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Rakesh Aggarwal

Publications and source records attributed to Rakesh Aggarwal.

33 records · Page 2Linked to original sources
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Hepatitis E virus is responsible for decompensation of chronic liver disease in an endemic region.

BACKGROUND: Hepatitis A virus infection in patients with previously stable chronic liver disease is associated with liver decompensation. Whether infection with hepatitis E virus (HEV) also does so is not known. METHODS: We studied 32 patients with decompensated liver disease and definite evidence of underlying cirrhosis for evidence of recent HEV infection. RESULTS: Of 32 patients, 14 (44%) had detectable IgM anti-HEV in their serum. In comparison, only 3 of 48 (6%) patients with stable cirrhosis and no recent decompensation had such antibodies (p<0.0001). Of the 14 patients with evidence of recent HEV infection, 11 had history of prodrome. The etiology of cirrhosis in these patients was: hepatitis B 6, hepatitis C 2, both hepatitis B and C 2, Wilson's disease 1, autoimmune 1 and cryptogenic 2. Two of these 14 patients died. Twelve patients survived, as compared to 9 of 18 patients without evidence of recent HEV infection (p<0.01). CONCLUSION: HEV infection is a frequent cause of decompensation in patients with liver cirrhosis in HEV-endemic regions.

Adolescent↗
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Etiological spectrum of sporadic malabsorption syndrome in northern Indian adults at a tertiary hospital.

BACKGROUND: The etiology of malabsorption syndrome (MAS) may differ in different geographical regions. Limited data are available on the etiological spectrum of MAS among Indian adults. METHODS: Ninety-nine consecutive adult patients with MAS (urine d-xylose <1 g/5 g/5 h with or without increased fecal fat (> or =7 g/24 h) were evaluated for cause of MAS using standard criteria. Past medical records were examined to know the nature of treatment received. RESULTS: The etiology of MAS was: tropical sprue 39, celiac disease 9, Crohn's disease 9, giardiasis 8, small intestinal bacterial overgrowth in absence of another cause of MAS 8, panhypogammaglobulinemia 2 (one with strongyloidiasis), intestinal lymphangiectasia 1, intestinal tuberculosis 4, idiopathic 15, acquired immunodeficiency syndrome 2, and amyloidosis 2. Twenty-eight patients had received anti-tubercular treatment earlier. CONCLUSIONS: Tropical sprue, celiac disease and Crohn's disease are common causes of MAS in Indian adults. Inappropriate anti-tubercular treatment is common in them and needs to be discouraged.

Adult↗
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Hepatitis B virus genotype A is more often associated with severe liver disease in northern India than is genotype D.

BACKGROUND: The clinical outcome of chronic hepatitis B may depend on hepatitis B virus (HBV) genotype. Data from India on this aspect are limited and contradictory. We studied the frequency of HBV genotypes and their clinical significance. METHODS: Stored sera from patients with chronic HBV infection were tested for HBV genotype using PCR-RFLP. Clinical data, and biochemical and serological parameters were retrieved from medical records; patients were classified as having chronic hepatitis or cirrhosis. RESULTS: Of 70 patients studied (mean age [SD] 38.4 [17.0] years; 63 men; ALT 140 [177] U/L), 32 had chronic hepatitis and 38 had cirrhosis. HBeAg was positive in 50/67 (75%), and anti-HBe in 12/66 (18%). Genotype A was the commonest (37; 53%), followed by D (32; 46%) and C (1; 1%). Patients with genotype A more often had ALT elevation exceeding 1.5 times normal (30/37 [81%] than those with genotype D (18/31 [58%]; p< 0.05). They also more often had positive HBeAg (32/37; 86%) and negative anti-HBe (33/36; 92%) than those with genotype D (18/29 [62%] and 21/29 [72%], respectively; p< 0.05 each). Of 37 patients with genotype A, 23 (62%) had cirrhosis and 14 (38%) had chronic hepatitis; of 32 patients with genotype D, 15 (47%) had cirrhosis and 17 (53%) had chronic hepatitis (p=ns). In the subgroup aged> 25 years, genotype A patients more often had cirrhosis than those with genotype D (23/28 [82%] vs 13/23 [57%]; p < 0.05). CONCLUSION: HBV genotypes A and D were the commonest in our population. Genotype A was more often associated with ALT elevation, HBeAg positivity, absence of anti-HBe and, among those aged 25 years and above, cirrhosis of liver, than was genotype D.

Adult↗
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Profile of liver involvement in dengue virus infection.

