Right ventricular thickness as predictor of global myocardial performance in systemic sclerosis: A Doppler tissue imaging study.

BACKGROUND: Cardiopulmonary involvement in systemic sclerosis (SSc) is a poor prognostic factor, due to pulmonary hypertension and right ventricular dysfunction. We assessed the echocardiographic parameters of right ventricular (RV) function in SSc and correlated echocardiographic findings to clinical features of the disease. METHODS: Thirty patients with SSc (cases) and 30 healthy, age-matched subjects (controls) were studied. Echocardiography, including tissue Doppler imaging, was used to evaluate cardiac function. RESULTS: Pulmonary hypertension could be documented in only 5 cases by Doppler echo, using Bernoulli principle. RV diastolic function was significantly deranged in cases. RV systolic function and left ventricle (LV) diastolic function were also significantly deranged in the cases. RV thickness was increased in patients with SSc. There were no significant differences in the echocardiographic variables between diffuse and limited subtypes of SSc. Myocardial performance index (MPI) of both ventricles were increased in cases. We could demonstrate RV thickness as the single most important predictor of MPI of both ventricles with sensitivity of 82% and specificity of 72% for RV-MPI and 63% for LV-MPI. Diastolic function was not found to be affected by disease duration or Rodnan skin score. CONCLUSION: Patients with SSc exhibit abnormal RV and LV diastolic functions as well as abnormal RV systolic function. RV wall thickness was found to be simple and the single best predictor of global myocardial performance. RV dysfunction may be a response to intermittent pulmonary arterial hypertension, lung parenchymal involvement, or secondary to LV diastolic dysfunction in SSc.

Causes of mortality among inpatients with systemic lupus erythematosus in a tertiary care hospital in North India over a 10-year period.

INTRODUCTION: Systemic lupus erythematosus (SLE) is a systemic autoimmune disorder with significant morbidity and mortality. The present study was undertaken to identify the causes of in-hospital mortality of patients with SLE. METHODS: This was a retrospective study. The hospital records of patients with SLE who died between 1998 and 2007 were reviewed. Demographic details, organ involvement, treatment received and evidence of infection were recorded. Disease activity was calculated using the SLE Disease Activity Index. The cause of death of each patient was determined and this information was classified into either deaths caused primarily due to SLE, deaths caused due to infection or those that were multi-factorial. RESULTS: Seventeen patients with SLE who were diagnosed according to the revised American College of Rheumatology criteria died between 1998 and 2007. Fifteen of these patients were female and two were male. The median age was 25 years. The average duration of hospital stay was 10.29 days. Seven patients (41%) died of active SLE (three from pulmonary hemorrhage, two had renal failure, one had myocarditis and one had severe thrombocytopenia with upper gastrointestinal bleed), three patients (18%) died from infections (one contracted Staphylococcal septicemia, another contracted tuberculous meningitis and the third patient had Pseudomonas septicemia) and in seven patients (41%) the etiology was multi-factorial (these showed both active SLE and evidence of infection). In total 10 patients had evidence of infection, two of these were community-acquired and the rest were hospital-acquired. CONCLUSION: Active SLE and/or infection are the major causes of death in hospitalised patients with SLE. To reduce patient mortality improvements in supportive care for patients with active SLE and measures to prevent hospital-acquired infections are required.

Profile of presentation of human immunodeficiency virus infection in north India, 2003-2007.

BACKGROUND: Clinico-epidemiological profile of the Human immunodeficiency virus (HIV) epidemic in India is varied and depends on multitude of factors including geographic location. We analyzed the characteristics of HIV-infected patients attending our Immunodeficiency Clinic to determine any changes in their profile over five years. SETTINGS AND DESIGN: A retrospective observational study. MATERIALS AND METHODS: The study sample included all patients with HIV infection from January 1, 2003 to December 31, 2007. Diagnosis of HIV was made according to National AIDS Control Organization guidelines. RESULTS: Of 3 067 HIV-infected patients, 1 887 (61.5%) were male and 1 180 (38.5%) were female patients. Mean age of patients was 35.1 ± 9.0 years. Majority (91.8%) of patients were in the age group of 15 to 49 years. Progressively increasing proportion of female patients was noted from year 2004 onward. Median CD4 count at presentation in year 2003 was 197/µl (Interquartile range [IQR] = 82.5-373) while in year 2007 it was 186.5/µl (IQR = 86.3-336.8). Mean CD4 count of male patients was 203.7 ± 169.4/µl, significantly lower as compared with female patients, which was 284.8 ± 223.3/µl (P value ≤0.05). Every year, substantial proportions of patients presenting to clinic had CD4 count<200/µl indicating advanced disease. Predominant route of transmission was heterosexual in 2 507 (81.7%) patients. Tuberculosis and oropharyngeal candidiasis were the most common opportunistic infections (OIs). Cryptococcal meningitis was the most common central nervous infection. Our patients had comparatively lower median CD4 counts at the time of presentation with various OIs. CONCLUSIONS: Patients had advanced stage of HIV infection at the time of presentation throughout five years. Females presented earlier during the course of HIV infection. There is need for early screening and increasing awareness in healthcare providers to make a diagnosis of HIV much sooner.

The -137G/C polymorphism of interleukin 18 promoter and risk of HIV-1 infection and its progression to AIDS.

