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Biomedical subjects

B K De

Publications and source records attributed to B K De.

At least 19 recordsLinked to original sources
PubMed2004

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.

Adolescent↗
PubMed2003

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.

Adult↗
PubMed2001

Randomized placebo-controlled trial of 2,3-dimercapto-1-propanesulfonate (DMPS) in therapy of chronic arsenicosis due to drinking arsenic-contaminated water.

BACKGROUND: Chronic arsenic toxicity, producing various clinical manifestations, is currently epidemic in West Bengal, India, Bangladesh, and other regions of the world. 2,3-Dimercapto-1-propanesulfonate, a chelating agent, increases excretion of arsenic in urine to several times the prechelation concentration but the therapeutic efficacy of 2,3-dimercapto-1-propanesulfonate in the management of chronic arsenic toxicity has been incompletely evaluated. We investigated the clinical use of 2,3-dmercapto-1-propanesulfonate in such patients. METHODS: Twenty-one consecutive patients with chronic arsenicosis were individually randomized into 2 groups: 11 patients (9 males and 2 females, age 30.63+/-11.4 years) received 2,3-dimercapto-1-propanesulfonate 100-mg capsules 4 times a day for 1 week and repeated in the 3rd, 5th, and 7th week with no drug during the intervening period. The other 10 patients (5 males and 5 females, age 34.4+/-14.41 years) were given placebo capsules (resembling 2,3-dimercapto-1-propanesulfonate) in the same schedule. The consumption of arsenic-contaminated water was terminated by all 21 subjects. Initial and posttreatment urinary arsenic excretion was determined in all cases. Sequential excretion of urinary arsenic was determined during the treatment of 2 drug- and 1 placebo-treated cases. The clinical features were evaluated by an objective scoring system before and after treatment. Routine investigation including liver function test and skin biopsy were also done before and after the treatment. Drug-associated toxicity was tabulated. RESULTS: Therapy with 2,3-dimercapto-1-propanesulfonate caused significant improvement in the clinical condition of chronic arsenicosis patients as evidenced by significant reduction of total clinical scores from 8.90+/-2.84 to 3.27+/-1.73; p < 0.0001. Exposure cessation alone with placebo treatment also reduced clinical scores (8.50+/-1.96 to 5.40+/-2.12; p < 0.003), but the posttreatment total clinical score of 2,3-dimercapto-1-propanesulfonate-treated patients (3.27+/-1.73) was significantly lower than that of placebo-treated patients (5.40+/-2.12; p < 0.01). The most significant improvement was noted in regard to the clinical scores of weakness, pigmentation, and lung disease. No difference was noted between groups in the hematological and biochemical parameters (which were normal) and skin histology before and after treatment. No 2,3-dimercapto-1-propanesulfonate-related adverse effects were noted. Total urinary excretion of arsenic in 2,3-dimercapto-1-propanesulfonate-treated cases increased significantly following drug therapy, with no increase in placebo-treated cases. CONCLUSION: 2,3-Dimercapto-1-propanesulfonate treatment caused significant improvement in the clinical score of patients suffering from chronic arsenic toxicity. Increased urinary excretion of arsenic during the period of therapy is the possible cause of this improvement.

Adult↗
PubMed2001

Performance characteristics of four free phenytoin immunoassays.

The measurement of the unbound or free phenytoin concentration is indicated in several situations, including uremia. In patients with uremia, metabolites of phenytoin and other substances accumulate and can displace phenytoin from its protein binding sites, with a consequent increase in the free fraction of drug. Some of the phenytoin metabolites that accumulate in uremia can cross-react with phenytoin immunoassays. In this study the authors evaluated four free phenytoin immunoassays compared with a high-performance liquid chromatography (HPLC) method: the Roche COBAS Integra, the Syva EMIT 2000, the Opus INNOFLUOR, and the Abbott TDx. All four methods demonstrated good precision, with interday coefficients of variation of < or = 5% and comparable recoveries using quality control material. Two of the methods, the EMIT 2000 and COBAS Integra, showed excellent agreement with the HPLC method using samples from patients both with normal renal function and with renal insufficiency. The other two methods, the INNOFLUOR and TDx, showed average positive biases for the therapeutic range of 3-7% and 21-22%, respectively, compared with the HPLC method for samples from patients with normal renal function, and average positive biases of 24-32% and 75-81%, respectively, with samples from patients with uremia.

