Prevalence of anxiety, depression, and their risk factors among lung cancer patients: A cross-sectional study in a tertiary care center, Kolkata

Background: Depression and anxiety disorders are common among lung cancer patients posing serious problem of treatment interruption, thereby poor prognosis and deterioration of quality of life. Objectives: The aim of the study was to find the prevalence of depression and anxiety among lung cancer patients and their respective determinants. Materials and Methods: An institution-based cross-sectional prospective study was conducted at the Department of Pulmonary Medicine of a tertiary care hospital at Kolkata over a period of 6 months. Patients were included by complete enumeration method, and an exit interview was conducted with the help of two standardized questionnaires: WHO Disability Assessment Schedule 2.0 to assess disability and Mini International Neuropsychiatric Interview English Version 5.0.0 DSM-IV to detect current major depressive episode (MDE) and generalized anxiety disorder (GAD). Collected data were entered and analyzed in SPSS 20.0 software. Results: A total of 210 patients were recruited. Nearly three-fourths of the study population (73.7%) were suffering from current GAD; a significant portion (42.1%) was suffering from current MDE. Both the disorders were diagnosed in 42.1% cases. Multivariate analyses revealed that patients who were currently unemployed or retired, time since diagnosis more than 1 month and suffering from higher degree of disability had higher risk of depression; while patients who were residing at urban area, currently not earning, financially dependent to others and suffering from higher degree of disability had greater risk of developing anxiety during the course of the disease. Conclusion: Both depression and anxiety were quite prevalent among lung cancer patients. Social and psychological supports are to be raised to achieve treatment success and a better quality of life by mitigating this problem.

Left pulmonary artery agenesis with pulmonary hypoplasia in an elderly patient: a rare case report.

Proximal interruption of the unilateral pulmonary artery is a rare congenital anomaly, which is often associated with other cardiovascular abnormalities. It is usually diagnosed in children but rarely discovered in adulthood as an isolated phenomenon, occurring more frequently on the right side and is often associated with a contralateral aortic arch. We are presenting a rare case of a sixty year old male who was diagnosed with left lung hypoplasia due to proximal interruption of left pulmonary artery with left sided aortic arch without any associated cardiovascular anomalies.

Pulmonary Lymphangitis Carcinomatosis In Primary Oesophagogastric Carcinoma.

Pulmonary Lymphangitis carcinomatosis is an unusual metastatic manifestation of Oesophagogastric carcinoma and it occurs due to diffuse spread of the tumour to the pulmonary lymphatic system. We described a case of a 28 year old woman, presenting with gradually progressive dyspnoea and cough where results of Chest X-ray and HRCT thorax were consistent with features of Lymphangitis carcinomatosis. Upper GI endoscopic evaluation showed a tumour originating from oesophagogastric junction and extending to cardia of stomach. Biopsy from tumour revealed adenocarcinoma. As there is no definitive therapy to this condition, patient was managed conservatively only to succumb few days after hospitalisation.

Gastro-duodenal mucosal changes associated with low-dose aspirin therapy: a prospective, endoscopic study.

OBJECTIVES: The association of low-dose aspirin use and gastro-intestinal bleeding is well described. However, the gastroduodenal mucosal changes associated with low-dose aspirin therapy have not been properly evaluated. We undertook a prospective, endoscopic study to evaluate gastro-duodenal mucosal lesions produced by low-dose aspirin. METHODS: Forty-seven patients with non-hemorrhagic cerebral infarct or transient ischemic attacks and normal upper gastrointestinal endoscopy were randomized to receive either enteric-coated (n=25) or plain (n=22) aspirin (150 mg/day). Follow-up endoscopy was done at 2, 4 and 8 weeks; gastro-duodenal mucosal lesions, if present, were scored. Forty-seven patients with hemorrhagic infarct who were not treated with aspirin served as controls. RESULTS: Twenty eight (60%) of 47 patients receiving aspirin had mucosal lesions; stomach alone was the most frequent site (32%), followed by both stomach and duodenum (23%). Frequency of mucosal changes in the stomach at 8 weeks (19%) was significantly lower (p<0.05) than those at 2 weeks (53%) and 4 weeks (55%). Coated (56%) and plain (63.6%) aspirin induced mucosal lesions with similar frequency. CONCLUSION: Administration of low-dose aspirin, either plain or enteric-coated, induces endoscopic gastro-duodenal mucosal lesions in a large majority of patients. The frequency of damage decreased after 8 weeks of therapy.

Treatment of chronic anal fissure with topical glyceryl trinitrate: a double-blind, placebo-controlled trial.

