Pulmonary involvement in chronic arsenic poisoning from drinking contaminated ground-water.

OBJECTIVES: Chronic arsenic poisoning, due to ingestion of contaminated ground-water, is a major public health problem in West Bengal. It causes multiorgan damage. The present study attempts to objectively investigate the pulmonary involvement by examining the lung function. The nature of lung changes was also evaluated. MATERIAL AND METHODS: One hundred and seven subjects with (cases) and 52 subjects without (controls) chronic arsenic poisoning were examined by spirometry. Forced expiratory volume-I second (FEVI), forced vital capacity (FVC) and peak expiratory flow rate (PEFR) were measured. Bronchoalveolar lavage (BAL) was performed in five cases with and five cases without pulmonary involvement. RESULTS: Thirty three (30.8%) cases and four (7.6%) controls (p<0.01) had respiratory involvement. The pattern of involvement in cases was: obstructive- 20(68.9%) (including three (10%) with bronchiectasis), restrictive- 1(3.5%), mixed- 8(27.6%), malignancy- 4(12.1%) (adenocarcinoma-I, squamous cell- 2, undifferentiated- I). FEVI (69.7+/-25.9 [n=105] vs 83.7+/-15.19 [n=51], p=0.0005), FVC (77.4+/-22.7 [n=105] vs 85.6+/-18.23 [n=51], p=0.025), FEVI/FVC (73.6+/-13.38 [n=105] vs 79.1+/-18.65 [n=52], p=0.007) and PEFR (53.9+/-21.52 [n= 103] vs 67.3+/-18.36 [n=51], p=0.0002) (percent of predicted) were all reduced more in cases compared to controls. Worsening of these parameters correlated with increasing degree of arsenic toxicity. Markers of inflammation (macrophage, lactate dehydrogenase, nitric oxide) were apparently more in the BAL fluid of those with lung involvement than in those without, though the arsenic content did not differ significantly. CONCLUSION: Chronic arsenic poisoning causes pulmonary involvement, predominantly obstructive, the degree of which worsens with increasing degree of arsenic toxicity. Inflammation, rather than direct toxicity, appears to be the underlying mechanism.

Disseminated tuberculosis presenting as hemobilia, successfully treated by arterial embolization.

Tuberculosis, specially disseminated tuberculosis, involves the liver frequently. Focal hepatic tuberculosis with local hemorrhage has been reported. We report on a twenty-one year female with disseminated tuberculosis presenting with initially non-localisable massive upper gastrointestinal bleeding, subsequently found to have pancreatitis, right sided pleural effusion and hemobilia which was treated successfully.

Management of the Budd-Chiari syndrome by balloon cavoplasty.

BACKGROUND: Obstruction of the suprahepatic inferior vena cava (IVC) by a membrane or stricture is the commonest cause of Budd-Chiari syndrome in the eastern hemisphere. We present our experience with the outcome of balloon cavoplasty in such cases. METHODS: We followed up 40 consecutive cases of Budd-Chiari syndrome over seven years. Doppler study of hepatic venous outflow tract (in all cases), liver biopsy (30 cases) and necropsy (two cases) were performed. Balloon cavoplasty was done in selected cases. RESULTS: Of 40 patients with BCS (mean age 35.2 [SD 8.7] years; 26 men) 5, 5 and 30 had fulminant, acute and chronic presentation, respectively. Inferior vena cavography was performed in 32 cases, and showed membranous obstruction of the IVC in 12, segmental occlusion of the IVC in 11 cases, and block in both the IVC and the main hepatic veins in the rest. Successful balloon cavoplasty was done in 18 cases with obstruction of the IVC (membrane or stricture); 15 of them are well over a mean follow up of 56 (14.6) months. Three patients developed restenosis; two of them, treated with redilatation, are doing well, and one died of septicemia and hepatic failure following a surgical bypass. Pressure gradient between the IVC and right atrium decreased significantly after cavoplasty (15.4 [2.8] vs 6.6 [2.0] mmHg; p< 0.001). CONCLUSION: Balloon cavoplasty gave encouraging results in the management of Budd-Chiari syndrome due to membranous obstruction or stricture of the IVC.

