influence the activity of central serotonergic systems modulate the intensity of buspirone induced cage climbing behaviour and catalepsy.

Effects of dextromethorphan on dopamine dependent behaviours in rats.

Dextromethorphan, a noncompetitive blocker of N-methyl-D- aspartate (NMDA) type of glutamate receptor, at 7.5-75 mg/kg, ip did not induce oral stereotypies or catalepsy and did not antagonize apomorphine stereotypy in rats. These results indicate that dextromethorphan at 7.5-75 mg/kg does not stimulate or block postsynaptic striatal D2 and D1 dopamine (DA) receptors. Pretreatment with 15 and 30 mg/kg dextromethorphan potentiated dexamphetamine stereotypy and antagonised haloperidol catalepsy. Pretreatment with 45, 60 and 75 mg/kg dextromethorphan, which release 5-hydroxytryptamine (5-HT), however, antagonised dexamphetamine stereotypy and potentiated haloperidol catalepsy. Apomorphine stereotypy was not potentiated or antagonised by pretreatment with 7.5-75 mg/kg dextromethorphan. This respectively indicates that at 7.5-75 mg/kg dextromethorphan does not exert facilitatory or inhibitory effect at or beyond the postsynaptic striatal D2 and D1 DA receptors. The results are explained on the basis of dextromethorphan (15-75 mg/kg)-induced blockade of NMDA receptors in striatum and substantia nigra pars compacta. Dextromethorphan at 15 and 30 mg/kg, by blocking NMDA receptors, activates nigrostriatal dopaminergic neurons and thereby potentiates dexampetamine stereotypy and antagonizes haloperidol catalepsy. Dextromethorphan at 45, 60 and 75 mg/kg, by blocking NMDA receptors, releases 5-HT and through the released 5-HT exerts an inhibitory influence on the nigrostriatal dopaminergic neurons with resultant antagonism of dexampetamine stereotypy and potentiation of haloperidol catalepsy.

Effects of buspirone on dopamine dependent behaviours in rats.

Buspirone, a partial agonist of 5-hydroxytryptamine autoreceptors, selectively blocks presynaptic nigrostriatal D2 dopamine (DA) autoreceptors. At doses which antagonised action of apomorphine in biochemical presynaptic nigrostriatal D2 DA autoreceptor test systems buspirone neither induced catalepsy nor antagonised apomorphine-induced turning behaviour in rats indicating that at these doses buspirone does not block postsynaptic striatal D2 and D1 DA receptors. This study determines whether at high doses buspirone blocks postsynaptic striatal D2 and D1 DA receptors and provides behavioural evidence for selective blockade of presynaptic nigrostriatal D2 DA autoreceptors by smaller doses of buspirone. We investigated in rats whether buspirone induces catalepsy and effect of its pretreatment on DA agonist induced oral stereotypies and on cataleptic effect of haloperidol and small doses (0.05, 0.1 mg/kg, ip) of apomorphine. Buspirone at 1.25, 2.5, 5 mg/kg, ip neither induced catalepsy nor antagonised apomorphine stereotypy but did potentiate dexamphetamine stereotypy and antagonised cataleptic effect of haloperidol and small doses of apomorphine. Buspirone at 10, 20, 40 mg/kg, ip induced catalepsy and antagonised apomorphine and dexamphetamine stereotypies. Our results indicate that buspirone at 1.25, 2.5, 5 mg/kg blocks only presynaptic nigrostriatal D2 DA autoreceptors while at 10, 20, 40 mg/kg, it blocks postsynaptic striatal D2 and D1 DA receptors. Furthermore, buspirone at 1.25, 2.5, 5 mg/kg by selectively blocking presynaptic nigrostriatal D2 DA autoreceptors, increases synthesis of DA and makes more DA available for release by dexamphetamine and during haloperidol-induced compensatory 'feedback' increase of nigrostriatal DAergic neuronal activity and thus potentiates dexamphetamine stereotypy and antagonizes haloperidol catalepsy.

Involvement of central serotonergic systems in dextromethorphan-induced behavioural syndrome in rats.