BACKGROUND: Topical glyceryl trinitrate (GTN) may produce healing of anal fissure by decreasing the high resting anal sphincter pressure in these patients. The present study assessed the efficacy of GTN in chronic anal fissure in a double-blind placebo-controlled trial. METHOD: Patients with chronic anal fissure (for more than 8 weeks) underwent measurement of maximum anal resting pressure (MARP) before and 12 minutes after application of either 0.2% GTN or placebo ointment in a randomized manner. They then received twice-daily local application of their respective ointment for 6 weeks. Symptoms and healing of fissure were assessed; patients were evaluated at 3 months for evidence of relapse. RESULTS: 19 adult patients (12 men) were studied; 10 received GTN and 9 placebo. Mean (SD) MARP decreased from 131.0 (32.3) cm H2O to 93.5 (28.4) cm H2O (p<0.05) with GTN and from 150.5 (36.9) cm H2O to 142.8 (35.0) cm H2O (p=ns) with placebo. Fissure healed in 7 of 10 patients treated with GTN and 2 of 9 patients treated with placebo (p<0.05). There was no relapse of fissure in either group. CONCLUSION: Local application of GTN was effective in healing chronic anal fissure.

Induction of oxidative stress in antitubercular drug-induced hepatotoxicity.

BACKGROUND AND AIM: Oxidative stress could play a role in the pathogenesis of antitubercular drug (ATD)-induced hepatotoxicity. We therefore studied the plasma level of reduced glutathione (GSH) and malondialdehyde (MDA) in patients with ATD-induced hepatotoxicity (cases), ATD-treated controls (disease controls) and in healthy volunteers. METHODS: This study was carried out in a case-control design. Twenty-one cases, 21 age- and sex-matched disease controls, and 10 healthy volunteers were enrolled. Plasma levels of GSH and MDA were measured. RESULTS: Plasma levels of GSH (median [range] 11.5 [6.2-21.2] mmol/dL) and MDA (1390 [560-2310] nmol/dL) of cases were significantly different (p<0.01) from GSH (18.4 [10.5-24.4]) and MDA (290 [240-550]) of disease controls. Further, plasma GSH and MDA levels of both the ATD-treated groups were different from those in healthy controls. CONCLUSION: Lower levels of plasma GSH and higher levels of MDA may be due to oxidative stress resulting from ATD therapy.

Oxidative stress in liver of mice exposed to arsenic-contaminated water.

BACKGROUND: Oxidative stress has been implicated in the initiation of hepatic damage caused by various agents. Not much data on oxidative stress in liver in chronic arsenic exposure are available in the literature. We therefore studied this aspect in a murine model. METHODS: BALB/c mice were given arsenic-contaminated (3.2 mg/L) or arsenic-free (< 0.01 mg/L, control) drinking water ad libitum. Batches of mice were sacrificed after 2 and 4 months, and blood samples and liver tissue were collected. Liver histology was examined and levels of hepatic reduced glutathione (GSH), malondialdehyde, and enzymes of the antioxidant defense system in the liver tissue were determined. Arsenic content in liver tissues obtained at 4 months was estimated. RESULTS: Two-month exposure to arsenic caused significant elevation of hepatic GSH (11.4 [0.8] micrograms/mg protein) compared to control mice (9.3 [0.4]; p < 0.01). Levels of enzymes related to GSH homeostasis were also elevated. At 4 months, hepatic GSH was significantly reduced (8.4 [0.5] micrograms/mg protein) when compared to control mice (9.3 [0.4]; p < 0.01). Arsenic content in the liver tissue after 4 months of exposure was significantly higher (0.40 [0.05] microgram/g) as compared to control mice (0.04 [0.04]; p < 0.01). CONCLUSION: The results suggest that the antioxidant defense system in the liver of mice is activated after exposure to arsenic for 2 months. However, prolonged exposure to arsenic probably causes overuse failure of this system, which might result in initiation of biochemical injury to the liver.

Esophageal and gastric dysmotility in non ulcer dyspepsia.

