Jejunal stricture complicating acute mesenteric venous thrombosis secondary to protein C deficiency and factor V Leiden gene mutation.

We report a patient with high small intestinal obstruction due to ischemic stricture, secondary to acute mesenteric venous thrombosis. Tests done for hypercoagulability revealed dual etiology (protein C deficiency and factor V Leiden gene mutation). The patient underwent surgical resection and has been on anticoagulation treatment. At 2 years' follow up, she remains asymptomatic.

Effect of tense ascites on esophageal body motility and lower esophageal sphincter pressure.

BACKGROUND: Esophageal motility and lower esophageal sphincter (LES) pressure change with rapid changes in intraabdominal pressure (IAP); the response of these to slow change in IAP is not known. AIMS: To study esophageal body motility and LES pressures in patients with cirrhosis with tense ascites in the basal state and after paracentesis. METHODS: Twenty four patients with cirrhosis of liver and tense ascites and 13 with cirrhosis without ascites (controls) were studied. Basal intragastric (IGP) and LES pressures, and esophageal body response to water swallows, were recorded using a water perfusion system; IAP was measured in patients with ascites. In patients with ascites, the study was repeated twice: after paracentesis of two liters of fluid and after adequate control of ascites. RESULTS: Basal IGP (p = 0.002) and duration of esophageal contraction (p = 0.01) were lower in controls, but basal LES pressures were similar in the two groups. After control of ascites, IAP (p = 0.02) and IGP (p = 0.005) decreased; amplitude and duration of distal esophageal contraction decreased (p < 0.05). The frequency of high-amplitude waves also decreased (p = 0.04). LES pressure remained unaltered. CONCLUSIONS: Esophageal contraction duration is increased in the presence of ascites, and decreases after control of ascites; LES pressure is not affected by ascites.

Acute lymphoblastic leukemia presenting with severe jaundice in an adult.

We report an adult patient of acute lymphoblastic leukemia presenting with liver dysfunction.

Early changes in esophageal motility after endoscopic variceal sclerotherapy or ligation.

INTRODUCTION: Endoscopic variceal sclerotherapy (EVS) and ligation (EVL) are reported to be associated with altered esophageal motility. Most studies have been in patients with alcoholic cirrhosis and ascites. AIMS: To study the early effect of EVS and EVL in patients with portal hypertension without ascites. METHODS: Forty six portal hypertensive patients without ascites underwent esophageal manometry 24 h prior to EVS or EVL and within 24 h of two subsequent sessions. Nineteen such patients but without prior gastrointestinal bleed were studied once as controls. RESULTS: The protocol was completed in 35 patients (cirrhosis--16, noncirrhotic portal hypertension--19; 27 men; mean age 36 years). Basal midexpiratory lower esophageal sphincter pressure was similar in the study group (mean [SD] 20.1 [9.1] mmHg) and controls (17.6 [6.0] mmHg); the pressure did not change following EVS or EVL. Amplitude of contractions in the lower 5 cm of the esophageal body was similar in the two groups (84.8 [43.1] mmHg and 95.9 [59.6] mmHg), and decreased (63.6 [34.0] mmHg; p = 0.03) after two sessions of variceal therapy. The duration of contraction did not change following intervention. Nonperistaltic waves > 2 of 10 swallows were present during the baseline study in 9 patients in each group; 13 and 21 patients (p < 0.02 compared to baseline) developed them after the first and second sessions of therapy, respectively. Percentage of abnormal waves also increased following therapy. Thirteen patients developed esophageal ulcers; there was no correlation between the presence of ulcers and dysmotility. There was no difference in the changes between the EVS and EVL groups, and between patients with cirrhosis and noncirrhotic portal hypertension. CONCLUSION: Both EVS and EVL affect esophageal motility; these changes do not cause significant esophageal symptoms.

Multiple abdominal venous thrombosis in HIV-seropositive patient.

HIV infection is known to be associated with endothelial dysfunction leading to thrombosis. We report a patient with multiple abdominal venous thrombosis and splenic hematoma who was seropositive for HIV-1. No cause for the hypercoagulable state was detected; prothrombin time, activated partial thromboplastin time, and levels of protein S, protein C and antithrombin III were normal. He tested negative for VDRL and anticardiolipin antibodies.

Consumption of 'country liquor' and its relation to alcoholic liver disease in Mumbai.