Dextromethorphan, a noncompetitive blocker of the N-methyl-D-aspartate (NMDA) type of glutamate receptor, at 45, 60 and 75 mg/kg, ip doses induced a behavioural syndrome characterised by reciprocal forepaw treading, lateral head-weaving, hind-limb abduction and flat body posture. Such type of behavioural syndrome is induced by 8-hydroxy-2- (di-n-propylamino) tetralin (8-OH-DPAT) by directly stimulating the central postsynaptic 5-hydroxytryptamine (5-HT, serotonin) receptors of the 5-HT1A type. Pretreatment with buspirone (5, 10 mg/kg, ip) and l-propranolol (10, 20 mg/kg, ip) antagonised the behavioural syndrome induced by 8-OH-DPAT and dextromethorphan. Pretreatment with p-chlorophenylalanine (100 mg/kg/day x 4 days) antagonised the behavioural syndrome induced by dextromethorphan and dexfenfluramine but had no significant effect on 8-OH-DPAT induced behavioural syndrome. This indicates that dextromethorphan induces the behavioural syndrome by releasing 5-HT from serotonergic neurons with resultant activation of the postsynaptic 5-HT1A receptors by the released 5-HT. Pretreatment with fluoxetine (10 mg/kg, ip) significantly potentiated the behavioural syndrome induced by dextromethorphan and 5-hydroxytryptophan but significantly antagonised dexfenfluramine induced behavioural syndrome. This indicates that dextromethorphan releases 5-HT by a mechanism which differs from that of dexfenfluramine. Dextromethorphan may be releasing 5-HT by blocking the NMDA receptors and thereby counteracting the inhibitory influence of l-glutamate on 5-HT release.

Effects of dexfenfluramine on dopamine dependent behaviours in rats.

5-hydroxytryptamine (5-HT) inhibits the synthesis and release of dopamine (DA) from rat nigrostriatal DAergic neurons. Dexfenfluramine releases 5-HT from brain 5-HTergic neurons. The present study was undertaken to determine whether dexfenfluramine, through the released 5-HT, modulates the intensity of the behaviours dependent on the functional status of the nigrostriatal DAergic system. The effect of pretreatment with dexfenfluramine on dexamphetamine and apomorphine stereotypies of the oral movement variety and on catalepsy induced by haloperidol and small doses (0.05 and 0.1 mg/kg ip) of apomorphine was studied in rats. We also investigated whether dexfenfluramine induces catalepsy in rats. Dexfenfluramine at 2.5, 5 and 10 mg/kg ip did not induce catalepsy and did not antagonise apomorphine stereotypy. However, 1 h pretreatment with 5-HT releasing doses of dexfenfluramine ie 5 and 10 mg/kg ip, antagonized dexamphetamine stereotypy and potentiated catalepsy induced by haloperidol and small doses of apomorphine. Our results, that dexfenfluramine at 2.5, 5 and 10 mg/kg ip neither induced catalepsy nor antagonised apomorphine stereotypy, indicate that dexfenfluramine at these doses does not block the postsynaptic striatal D2 and D1 DA receptors. They also indicate that the 5-HT released by 5 and 10 mg/kg dexfenfluramine does not exert an inhibitory effect at or beyond the postsynaptic striatal D2 and D1 DA receptor sites. However, 5 and 10 mg/kg doses of dexfenfluramine, through the released 5-HT, inhibit the synthesis and release of DA from the nigrostriatal DAergic neurons and thus antagonise dexamphetamine stereotypy and potentiate catalepsy induced by haloperidol and small doses of apomorphine.

Oxidants and antioxidants in hypoxic ischaemic encephalopathy.

In the present study, the role of serum lipid peroxide and serum nitric oxide as oxidants and erythrocytic superoxide dismutase & serum vitamin E as antioxidants were determined in the 50 neonates with hypoxic ischaemic encephalopathy. (HIE) as against 25 healthy neonates as controls 50 patients of HIE were further divided into two groups i. e. mild and moderate HIE patients. All subjects were in the age group of 37-41 weeks of gestation. The levels of serum lipid peroxide, serum nitric oxide and erythrocytic superoxide dismutase were significantly elevated in both groups of neonates with HIE than those of controls (P<0.001), whereas serum vitamin E levels were significantly decreased in both groups of HIE patients than those of controls (P<0.001). A positive correlation was obtained between serum lipid peroxide and erythrocytic superoxide dismutase (r=+0.86). Alterations in the status of oxidants and antioxidants indicate role of free radicals in the development of HIE.