BACKGROUND: The pathophysiology of non ulcer dyspepsia is poorly understood. Data on gastrointestinal motility alterations in this condition in the Indian population are scanty. We studied esophageal and gastric motility in patients with non ulcer dyspepsia. METHODS: 58 consecutive patients with non ulcer dyspepsia (according to the Rome criteria) were studied; 10 healthy volunteers were studied as controls. Esophageal transit of solid and liquid boluses (in all patients) and solid-phase gastric emptying (in 20 patients) were studied using scintigraphic techniques. RESULTS: Delayed esophageal transit and delayed gastric emptying were observed in 32 (55%) and 9 (45%) patients, respectively. Delay of both esophageal and gastric transit was found in 5 patients. Mean (SD) esophageal transit for liquid bolus was significantly delayed in patients (9.3 [3.7] s) compared to controls (7.0 [2.0] s; p < 0.01). Mean (SD) gastric emptying time (T50) was significantly delayed in patients (61.6 [13.6] min) compared to controls (50.0 [5.0] min; p < 0.001). Esophageal and gastric delayed transit was found in about two thirds of patients with dysmotility-like dyspepsia, but there were no significant difference in these abnormalities among different subgroups of dyspepsia. CONCLUSION: High prevalence of esophageal and gastric transit delay was found in non ulcer dyspepsia, particularly in the dysmotility subgroup.

Histopathology of skin lesions in chronic arsenic toxicity--grading of changes and study of proliferative markers.

Chronic arsenic toxicity (CAT) manifests predominantly as cutaneous lesions in the form of melanosis, keratosis and neoplastic changes. We have studied skin biopsies from 42 patients of CAT. Histological study of H/E stained sections showed--hyperkeratosis in 13, parakeratosis in 13, acanthosis in 12, papillomatosis in 24, elongation of reteridges in 21, increased basal pigmentation in 27 and dysplastic changes in 8 cases. Squamous cell carcinoma was present in 2, basisquamous in 1 and basal cell carcinoma in 1 case. Changes of skin lesions after drug DMSA and DMPS therapy compared to placebo were studied. The result was inconclusive. Proliferative activity of skin lesions in CAT were studied by AgNOR stain to assess the biological behaviour of the lesions. AgNOR score showed--normal control 1.08, benign changes (e.g. Hyperkeratosis, parakeratosis, acanthosis, papillomatosis etc.) without dysplasia--1.35, mild to moderate dysplasia--1.735, severe dysplasia--3.0 and carcinoma--3.56. Thus, AgNOR score gives some idea on the biological behaviour of CAT lesions. It is suggested that AgNOR staining should be done regularly along with H&E staining for proper assessment of the cases.

Development of an animal model of hepatic fibrosis by excretory-secretory antigen of Ascaris suum.

OBJECTIVE: The excretory-secretory (ES) antigens of Ascaris suum are known to cause hepatic damage in animals. The present study was aimed at developing an animal model of hepatic fibrosis with these antigens. METHODS: Three doses of ES antigens of A. suum were injected into 24 golden hamsters on days 0, 10 and 20. Batches of 8 animals each were sacrificed at 3 days, 45 days and 90 days after the third injection, after collection of blood. Three groups of 6 control animals each were injected with normal saline and were sacrificed similarly. Liver biochemistry, leukocyte migration inhibition test on cells separated from spleen, and liver histology were carried out. RESULTS: Serum ALT levels in experimental animals were significantly higher than those in control animals at days 3, 45 and 90 after the last antigen dose; AST levels were elevated 45 and 90 days after the last dose of ES antigen. Leukocyte migration inhibition in experimental animals was 58.2 (8.5)%, 51.6 (11.2)% and 50.5 (12.8)% at days 3, 45 and 90 after the last antigen dose. Marked centrivenular degeneration and necrosis were observed in liver tissue in all the experimental animals sacrificed 72 h after the last antigen dose. Condensation of reticulin around the portal zone with extension into the liver lobule was observed in 4 of 8 and 7 of 8 experimental animals sacrificed 45 and 90 days, respectively, after the last dose. Control animals did not have such lesions. CONCLUSION: An animal model of hepatic fibrosis could be produced by repeated injection of ES antigens of A. suum.

Oxidative stress in gastric mucosa in Helicobacter pylori infection.