BACKGROUND: Data are scarce on liver involvement in adult patients with dengue virus infection. METHODS: During a recent outbreak of dengue fever in Uttar Pradesh, India, we looked for evidence of liver dysfunction among patients with dengue fever. RESULTS: A total of 45 patients with dengue fever (age 7-65 [median 33] years; 29 men; 39 adults) were studied, including 23 with uncomplicated dengue fever, 15 with dengue haemorrhagic fever and 7 with dengue shock syndrome. The median platelet count was 34 x 10(9)/L (9-99 x 10(9)). Seven patients (15%) had jaundice, 11 (24%) hepatomegaly and 9 clinically detectable ascites; none had splenomegaly. Twelve patients (30%) had hyperbilirubinaemia. Serum alanine and aspartate aminotransferase activities were elevated in 43 patients (96%) each; 5-fold elevated levels were more frequent in severe disease. Hypoalbuminaemia was found in 31/41 patients (76%). Seven patients died, including 2 with acute liver failure. CONCLUSION: Our data show that liver injury is common in adult patients with dengue infection. Further studies are needed to determine the mechanism of liver injury in this disease.

Adolescent↗
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Safety and efficacy of an indigenous human recombinant interferon alpha 2b (Shanferon) in patients with chronic hepatitis B.

Interferon treatment is the established option for the treatment of patients with chronic hepatitis B without decompensated liver disease. However, such treatment is expensive. We report here our data of a multi-center, open-label trial of the use of an indigenously produced interferon in the treatment of chronic HBeAg-positive chronic hepatitis B. Adult patients with chronic HBeAg-positive hepatitis B with elevated serum transaminase activity and positive serum HBV DNA test were treated with 5 MU/day of an indigenously produced interferon (Shanferon; Shantha Biotechnics, Hyderabad, India) for 4 months, and were then followed up for 6 months. Of the 39 patients enrolled, 36 completed the treatment and 33 completed the post-treatment follow-up. Of the 33 patients who completed the study, end-of-treatment biochemical and virological responses were observed in 10 (30%) and 5 (15%) respectively. Sustained biochemical and virological responses were observed in 15 (45%) and 7 (21%), patients respectively. Adverse effects led to the discontinuation of treatment in only one patient. Our data suggest that safety and efficacy of the indigenously produced interferon were similar to those previously reported results with interferon from other sources.

Adolescent↗
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Low frequency of factor V Leiden and prothrombin G20210A mutations in patients with hepatic venous outflow tract obstruction in northern India: a case-control study.

BACKGROUND: Factor V Leiden (FVL) and prothrombin gene (G20210A) mutations are known to be associated with venous thromboembolism. Several studies have shown an association of these mutations with hepatic venous outflow tract obstruction (HVOTO). We studied the prevalence of these mutations among patients with HVOTO in northern India in comparison with healthy population. METHODS: Genomic DNA from patients with HVOTO and healthy controls was analyzed for the presence of FVL and prothrombin gene G20210A mutations, using PCR and restriction-fragment length polymorphism. RESULTS: Fifty-nine patients with HVOTO (age 5-69 years, median 27; 39 male) and 49 unrelated healthy controls from the same geographic region were studied. Of the 59 patients, 19 had a block in the hepatic vein, 7 in inferior vena cava, and 33 had mixed block. Presentation was with acute thrombosis in 9 patients and with long-standing obstruction in 50 patients. Among 49 controls, heterozygous and homozygous FVL mutations were observed in 2 and 0 subjects, respectively, with an allele frequency of 2% (2 of 98). In comparison, among 59 patients with HVOTO, four had heterozygous and none had homozygous FVL mutation, with an allele frequency of 3.4% (p=ns versus controls). The G20210A prothrombin gene mutation was not found in any of the patients or controls. CONCLUSION: FVL and prothrombin G20210A mutations appear to have no role in the pathogenesis of HVOTO in our patients with Budd-Chiari syndrome, consisting largely of those with long-standing obstruction of the inferior vena cava.

Adolescent↗
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Superior sagittal sinus thrombosis and Budd-Chiari syndrome due to paroxysmal nocturnal hemoglobinuria managed with transjugular intrahepatic portosystemic shunt: a case report.

BACKGROUND: Paroxysmal nocturnal hemoglobinuria (PNH), caused by somatic mutation of hematopoietic cells, is associated with complement-mediated hemolysis and a hypercoagulable state. Thrombotic complications in this disease are associated with reduced survival. We report a patient with PNH complicated by intracranial venous thrombosis and Budd-Chiari syndrome, who was managed with transjugular intrahepatic portosystemic shunt. CASE PRESENTATION: A 26-year-old man presented with thrombosis of the superior sagittal and right sigmoid sinuses. Initial investigations did not reveal any underlying cause. Nine months later, he developed hepatic venous thrombosis. At this time, Ham test was positive. Flow cytometry confirmed the diagnosis of PNH. The patient was treated with transjugular intrahepatic portosystemic shunt; one episode of stent blockage one month later was managed successfully with balloon dilatation and restenting. CONCLUSION: PNH should be considered in patients with unexplained venous thrombosis. Thrombosis in these patients needs to be managed with prolonged anticoagulation. For Budd-Chiari syndrome in patients with underlying PNH, transjugular intrahepatic portosystemic shunt may be a good option but caution is needed to prevent stent occlusion.