Development of carcinoma in chronic calcific pancreatitis.

Development of carcinomas of the pancreas over an underlying chronic pancreatitis is a rare event. Diminution of pancreatic calcification, following the development of carcinoma, has been previously reported only once. We report another such case.

Colonoscopic polypectomy. North Indian experience.

Colonoscopic snare polypectomy was carried out in 70 patients (40 children, 30 adults). There was a male preponderance in both the groups with a combined male: female ratio of 4.4:1. The majority of patients (85%) were aged 20 years or below. All patients presented with intermittent bleeding per rectum, ranging from 2 months - 6 years (mean 1.2 +/- 1.1 years) in children and 1-14 years (1.9 +/- 2.3) in adults. The majority of patients polyps were located in the rectum (73%) or in the rectosigmoid region (21%). Polyps were significantly more common in the rectum (80% vs 63%; P less than 0.01) and less frequent in the rectosigmoid (15% vs 30%; p less than 0.01) in children as compared to adults. A single polyp was present in 49 (70%) patients; 17 (24%) had 2-10 polyps, while 4 patients (2 children, 2 adults) had more than ten polyps. Most patients (94%) had polyps of less than 2 cm size. Histologically, the most polyps (91.5%) were of the juvenile variety; 39 (97.5%) children and 25 (83%) adults had this variety of polyp. The remaining 5 (17%) adults and one (2.5%) child had adenomatous polyps. The difference in the polyp histology between the two age groups was statistically significant (p less than 0.05). Only one patient (1.4%) had excessive bleeding following polypectomy. The present study suggests two important differences in the nature of polyps as compared to the West: 1) our patients were much younger, and polyps were rare after 40 years; and (2) histologically, the commonest polyps were of the juvenile variety (91.5%) while adenomatous polyps were rare (8.5%).

Conventional versus on-demand therapy for duodenal ulcer: results of a controlled therapeutic trial.

To compare the efficacy of conventional versus on-demand (symptomatic) treatment of duodenal ulcer, 81 patients were randomized into two groups. Group A (n = 40) patients were treated with ranitidine 150 mg twice daily until complete ulcer healing was achieved. Group B (n = 41) received a similar dose of ranitidine until complete relief of pain was achieved, irrespective of ulcer healing. Recurrence of ulcer in group A was treated with a full course of treatment until complete healing of the ulcer was achieved again, whereas, in group B, treatment was given only until pain recurrence was symptomatically controlled. Endoscopic examination was performed each month. Analysis of the results at 8 wk and 28 wk showed that 1) ulcer healing in group A was significantly superior to that in group B up to 24 wk, but at 28 wk the difference was no longer statistically significant (95% vs 70%), 2) the number of painful days were similar in the two groups, 3) group A patients took treatment for a significantly longer period than those in group B, 4) the cost of treatment per patient in group A was significantly greater than that in group B, 5) the recurrence rate assessed in patients followed for 28 wk after complete ulcer healing was similar in the two groups, and 6) the ulcer-related complications were not significantly different in the two groups. These findings indicate that, although on-demand treatment results in slower ulcer healing, it is not associated with an increase in the duration of pain and incidence of complications. A major advantage of this approach was a significant reduction in the cost of treatment. It is concluded that on-demand treatment is an attractive alternative therapeutic approach in the management of duodenal ulcer disease.

Gastric acid response to modified sham feeding in patients with duodenal ulcer: is increased vagal tone the cause of basal acid hypersecretion?