Anticonvulsants↗
PubMed2000

Purification and characterization of Streptococcus pneumoniae palmitoylated pneumococcal surface adhesin A expressed in Escherichia coli.

All Streptococcus pneumoniae isolates tested to date express a species-common lipoprotein designated as pneumococcal surface adhesin A (PsaA). This protein is cell-associated, hydrophobic, immunogenic, and genetically conserved. It is currently under investigation as a potential component in third-generation pneumococcal vaccine formulations. To overcome the problem of low-level expression of native hydrophobic PsaA in S. pneumoniae, and also of the recombinant PsaA (rPsaA) in Escherichia coli, we generated a stable E. coli construct expressing functional palmitoylated rPsaA ( approximately 10 mg/l of fermentation culture) using Borrelia burgdorferi outer surface protein A (OspA, a hydrophobic lipoprotein) signal peptide. By Western blot analysis, the chimeric rPsaA ( approximately 34 kDa) was detected in the cell lysate using anti-PsaA antibodies. It was partially purified by extracting the cell pellet with PBS/Triton X(R)-114 buffers, followed by anion exchange filter chromatography. A trypsin digestion profile of rPsaA closely resembled that of the native protein, as revealed by SDS-PAGE/silver staining. Lipidation of rPsaA was confirmed by labeling recombinant E. coli cells with [(3)H] palmitic acid and analyzing the labeled E. coli cells by Western blotting coupled with autoradiography. Further, analysis of purified rPsaA by mass spectrometry (MALDI-TOF) revealed a heterogenous spectrum with a major peak (M+H)(+1) of mass 33,384 Da (theoretical mass of palmitoylated rPsaA=33,361 Da). Purified rPsaA was immunogenic in CBA/NCAHN-XID female mice following intranasal immunization with or without adjuvant, as determined by measurement of anti-PsaA serum IgG levels. These anti-PsaA antibodies reacted with both native and rPsaA polypeptides. Our data strongly suggest that E. coli-expressed rPsaA is palmitoylated and closely resembles the native protein in structure and immunogenicity. It was also observed to elicit measurable protection against nasopharyngeal carriage with S. pneumoniae.

Adhesins, Bacterial↗
PubMed2000

Hepatopulmonary syndrome in inferior vena cava obstruction responding to cavoplasty.

Reports show that hepatopulmonary syndrome mostly occurs in the setting of advanced hepatic dysfunction, with the associated vasoactive substance imbalance believed to be responsible for its pathogenesis. However, hepatopulmonary syndrome has also been reported in cases of mild hepatic dysfunction or noncirrhotic portal hypertension, indicating that portal hypertension also plays a part in the pathogenesis. Liver transplantation remains the only therapeutic option of proven benefit. We describe 2 cases of hepatopulmonary syndrome in the setting of inferior vena cava (suprahepatic) obstruction, but with minimal hepatic dysfunction. After balloon cavoplasty, 1 patient showed, in addition to improvement of the features of hepatic outflow obstruction, significant reduction of dyspnea, cyanosis, and hypoxemia with arterial blood gas normalization within 2 weeks and intrapulmonary shunt reversal within 8 weeks. This implies that hemodynamic alterations (such as portal hypertension) independently contribute to the pathogenesis of hepatopulmonary syndrome in at least some of the cases. Therapies aimed at correcting these abnormal hemodynamics may be important in the treatment of this condition, especially when the hepatic functional status by itself does not warrant a liver transplant.

Adult↗
PubMed2000

Clinical and haemodynamic aspects of hepatopulmonary syndrome in Indian patients with cirrhosis.