BACKGROUND: Infection with Helicobacter pylori is believed to be associated with generation of reactive oxygen molecules which leads to oxidative stress in the gastric mucosa; but the relation between oxidative stress and gastrointestinal mucosal damage has not been documented. AIM: To look for evidence of oxidative stress and lipid peroxidation in the gastric mucosa in H. pylori-associated peptic ulcer. METHODS: 34 duodenal ulcer (DU) patients with H. pylori infection, 14 DU patients without H. pylori infection and 10 healthy subjects without H. pylori infection were studied. H. pylori infection was diagnosed by histology and rapid urease test on endoscopic biopsies from the gastric body and antrum. Reduced glutathione (GSH) and malondialdehyde (MDA) content were measured in biopsies taken from the gastric antrum. Statistical analysis was done using Student's t test. RESULTS: Tissue levels of GSH were significantly lower (91.7 [35.4] nmole/100 mg versus 147.3 [41.2] nmole/100 mg; p < 0.001) and MDA higher (163.0 [83.4] nmole/100 mg versus 109.2 [51.3] nmole/100 mg; p < 0.01) in patients with DU associated with H. pylori infection as compared to those without H. pylori infection. GSH levels were significantly lower and MDA levels higher in DU patients with or without H. pylori infection as compared to control subjects. Serum MDA levels in DU patients with H. pylori infection were also significantly higher than in patients without H. pylori infection. CONCLUSION: Depletion of gastric mucosal glutathione in H. pylori-infected DU patients may be due to failure of the antioxidant defense system. Failure of the glutathione-dependent defense system results in accumulation of free radicals which can initiate membrane damage by lipid peroxidation.

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.

Prevalence of hepatitis B infection in the general population: a rural community based study.

BACKGROUND: Available seroprevalence studies of hepatitis B in Indian population has limitations. A community based door to door epidemiological study was conducted between December 1997 and January 1988 to look for the dynamics of hepatitis B exposure in a single village of West Bengal. METHODS: In all, 960 inhabitants out of 1261 (according to 91 census) in a village of Birbhum district in West Bengal were interviewed and their blood were tested by ELISA for HBV exposure. Odds ratio was calculated to estimate the relative risks for each potential factor facilitating virus transmission. RESULTS: Participation rate in the present study was 76.1%. Over all HBsAg carrier rate was found to be 5.3%. Only 2/51 (3.9%) carriers were HBeAg positive. Injection by glass syringe (odds ratio = 3.01), age < 20 years (odds ratio = 1.41) and male sex (odds ratio = 1.57) were significant risk factor. CONCLUSION: The results of this rural, predominantly poor, agrarian worker based community data reveals a fairly large reservoir of infection (5.3%). It is mainly built-up early in life. Injection practices need to be safer in addition to HBV vaccination to fight this menace.

Response to low-dose interferon in chronic liver disease due to hepatitis B virus infection.

BACKGROUND: Interferon is at present the only effective therapy for chronic hepatitis B virus (HBV) infection. Data regarding its efficacy in India are scant. The present study was undertaken to assess the efficacy of low-dose interferon in chronic liver disease due to HBV infection. METHODS: Twenty four patients with histologic evidence of chronic hepatitis with or without cirrhosis, and persistent elevation of serum aminotransferases and persistent positivity for HBsAg and HBeAg for more than six months, were included. Fourteen patients were treated with interferon alpha-2b, 3 million units thrice weekly for 16 weeks; ten patients who could not afford the drug were followed up as controls without specific therapy. Patients were examined weekly for the first 4 weeks, followed by two weekly for 12 weeks and then every two months. Blood tests for viral markers and liver biochemistry were done at 0, 4, 8, 12, 16 weeks and then at two-month intervals for at least one year after therapy. Patients who cleared HBeAg were followed up for 2.2 (1-4) years for HBsAg clearance. RESULTS: HBeAg clearance occurred in 9 patients (64%) in the interferon group, and in one control patient (p < 0.01). HBsAg clearance occurred in only one patient in the treatment group during follow up of mean 2.4 years. No patient in the control group cleared HBsAg. Patients having high ALT level at the beginning of treatment had significantly higher HBeAg clearance rate (7 of 7) than patients with low ALT levels (2 of 7; p < 0.05). CONCLUSION: Low-dose interferon therapy is effective in attaining HBeAg, but not HBsAg, clearance in chronic HBV infection.

Prevention of carbon tetrachloride-induced hepatic injury in mice by Picrorhiza kurrooa.