Etiology based prevalence of Budd-Chiari syndrome in eastern India.

BACKGROUND: Diagnosis of Budd-Chiari syndrome (BCS) is often missed unless its possibility has been kept in mind. Obstruction of inferior vena cava (IVC) is reportedly the most frequent cause of BCS in Afro-Asian variety. AIM: An attempt was made to classify BCS (in an eastern Indian population) etiopathologically. PATIENTS AND METHODS: Thirty consecutive cases of BCS presenting over a period of five years were included. Following a thorough physical examination, necessary investigations (including coagulation profile, ultrasonography (with Doppler study) of hepatobiliary tract, hepatic vein and IVC angiography (n = 22) and liver biopsy (n = 26, including autopsy in two cases) were performed. RESULTS: Mean age at presentation was 32.7 +/- 10.36 years (range 12-60 years) with M:F = 21:9. Clinical presentations included, hepatomegaly in 28 (93.3%), ascites in 27 (90%), splenomegaly in 15 (50%), pain in abdomen in 26 (86.6%), jaundice in 10 (33.3%), back veins in 20 (66.6%) and gastrointestinal bleeding in three (10%) cases. Amongst the total of 30 patients, four, six and 20 cases presented as fulminant, acute and chronic BCS respectively. Twenty four cases of BCS could be diagnosed by ultrasonography alone, while the remainder required angiography for diagnosis. IVC and hepatic vein angiography revealed membranous obstruction in nine, partial stricture of IVC in six, and IVC and/or hepatic vein block in others. The etiopathological nature in 30 cases were as follows: idiopathic membranous obstruction in nine (30%), hepatocellular carcinoma in six (20%), idiopathic stricture in six (20%) cases and one case (3.3%) each of the following: cholangiocarcinoma, renal cell carcinoma, chronic pancreatitis, hydatid cyst in liver, protein S deficiency, oral contraceptive use, nephrotic syndrome (with antithrombin III deficiency), polycythemia rubra vera and chronic lymphatic leukemia. CONCLUSION: Idiopathic membranous obstruction and stricture of IVC are the commonest cause of BCS in the eastern part of India. Hepatocellular carcinoma is also a common cause, presenting in the fulminant form. Ultrasonography may be a helpful screening test for BCS, but IVC and hepatic vein catheterisation is essential for a complete work up of these patients.

Hepatic manifestations in chronic arsenic toxicity.

OBJECTIVE: The hepatotoxic action of arsenic, when used as a therapeutic agent, has long been recognized. Data on liver involvement following chronic exposure to arsenic-contaminated water are scanty. We report the nature and degree of liver involvement on the basis of hospital-based and cohort follow-up studies in patients who consumed arsenic-contaminated drinking water for 1 to 15 years. METHODS: 248 patients with evidence of chronic arsenic toxicity underwent clinical and laboratory examinations including liver function tests and HBsAg status. Liver biopsy was done in 69 cases; in 29 patients, liver arsenic content was estimated by neutron activation analysis. A cohort follow up of 23 patients who took arsenic-free water for 2-12 years was also carried out. RESULTS: Hepatomegaly was present in 190 of 248 patients (76.6%). Noncirrhotic portal fibrosis (91.3%) was the predominant lesion in liver histology. The maximum arsenic content in liver was 6 mg/Kg (mean 1.46 [0.42], control value 0.16 [0.04]; p < 0.001); it was undetected in 6 of 29 samples studied. Cohort follow-up studies showed elevation of globulin in four cases and development of esophageal varices in one case. CONCLUSION: We report the largest number of patients with liver disease due to chronic arsenicosis from drinking arsenic-contaminated water. Noncirrhotic portal fibrosis is the predominant lesion in this population.

Primary pulmonary hypertension in cirrhosis of liver.