BACKGROUND: Hepatopulmonary syndrome consists of the triad of hepatic dysfunction and/or portal hypertension, intrapulmonary vascular dilatation and hypoxaemia, in the absence of detectable primary cardiopulmonary diseases. In the present study, we examined the frequency of hepatopulmonary syndrome among Indian patients with cirrhosis, and studied clinical predictors and pulmonary haemodynamic alterations. METHODS: Forty-five patients with cirrhosis and no cardiopulmonary diseases were investigated by air-contrast echocardiography. Where patients were positive, arterial blood gas analysis was carried out. Positive contrast echocardiography with PO2 < 70 mmHg confirmed the diagnosis of hepatopulmonary syndrome. Three cases with the syndrome and 24 without were assessed for haemodynamic status by hepatic and pulmonary catheterization. RESULTS: Four of 45 cases of cirrhosis (8.9%) had positive contrast echocardiographies, including three (6.7%) with hepatopulmonary syndrome and one 'subclinical' case (positive contrast echocardiography without hypoxaemia). Under haemodynamic study, the mean pulmonary arterial and pulmonary capillary wedge pressures appeared to be lower among those patients with hepatopulmonary syndrome. CONCLUSIONS: In this small study, the frequency of hepatopulmonary syndrome was relatively low (6.7%). Cyanosis was the only reliable clinical indicator, and there was no clear relationship with the severity of cirrhosis by Child's grading.

Adolescent↗
PubMed2000

Arsenic in drinking water and the prevalence of respiratory effects in West Bengal, India.

BACKGROUND: A large population in West Bengal, India has been exposed to naturally occurring inorganic arsenic through their drinking water. A cross-sectional survey involving 7683 participants of all ages was conducted in an arsenic-affected region between April 1995 and March 1996. The main focus of the study was skin keratoses and pigmentation alterations, two characteristic signs of ingested inorganic arsenic. Strong exposure-response gradients were found for these skin lesions. The study also collected limited information concerning respiratory system signs and symptoms, which we report here because increasing evidence suggests that arsenic ingestion also causes pulmonary effects. METHODS: Participants were clinically examined and interviewed, and the arsenic content in their current primary drinking water source was measured. There were few smokers and analyses were confined to non-smokers (N = 6864 participants). RESULTS: Among both males and females, the prevalence of cough, shortness of breath, and chest sounds (crepitations and/or rhonchi) in the lungs rose with increasing arsenic concentrations in drinking water. These respiratory effects were most pronounced in individuals with high arsenic water concentrations who also had skin lesions. Prevalence odds ratio (POR) estimates were markedly increased for participants with arsenic-induced skin lesions who also had high levels of arsenic in their current drinking water source (> or = 500 microg/l) compared with individuals who had normal skin and were exposed to low levels of arsenic (<50 microg/l). In participants with skin lesions, the age-adjusted POR estimates for cough were 7.8 for females (95% CI : 3.1-19.5) and 5.0 for males (95% CI : 2.6-9.9); for chest sounds POR for females was 9.6 (95% CI : 4.0-22.9) and for males 6.9 (95% CI : 3.1-15.0). The POR for shortness of breath in females was 23.2 (95% CI : 5.8-92.8) and in males 3.7 (95% CI : 1.3-10.6). CONCLUSION: These results add to evidence that long-term ingestion of inorganic arsenic can cause respiratory effects.

Adolescent↗
PubMed2000

Propranolol in primary and secondary prophylaxis of variceal bleeding among cirrhotics in India: a hemodynamic evaluation.

OBJECTIVE: In the present study, we attempted to complete the hemodynamic assessment of propranolol response in cirrhotics with esophageal varices at high risk of bleeding, in one sitting, so as to identify nonresponders at the earliest. Some noninvasive indicators of this response were also evaluated. METHODS: Hepatic venous pressure gradient (HVPG) was measured in 33 such cases (18 nonbleeders, 15 bleeders) before and 90 min after an oral dose of 80 mg propranolol, and reduction by > or =20% taken as responder. RESULTS: Twenty-two patients (66.67%) responded (HVPG reduction > or =26%), whereas 11 (33.33%) did not (HVPG reduction < or =6%). Postdrug HVPG between responders and nonresponders showed a significant difference (p < 0.001). Neither baseline HVPG (p > 0.1), baseline CI (p = 0.665), nor baseline stroke volume index (p > 0.1) could predict responder status. Difference of HVPG reduction (percent) between bleeders (21.49 +/- 35.53) and nonbleeders (40.58 +/- 23.95) approached, but did not reach, statistical significance (p = 0.076). However, logistic regression showed this difference to be significant (p = 0.026). Age of responders was found to be significantly lower than that of nonresponders (p approximately equals 0.05). During a follow-up of 9-38 months, only one of 22 responders (on propranolol) had an episode of variceal bleed. None in whom HVPG fell to < or = 12 mm Hg bled. CONCLUSION: The study suggests that single-sitting hemodynamic assessment of acute response to high-dose oral propranolol clearly differentiates between responders and nonresponders. Moreover, it appears that prior history of variceal bleeding and old age negatively influences the effect of propranolol.