In order to test the hypothesis that increased basal vagal tone causes basal acid hypersecretion in duodenal ulcer (DU), the effect of sham feeding on gastric acid secretion was studied in 26 patients with DU and 20 healthy controls. Basal acid output (BAO), sham feeding-stimulated acid output (SAO) and peak histamine-stimulated acid output (PAO) were significantly higher in DU patients compared with healthy controls (P less than 0.01). The BAO/PAO ratio in DU patients (0.28 +/- 0.03) was not significantly different from that of healthy subjects (0.19 +/- 0.03), indicating that the higher BAO in DU patients group, as a whole, was due to a higher parietal cell mass. The basal subtracted response to sham feeding expressed as a fraction of secretory capacity [(SAO-BAO)/PAO], which correlates inversely with the basal vagal tone, was not significantly different in the patients and control subjects (0.27 +/- 0.03 versus 0.3 +/- 0.03; P greater than 0.05). Based on the data from the healthy controls, a ratio of BAO/PAO greater than 0.44 was defined as abnormal (using 95% confidence limits) and it indicated marked basal acid hypersecretion. Four of 26 DU patients had basal acid hypersecretion (that is, BAO/PAO greater than 0.44), but only two of them did not show an increase over their basal rate of secretion in response to sham feeding. All other DU patients, including two with marked basal acid hypersecretion, and all healthy controls showed an appreciable increase in their acid secretion in response to sham feeding.(ABSTRACT TRUNCATED AT 250 WORDS)

Long-term treatment of irritable bowel syndrome: results of a randomized controlled trial.

To examine the long-term management of irritable bowel syndrome we conducted a two-part controlled therapeutic trial on 28 patients who had recovered completely after four to six weeks of treatment with ispaghula husk and propantheline. In part I patients were randomly divided into two groups. Group A received a placebo capsule while Group B continued with treatment as before. After six months the response to treatment was assessed according to a scoring system. The overall relapse rate in Group B was 46 per cent compared to 82 per cent in group A. With continued treatment patients in Group B became asymptomatic from the fourth month while patients in Group A continued to deteriorate. In part II, patients who had relapsed whilst on placebo received active treatment. Six of the seven who agreed to continue with the study became asymptomatic within four weeks. However, all the patients who were asymptomatic while on active treatment relapsed on discontinuation and again recovered on reinstitution of active treatment. We conclude that irritable bowel syndrome is a chronic relapsing disorder and that treatment with a combination of ispaghula husk and propantheline is effective, both in relieving symptoms and in the maintenance of remission.

Pancreaticobiliary ductal union in biliary diseases. An endoscopic retrograde cholangiopancreatographic study.

To assess whether the anatomy of the pancreaticobiliary ductal drainage into the duodenum has any relationship with biliary diseases we analyzed 259 endoscopic retrograde cholangiopancreatograms. These included 102 normal examinations (control group), 95 patients with gallstone disease, and 21 patients with carcinoma of the gallbladder. In the control group, 64 (63%) subjects had a common channel and 38 (37%) had separated openings for the common bile duct and the main pancreatic duct. By contrast, the prevalence rate of a common channel was significantly lower in gallstone disease [28 (30%); p less than 0.001]. No such difference, compared with controls, was observed in patients with carcinoma of the gallbladder. The length of the common channel in the control group (mean +/- SD, 4.7 +/- 2.5 mm) was similar to that in gallstone disease (4.6 +/- 2.6 mm). However, patients with carcinoma of the gallbladder had a significantly longer common channel (8.3 +/- 4 mm; p less than 0.001) compared with the control group. An abnormally long common channel (greater than or equal to 8 mm) was seen more frequently in carcinoma of the gallbladder (8 of 21; 38%) compared with normal subjects (3 of 102; 3%) and patients with gallstones (1 of 95; 1%); the difference was highly significant (p less than 0.001 for each). These observations suggest a close association between the anatomy of the distal ends of the common bile duct and main pancreatic duct and the development of gallstones and carcinoma of the gallbladder.

Evaluation of the incidence and significance of the "mosaic pattern" in patients with cirrhosis, noncirrhotic portal fibrosis, and extrahepatic obstruction.