Adult↗
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HFE, hepcidin and ferroportin gene mutations are not present in Indian patients with primary haemochromatosis.

BACKGROUND: Primary haemochromatosis is characterized by iron overload in the body tissues. It is common in populations of northern European descent. In such populations, 85%-90% of patients with this disease have a C282Y mutation in the HFE gene. In India, the disease is uncommon and the genetic defects associated with it are unknown. We therefore looked for mutations in the HFE and other genes involved in iron metabolism in Indian patients with primary haemochromatosis. METHODS: Five patients (including a brother-sister pair) with primary haemochromatosis diagnosed on clinical, biochemical and histological findings were studied. Genomic DNA was analysed by sequencing for the presence of mutations in all the 6 exons of the HFE gene and for previously described mutations in genes encoding hepcidin antimicrobial peptide and ferroportin. RESULTS: No patient had the C282Y mutation. One had homozygous H63D mutation. No other mutation was found in any HFE exon. Two previously reported splice site mutations in the HFE gene (IVS3 + 1 G/T and IVS5+1 G/A) were not detected. Four of the 5 patients had an HFE splice site mutation (IVS2 + 4 T/C; homozygous 2, heterozygous 2); however, this change was as frequent in 29 healthy subjects (homozygous 9, heterozygous 7), and was present in only 1 of the sibling pair patients, indicating that this represented a polymorphism. No patient had any of the previously described mutations in the genes for hepcidin and ferroportin. CONCLUSION: Our patients with primary haemochromatosis lacked mutations in the HFE, hepcidin and ferroportin genes. Further genetic analysis may help identify novel mutations responsible for primary haemochromatosis in these patients.

Adult↗
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Antibody testing in Indian children with celiac disease.

BACKGROUND: We prospectively evaluated the usefulness of IgA tissue transglutaminase antibodies (IgA tTG) in the initial diagnosis of celiac disease (CD) and compared its diagnostic potential with that of IgA anti-endomysial antibodies (IgA EMA) and anti-IgA and IgG gliadin antibodies (AGA and AGG, respectively). METHODS: Sera of 23 untreated children fulfilling the revised ESPGHAN criteria for diagnosis of CD (Group I; mean age 10.8 y); 19 disease controls (Group II; mean age 8.5 y) presenting with chronic diarrhea, short stature or both; and 22 healthy children (Group III; mean age 8.8 y) were studied. These were tested in a blinded manner for AGA, AGG, IgA tTG (guinea pig as antigen) and IgA EMA. RESULTS: In Group I, IgA EMA was positive in 19, IgA tTG in 17, AGA in 14 and AGG in 17 patients. In Group II, these tests were positive in 1, 0, 2 and 14 patients, respectively and in Group III, in 0, 0, 0 and 1 child, respectively. Analyzing data from Group I and II, IgA EMA, IgA tTG, AGA and AGG had sensitivity rates of 83%, 74%, 61% and 74%, respectively; the specificity rates were 95%, 100%, 89% and 26%; positive predictive values were 95%, 100%, 88% and 55% and negative predictive values were 82%, 74%, 65% and 45%, respectively. CONCLUSION: IgA tTG is useful for the diagnosis of CD, with sensitivity and specificity rates comparable to those of EMA and this test is well suited for use in tropical countries like India.

Adolescent↗
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Factor V Leiden and prothrombin gene G20210A mutations are uncommon in portal vein thrombosis in India.

BACKGROUND: Extra-hepatic portal vein obstruction due to portal vein thrombosis (PVT) is an important cause of portal hypertension in several regions including India. The cause of thrombosis in these patients remains unclear. We studied the frequency of mutations in genes for coagulation factors V and II (prothrombin) in 61 Indian patients with PVT and 49 healthy control subjects. METHODS: The presence of factor V Leiden mutation and of G20210A prothrombin gene mutation was determined using polymerase chain reaction followed by restriction fragment length polymorphism. Chi-squared test was used to compare patients and controls. RESULTS: Of the 61 patients (median age 11 years; 47 male) studied, 49 were children. One of 61 (1.6%) patients with PVT was heterozygous for factor V Leiden mutation and none had the G20210 prothrombin gene mutation. The frequencies of these mutations were not different from those in control subjects (2/49 and 0/46, respectively). CONCLUSION: Factor V Leiden and G20210 prothrombin gene mutations are infrequent in Indian patients with PVT. Thus, these mutations are unlikely to be responsible for PVT in the Indian population.

Adolescent↗