Administration, Oral↗
PubMed2000

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.

Adolescent↗
PubMed1999

Endoscopic variceal ligation for primary prophylaxis of oesophageal variceal bleed: preliminary report of a randomized controlled trial.

BACKGROUND: Prevention of variceal bleeding, a major cause of morbidity and mortality, is an important goal in the management of patients with portal hypertension (PHT). Although propranolol has been found useful in preventing the first episode of variceal bleeding (primary prophylaxis) in cirrhotic PHT, it has limitations which include side effects, contraindications, non-compliance and failure in some patients. Endoscopic variceal ligation (EVL) has not been used for primary prophylaxis. METHODS: Thirty cirrhotic patients with PHT, grade III to IV oesophageal varices, hepatic venous pressure gradient > or = 12 mmHg and no prior history of upper gastrointestinal bleeding were randomized to receive propranolol (to reduce their pulse rate by 25% from baseline, n = 15) and EVL (weekly to fortnightly until variceal eradication, n = 15). The two groups were comparable. All the patients in EVL group had variceal eradication during 3.8 +/- 2.2 sessions. RESULTS: There was no major complication or interval bleeding. During a follow-up period of 17.6 +/- 4.7 months, varices recurred in three, two of which bled (successfully treated by EVL). In contrast, during this period of follow up one patient in the propranolol group had variceal bleeding (P=NS). Side effects of propranolol included symptomatic bradycardia requiring reduction of dose in one of 15 patients. CONCLUSIONS: Although sample size in this study is small, it seems that EVL may be a good option for primary prophylaxis for variceal bleeding in patients with cirrhotic PHT; further studies on a larger number of patients and longer follow up are required.

Adrenergic beta-Antagonists↗
PubMed1999

Analytic performance of two automated nonpretreatment digoxin immunoassays.

The analytic performance of two automated nonpretreatment digoxin methods, AxSYM Digoxin II and Vitros digoxin immunoassays, was assessed. Both assays had analytic sensitivities of less than 0.2 microg/L, were linear from digoxin concentrations of 0.5 to 4.0 microg/L, and showed acceptable precision, with a maximum total coefficient of variation (CV) of 8.9% and 6.4% for the AxSYM and Vitros, respectively. Comparison of the two methods using samples from patients receiving digoxin gave the following relationship: Vitros = 0.91 x AxSYM + 0.23 (r = 0.97, Sy,x = 0.12). Digoxinlike immunoreactive factor (DLIF) crossreactivity was examined in specimens from patients who had hepatic disease, renal insufficiency, had undergone cardiac surgery, and in neonatal cord blood samples. Minimal crossreactivity was observed for most samples and the average crossreactivity for each group of samples was comparable for the two methods. The recovery of digoxin added to samples from each group of DLIF was similar, except for that from cord blood samples, for which recovery was significantly lower with the AxSYM method. Titration of a digoxin-spiked serum pool with digoxin-immune Fab showed a similar decrease in the measured digoxin concentration for both methods. Overall, the analytic performance characteristics of these two methods were comparable.

Anti-Arrhythmia Agents↗
PubMed1999

Falsely increased immunoassay measurements of total and unbound phenytoin in critically ill uremic patients receiving fosphenytoin.

BACKGROUND: Fosphenytoin, a phosphate ester prodrug of phenytoin, is metabolized to phenytoin in vivo. Phenytoin metabolites accumulate in renal insufficiency and cross-react in some phenytoin immunoassays. Our aim was to determine the accuracy of phenytoin immunoassays in renal patients treated with fosphenytoin. METHODS: We measured phenytoin with HPLC and with the aca, ACS:180, TDx phenytoin II, Vitros, and AxSYM methods. Specimens were collected 2-120 h after fosphenytoin administration from 17 patients with renal insufficiency. RESULTS: The AxSYM, TDx phenytoin II, ACS:180, and Vitros assays displayed falsely increased phenytoin results up to 20 times higher than the HPLC results. The aca Star results for these specimens were comparable to the HPLC results. Although fosphenytoin can cross-react with phenytoin immunoassays, no fosphenytoin was detected by a sensitive HPLC method in any sample that was tested for its presence. CONCLUSION: These results are consistent with the formation of one or more novel metabolites or adducts of fosphenytoin that accumulate in some critically ill patients with renal insufficiency and that display significant cross-reactivity with some, but not all, phenytoin immunoassay methods.