Mosaic pattern of gastric mucosa has been reported to be a sensitive and specific criterion for the diagnosis of portal hypertension and an important marker of nonvariceal upper gastrointestinal bleeding. So that the validity of this endoscopic sign could be assessed, 136 patients with portal hypertension, 25 chronic alcoholics without portal hypertension, and 366 controls were carefully endoscoped. Mosaic pattern was significantly (p less than 0.01) more common in portal hypertension patients (7.4%) than in controls (1.4%). It was not seen in chronic alcoholics. The incidence of mosaic pattern was 10.9% in cirrhotics, 2.9% in noncirrhotic portal fibrosis, and 5.4% in extrahepatic portal obstruction patients; the differences were not significant. Mosaic pattern was significantly (p less than 0.01) more often seen in postsclerotherapy (13.8%) than in presclerotherapy patients (2.6%). Bleeding from nonvariceal causes was uncommon, and was seen in only one patient (0.8%) showing mosaic pattern. Endoscopic gastric biopsies from areas showing mosaic pattern did not reveal any vascular abnormalities. In conclusion, gastric mucosal lesions are not very common in Indian patients with portal hypertension. In our experience, "mosaic pattern" is not a useful diagnostic feature in portal hypertension patients.

Endoscopic sclerotherapy for varices in children.

Thirty-one children with variceal bleeding due to portal hypertension (extrahepatic obstruction 19, non-cirrhotic portal fibrosis five, and cirrhosis of liver seven patients) were treated with endoscopic sclerotherapy with absolute alcohol. Acute variceal bleeding was successfully controlled in 10 patients by emergency sclerotherapy. A 3 weekly schedule of sclerotherapy could achieve obliteration of varices in all the patients. The mean (+/- SD) number of sclerotherapy courses and the time required for variceal eradication was 4.5 +/- 1.7 and 14.4 +/- 3.9 weeks, respectively. During a mean follow-up of 23.3 +/- 11.4 months, variceal recurrence was seen in three (9.7%) patients, two with cirrhosis and one with noncirrhotic portal fibrosis. Recurrence was not seen in any patient with extrahepatic obstruction. Five (16.1%) patients had a rebleed that could be controlled with emergency sclerotherapy. Esophageal stricture developed in four (12.9%) patients and could be dilated easily in all of them. The other complications of sclerotherapy included retrosternal pain, dysphagia, and fever; these were mild and short lasting. Survival in patients with extrahepatic obstruction and noncirrhotic portal fibrosis was 100%. The only death was in a cirrhotic, who died due to terminal hepatic failure. In conclusion, endoscopic sclerotherapy can be recommended as a safe and effective treatment in children for the control of acute variceal bleeding and for variceal obliteration.

Spontaneous expulsion per rectum of an ileal lipoma.

We report a case of spontaneous expulsion of a lipoma in a 32 year old male patient who presented with recurrent attacks of subacute intestinal obstruction. During one such episode the patient developed unusually severe abdominal pain and expelled a fleshy mass per rectum which, on histopathology, was found to be a lipoma attached to a necrosed portion of the small intestine. The pain disappeared immediately; a subsequent barium meal examination revealed normal appearances and the patient has remained completely symptom free 10 months after the incident.

Ethanolamine oleate versus absolute alcohol as a variceal sclerosant: a prospective, randomized, controlled trial.

Forty-seven patients with esophageal variceal bleeding were randomly allocated to undergo sclerotherapy on a 3 weekly schedule with either 5% ethanolamine oleate (23 patients) or absolute alcohol (24 patients), in an attempt to compare the efficacy and safety of the two sclerosants. Sclerotherapy with absolute alcohol eradicated esophageal varices significantly earlier compared with ethanolamine oleate (12.9 +/- 5.2 vs 22.3 +/- 8.2 wk, respectively, p less than 0.001). The mean number of injection courses and the mean amount of sclerosant required for variceal obliteration was also significantly (p less than 0.001) less in the alcohol-injected group. Although the total number of rebleeding episodes were significantly (p less than 0.05) less in the alcohol-injected group, the frequency of rebleeding was not significantly different between the two groups (20.8% vs 30.4%, respectively, p greater than 0.05). Two (8.1%) patients died due to rebleeding in the ethanolamine-injected group, whereas in the alcohol group, none died. There was no significant difference in the frequency of complications with the two sclerosants. Besides the relative ease of rapid injection due to its aqueous nature, alcohol is readily available and relatively economical (total cost of sclerosant per patient; alcohol US $0.50, ethanolamine US $60). In conclusion, absolute alcohol appears to be a useful alternative to 5% ethanolamine oleate as a variceal sclerosant.