OBJECTIVE: Picrorhiza kurrooa (Pk) has been used in liver diseases in the Indian indigenous system of medicine. We undertook this study to determine whether Pk extract possesses hepatoprotective function and if so to determine its nature and mechanism. METHODS: Liver injury was induced in 16 mice by thrice-a-week injection of carbon tetrachloride (CCl4) for nine weeks. Eight of them were given daily feeding of Pk extract (12 mg/Kg) 10 days prior to CCl4 injection. Control mice (n = 6) were injected with olive oil for the same period. Serum markers of liver injury and histology of liver tissues were studied. Hepatic glutathione (GSH), total thiol (-SH), glucose 6-phosphate dehydrogenase (G6PD), catalase, lipid peroxidation and plasma membrane-bound Na+/K+ ATPase were also determined. RESULTS: CCl4 treatment resulted in significant elevation of serum ALT and AST. Liver GSH [6.3 (0.7) vs control 10.5 (1.1) micrograms/mg protein], -SH, G6PD, catalase and membrane-bound Na+/K+ AT-Pase [164.3 (23.2) vs control 358.4 (12.9) nmole pi released/min/mg protein] were significantly reduced. Significant increase of lipid peroxidation [3.0 (0.6) vs control 1.0 (0.3) nmole MDA/mg protein] and histologic changes characteristic of liver injury were also seen. Feeding of Pk extract in CCl4-treated mice caused significantly less alteration of serum ALT, AST, liver GSH [8.9 (0.7) micrograms/mg protein], -SH, G6PD, catalase and membrane-bound Na+/K+ ATPase [270.8 (21.3) nmole pi released/min/mg protein]. Histologic lesions of liver and lipid peroxidation [1.7 (0.4) nmole MDA/mg protein] were also significantly less in these animals. CONCLUSION: The extract of Pk appears to offer significant protection against liver damage by CCl4. It probably acts as free-radical scavenger and inhibitor of lipid peroxidation of liver plasma membrane.

Chronic arsenic toxicity in west Bengal--the worst calamity in the world.

Since 1983 large number of people are being encountered with arsenic toxicity due to drinking of arsenic contaminated water (0.05-3.2 mg/l) in 6 districts of West Bengal. Clinical and various laboratory investigations were carried out on 156 patients to ascertain the nature and degree of morbidity and mortality that occurred due to chronic arsenic toxicity. All the patients studied had typical rain drop like skin pigmentation (being inclusion criteria) while thickening of palm and sole were found in 65.5% patients. Other features included weakness (70%), gastro-intestinal symptoms (58.6%), involvement of respiratory system (57.08%) and nervous system (50.6%). Lung function tests showed restrictive lung disease in 53% (9/17) and combined obstructive and restrictive lung disease in 41% (7/17) of patients. Abnormal electromyography was found in 34.8% (10/29) and altered nerve conduction velocity in 34.8% (10/29) of cases. Enlargement of liver was found in 120 cases (76.9%) while splenomegaly in 31.4% cases. Liver function test showed elevated globulin level in 15.8% and alkaline phosphatase in 51.3%, alanine amino transferase (ALT) in 11.8% and aspartate amino transferase (AST) in 27.6% of cases. Evidence of portal hypertension was found in 33.3% patients. Liver biopsy reports of 45 patients showed non-cirrhotic portal fibrosis in 41, cirrhosis in 2 and normal histology in 2 cases. There was no correlation between the quantity of arsenic taken through water and the level of arsenic in hair, nail, liver tissues and the degree of fibrosis. There were 5 deaths of which one had skin cancer. The various non-cancer manifestations which were observed in these patients were much severe than those reported in similar cases in other parts of the world.

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.

Histological changes in hamster liver by ES antigen of Ascaris suum.

Polyacrylamide gel electrophoresis with SDS (PAGE-SDS) of the ES antigens of A. suum revealed several protein molecules which differed from those obtained in ES antigens of A. lumbricoides. Nature of liver damage caused by ES antigens of A. suum was studied in hamsters to find out the nature of damage and to compare with those caused by ES antigens of A. lumbricoides. Feeding of ES antigens of A. suum was carried out in 7 hamsters for 75 days. After such feeding gross hepatic damage was noticed. This was characterized by pericentrivenular degeneration and necrosis of liver parenchyma, the lesions being different and much more severe than those observed in hamster challenged by ES products of A. lumbricoides. The lesions appear to be immune mediated.

Hepatic lesions caused by excretory and secretory products of Ascaris lumbricoides in golden hamster.

OBJECTIVE: To ascertain the role of excretory and secretory (ES) products of Ascaris lumbricoides in liver damage. METHODS: The ES products of A lumbricoides were collected in vitro and their SDS-PAGE analysis was done. Feeding and subcutaneous injection of ES products were done in hamsters. Estimation of serum proteins, alkaline phosphatase and alanine aminotransferase and histology of liver were carried out. Control animal experiments were done concurrently. RESULTS: The ES products of A lumbricoides contained several proteins ranging in molecular weight from 14 to 205 Kd. Prolonged feeding of ES products caused elevation of ALT and amyloid deposition in the liver, whereas short term feeding or subcutaneous challenge caused focal cell necrosis and granuloma formation in the liver. CONCLUSION: ES products of A lumbricoides can produce liver damage.