Acute Kidney Injury↗
PubMed1998

Arsenic levels in drinking water and the prevalence of skin lesions in West Bengal, India.

BACKGROUND: A cross-sectional survey was conducted between April 1995 and March 1996 to investigate arsenic-associated skin lesions of keratosis and hyperpigmentation in West Bengal, India, and to determine their relationship to arsenic water levels. METHODS: In all, 7683 participants were examined and interviewed, and the arsenic levels in their drinking water measured. RESULTS: Although water concentrations ranged up to 3400 microg/l of arsenic, over 80% of participants were consuming water containing <500 microg/l. The age-adjusted prevalence of keratosis was strongly related to water arsenic levels, rising from zero in the lowest exposure level (<50 microg/l) to 8.3 per 100 for females drinking water containing >800 microg/l, and increasing from 0.2 per 100 in the lowest exposure category to 10.7 per 100 for males in the highest exposure level (> or =800 microg/l). However, 12 cases with keratosis (2 females and 10 males) were drinking water containing <100 microg/l of arsenic. Findings were similar for hyperpigmentation, with strong dose-response relationships. Among those with hyperpigmentation, 29 cases were exposed to drinking water containing <100 microg/l. Calculation by dose per body weight showed that men had roughly two to three times the prevalence of both keratosis and hyperpigmentation compared to women apparently ingesting the same dose of arsenic from drinking water. Subjects who were below 80% of the standard body weight for their age and sex had a 1.6 fold increase in the prevalence of keratoses, suggesting that malnutrition may play a small role in increasing susceptibility. CONCLUSION: The surprising finding of cases who had arsenic-associated skin lesions with apparently low exposure to arsenic in drinking water needs to be confirmed in studies with more detailed exposure assessment. Further research is also needed concerning susceptibility factors which might be present in the exposed population.

Adolescent↗
PubMed1998

Randomized placebo-controlled trial of 2,3-dimercaptosuccinic acid in therapy of chronic arsenicosis due to drinking arsenic-contaminated subsoil water.

INTRODUCTION: Chronic arsenic toxicity producing various clinical manifestations is currently epidemic in West Bengal, India, Bangladesh, and other regions of the world. Animal studies have indicated that 2,3-dimercaptosuccinic acid can be used as an oral chelating agent. A prospective, double-blind, randomized controlled trial was carried out to evaluate the efficacy and safety of 2,3-dimercaptosuccinic acid for chronic arsenicosis due to drinking arsenic-contaminated (> or = 50 micrograms/L) subsoil water in West Bengal. METHOD: Twenty-one consecutive patients with chronic arsenicosis were individually randomized (random number; assignment made by individual not evaluating patients) into 2 groups: 11 patients (10 male, age 25.5 +/- 8 years) received 2,3-dimercaptosuccinic acid 1400 mg/d (1000 mg/m2) in the first week and 1050 mg/d (750 mg/m2) during the next 2 weeks with a repeat course 3 weeks later. The other 10 patients (all male, age 32.2 +/- 9.7 years) were given placebo capsules for the same schedule. The clinical features were evaluated by an objective scoring system before and after treatment. Routine investigations including liver function tests, arsenic concentrations in urine, hair, and nails, and skin biopsy evaluations were also completed. RESULTS: Though there was improvement in the clinical score of 2,3-dimercaptosuccinic acid-treated patients, similar improvement was observed in the placebo-treated group. There were no statistical differences in the clinical scores between the 2 groups at the beginning and at the end of treatment. Similarly, no differences were found for the other investigated parameters. CONCLUSION: Under the conditions of this study, 2,3-dimercaptosuccinic acid was not effective in producing any clinical or biochemical benefit or any histopathological improvement of skin lesions in patients with chronic arsenicosis.

Adolescent↗
PubMed1998

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.

Adolescent↗