BACKGROUND: Primary pulmonary hypertension (PPH) is a grave association of portal hypertension, and is potentially fatal in liver transplant candidates. AIM: To investigate the prevalence of PPH among cirrhotics with portal hypertension. METHODS: 43 cirrhotics with portal hypertension (Child B 22, C 14), after screening for cardiopulmonary diseases, were evaluated by hemodynamic study. RESULTS: PPH was detected in 2 cases (4.7%), both in Child B, hepatitis B and C viruses being the etiologies. Neither had portal axis thrombosis. Two other cases also had pulmonary hypertension, but with high pulmonary capillary wedge pressure (PCWP). The 41 cases without and 2 cases with PPH had, respectively, mean pulmonary artery pressure (MPAP) 16.3 (5.9) mmHg, 26 mmHg and 33 mmHg; PCWP 11.5 (6.7) mmHg, 12 mmHg and 11 mmHg; transpulmonary pressure gradient 4.8 (2.6) mmHg (n = 27), 14 mmHg and 22 mmHg; and pulmonary vascular resistance 80.2 (55.8) dyne.sec.cm-5 (n = 27), 155.6 dyne.sec.cm-5 and 366.7 dyne.sec.cm-5. No correlation of MPAP was found with either Child-Pugh scoring (r2 = 0.0347) or with hepatic venous pressure gradient (r2 = 0.0021). CONCLUSION: PPH has a prevalence of 4.7% among cirrhotics with portal hypertension; it bears no relation with severity of liver disease.

Portal hypertensive gastropathy and gastric varices before esophageal variceal sclerotherapy and after obliteration.

OBJECTIVES: To evaluate the frequency and clinical importance of portal hypertensive gastropathy (PHG) and gastric varices (GV) before endoscopic sclerotherapy (EST) and after esophageal variceal obliteration. METHODS: Patients with portal hypertension (PHT) with variceal bleed were prospectively evaluated for PHG and GV before EST with intravariceal injection of absolute alcohol and after esophageal variceal obliteration. Gastric varices and PHG were characterized and graded according to previously established criteria. Patients were followed up for 12-48 (mean 37) months after variceal obliteration. RESULTS: Of 70 patients with PHT 26 had PHG before (severe in two) [18/37 in cirrhosis, 6/20 in non-cirrhotic portal fibrosis (NCPF), and 2/13 in extrahepatic portal vein obstruction (EHPVO)] and 50 had PHG after variceal obliteration (severe in 22) (27/37 in cirrhosis, p = 0.03 before versus after esophageal variceal obliteration; 16/20 in NCPF, p < 0.01; and 7/13 in EHPVO, p = ns). Type I GV (continuation of esophageal varix into the stomach) was found in 25/70 before and 5/70 after esophageal variceal obliteration (p < 0.001); in contrast, other types of GV were seen in 14/70 before and 29/70 after (p < 0.01). Overt bleeding from GV and PHG during follow-up after variceal obliteration occurred in 6 and 4 patients, respectively. CONCLUSIONS: Esophageal variceal obliteration by EST increases the frequency of PHG and GV (except type I GV which get obliterated); both PHG and GV have potential to cause rebleeding.

Primary pulmonary hypertension in non-cirrhotic portal fibrosis.

BACKGROUND: Primary pulmonary hypertension (PPH) has been reported in association with cirrhosis and extrahepatic portal venous obstruction; reports of PPH in noncirrhotic portal fibrosis (NCPF) are few. AIM: To evaluate pulmonary arterial pressure in patients with NCPF. METHODS: Twenty two patients with NCPF underwent hemodynamic studies for pulmonary arterial pressure after excluding secondary causes of pulmonary hypertension. Hemodynamic studies were carried out through the femoral route using 7F Swan-Ganz catheter. Splenoportal venography was done by percutaneous splenic puncture. RESULTS: The mean pulmonary arterial pressure was 12.9 +/- 3.1 mmHg with pulmonary capillary wedge pressure of 8.3 +/- 2.1 mmHg in 20 of 22 cases; in the remaining two cases, the corresponding pressures were 30 mmHg and 28 mmHg and 13 mmHg and 12 mmHg, respectively. CONCLUSION: Two of 22 patients with NCPF had PPH. PPH can thus develop without hepatocellular failure or recurrent embolization from portal axis thrombosis as has been described in cirrhosis.