The amount of alcohol intake required for the development of liver disease has been determined in Western populations; corresponding figures in Indians, many of whom consume locally brewed liquors, are not known. We studied 328 patients from a public hospital in Mumbai who admitted to regular alcohol consumption, to determine the pattern of alcohol consumption and its relation to liver disease. Liver disease was more common in those who consumed illicitly-brewed as compared to licit liquor. Daily drinking, volume of consumption > 200 ml per day, and duration of drinking > 14 years were each significantly more common in those with liver disease. A cumulative intake of > 2000 ml. years, calculated as the product of volume (ml per day) and duration (years), was a reliable cut-off level for association with liver disease (sensitivity 65%, specificity 77%) and cirrhosis (sensitivity 70%, specificity 59%). The content of alcohol in these liquors, estimated in 23 samples, ranged from 23-36.1 g/100 ml, being lower in the illicit liquors. Thus, in Mumbai, alcoholic liver disease occurs more commonly with consumption of illicit liquor (despite its lower alcohol content); liver involvement appears earlier and with lower consumption levels than in the West.

Manometric mapping of normal esophagus and definition of the transition zone.

BACKGROUND: The normal esophagus has not been manometrically mapped. The transition zone between esophageal smooth and skeletal muscles has also not been defined manometrically. AIMS: To manometrically map the normal esophagus and to define the transition zone. METHODS: Thirty normal adults [23 men; mean age 34.8 (10.4) years] underwent manometry using a water-perfused system. The lower esophageal sphincter (LES) was studied by station pull-through, and esophageal body musculature was evaluated at 1-cm intervals with five wet swallows at each level. The transition zone was identified as an area where the wave-forms did not resemble typical skeletal or smooth muscle wave-forms. RESULTS: The basal mid-expiratory LES pressure was 18.7 (7.2) mmHg, and its length was 3.6 (1.2) cm. Based on our findings, we defined the transition zone as an area where either the amplitude of contraction was < 40 mmHg or, if the amplitude was 40-50 mmHg, the rate of change of pressure from baseline to peak of the wave was < 50 mmHg/s. The lengths of the skeletal, transition and smooth muscle zones were 2.8 (1.2), 4.0 (1.7) and 12.5 (2.7) cm, respectively. The amplitude and dp/dt of contraction and transmission velocity were lowest in the transition zone (p < 0.05). CONCLUSIONS: We have manometrically mapped the normal esophageal muscle zones; the parameters obtained may be used as reference values. The manometric criteria for the transition zone have also been defined.

Vagal dysfunction following endoscopic variceal sclerotherapy.

BACKGROUND: Sclerotherapy is associated with complications which involve adjacent structures like the pleura. The effect of sclerotherapy on function of the vagus nerve, which lies in close proximity to the thoracic esophagus, is not clear. AIM: To study gastric acid secretion as a marker of vagal function in portal hypertensive patients who have undergone sclerotherapy. METHODS: Portal hypertensive patients who had undergone at least three sessions of sclerotherapy were evaluated by mapping gastric acid-secreting mucosa by the Congo red test and by estimating gastric acid secretion using the modified sham feeding test. Patients with portal hypertension who had never been subjected to endoscopic sclerotherapy were recruited as controls. RESULTS: On Congo red test, complete or substantial reduction in acid-secreting mucosa was observed in eight patients in comparison to none of the controls. Significantly lower acid secretion on modified sham feeding test was observed in these eight patients. CONCLUSION: A lower gastric acid secretion, probably secondary to vagal dysfunction, is seen in patients who have undergone multiple sessions of sclerotherapy; vagus nerve involvement may be secondary to periesophageal inflammation.

Helicobacter pylori gastritis masquerading as gastric lymphoma.

A 30-year-old man presented with acute acid-peptic symptoms. Endoscopy and radiological studies revealed generalized thickening of gastric folds with multiple superficial ulcerations and infiltration of the distal stomach simulating gastric neoplasm. Endoscopic biopsies revealed acute gastritis with foveolar hypertrophy with numerous Helicobacter pylori. The symptoms and endoscopy findings resolved completely with combination triple-drug therapy for H pylori.

Sublingual nifedipine and captopril in hypertensive urgencies and emergencies.

Fifty two patients of severe hypertension, diastolic blood pressure > or = 115 mmHg, with or without acute complications, were treated with sublingual nifedipine 10 mg or sublingual captopril 25 mg in a randomized prospective in patient study with careful clinical monitoring. Both the drugs were safe and effective in rapidly lowering blood pressure. Nifedipine appeared to be superior to captopril with earlier onset of action, greater magnitude of response and longer duration of action. No significant side effects were observed in either of the two groups.