A growing body of evidence suggests that host genetic factors play an important role both in susceptibility to human immunodeficiency virus 1 (HIV-1) infection and in progression to AIDS. Interleukin 18 (IL-18) is a pleiotropic proinflammatory cytokine that serves as an important regulator of immune responses. It plays a key role in induction of both Th1 and Th2 cytokines and, thereby, modulates their immune responses. Single nucleotide polymorphisms in the IL-18 gene promoter region may lead to an altered transcriptional activity and IL-18 production, and so this may account for individuals' variation to the risk of HIV-1 infection. With this perspective, the -137G/C polymorphism in the promoter region of the IL-18 gene was studied in 500 patients with HIV-1/AIDS and an equal number of sex and age matched healthy controls using sequence specific polymerase chain reaction analysis. We did not observe any significant association of the heterozygous G/C genotype with the risk of HIV-1-infection/AIDS. However, statistically significant associations of the G allele and homozygous G/G genotype of -137 G/C polymorphism of IL-18 promoter with increased risk of HIV-1/AIDS were identified. The data of the present study suggest that IL-18 -137 G allele and G/G genotype seem to be involved in the pathogenesis of HIV-1 infection among North Indians.

IL-18 Gene Promoter Region 607C/A Polymorphism in HIV-1 Infected North Indian Population.

Several host genetic factors play an important role in susceptibility to human immunodeficiency virus type 1 (HIV-1) infection and in its progression to acquired immune deficiency syndrome (AIDS). The interleukin-18 (IL-18) is a multifunctional proinflammatory cytokine that regulates immune responses and plays a pathogenic role in HIV-1 infection by enhancing viral replication. Single nucleotide polymorphisms (SNPs) in the IL-18 gene promoter region may lead to altered transcriptional activity and IL-18 production, and may account for variation in the risk of HIV-1 infection. We have investigated the association between IL-18 promoter polymorphism -607C>A and HIV-1 infection through a case-control study of 500 patients with HIV-1/AIDS and an equal number of age and sex matched controls in a north Indian population. Genotyping using sequence specific primer-polymerase chain reaction (SSP-PCR) showed a statistically significant reduced risk of HIV-1 infection for the A>A genotype [odds ratio (OR) = 0.57, 95% confidence interval (95% CI) = 0.33-0.98, p = 0.040], but not for the C>A genotype (OR = 0.87, 95% CI = 0.66-1.14, p = 0.321). We concluded that the -607A allele of the IL-18 gene promoter polymorphism may play a protective role against the progression of HIV-1 infection in this population.

CD4 cell count recovery in HIV/TB co-infected patients versus TB uninfected HIV patients.

BACKGROUND: There is lack of data comparing the improvement in CD4 count following antitubercular (ATT) and antiretroviral therapy (ART) in patients presenting with Human Immunodeficiency Virus/Tuberculosis (HIV/TB) dual infection compared with CD4 matched cohort of TB uninfected HIV patients initiated on ART. We sought to test the hypothesis; TB additionally contributes to reduction in CD4 count in HIV/TB co-infected patients and this would result in greater improvement in count following treatment compared with CD4 matched TB uninfected individuals. MATERIALS AND METHODS: In a retrospective cohort study design we studied the change in CD4 cell counts in two groups of patients - those with CD4 cell count >100 cells / mm 3 (Group 1) and <100/mm 3 (Group 2) at presentation. In each group the change in CD4 cell count in dually infected patients following six-month ATT and ART was compared to cohorts of CD4 matched TB uninfected patients initiated on ART. RESULTS: In Group 1 (52 patients) dually infected subjects' CD4 count improved from 150 cells/ mm 3 to 345 cells/mm 3 (P=0.001). In the control TB uninfected patients, the change was from 159 cells/mm 3 to 317 cells/mm 3 (P=0.001). Additional improvement in dually infected patients compared to the control group was not statistically significant (P=0.24). In Group 2 (65 patients) dually infected subjects count improved from 49 cells/mm3 to 249 cells/mm 3 (P=0.001) where as in control TB uninfected patients improvement was from 50 cells/ mm 3 to 205 cells/mm 3 (P=0.001), there being statistically significant additional improvement in dually infected subjects (P=0.01). CONCLUSION: Greater increment in CD4 counts with ATT and ART in dually infected patients suggests that TB additionally influences the reduction of CD4 counts in HIV patients.

The influence of variations in the DNA repair (XRCC1) gene on HIV-1/AIDS among Indian population.

Genetic polymorphisms in DNA repair genes may influence individual variations in the DNA repair capacity. Polymorphisms in the XRCC1 gene that cause amino acid substitutions may impair the interaction of its proteins (XRCC1) with the other enzymatic proteins and consequently alter DNA repair function, which may be associated with the risk of HIV-1/AIDS disease. In this study, we aimed to determine the frequency of polymorphisms in XRCC1 codon 399 in a sample of Indian population with HIV-1/AIDS to evaluate its association with the disease. Polymerase chain reaction and restriction fragment length polymorphism were used to analyse XRCC1 Arg399Gln polymorphisms in 300 positively diagnosed cases with HIV-1/AIDS and an equal number of negatively diagnosed controls of the matched age. The XRCC1 homozygous variant genotype Gln399Gln was associated with an increased risk of HIV-1/AIDS disease (OR = 1.8, 95% CI 1.10-2.94), while no association was found with the Arg399Gln genotype. Polymorphisms in the XRCC1 homozygous variant genotype for the 399Gln allele were associated with the risk of HIV-1/AIDS disease in a sample of North Indian population.

Immunophenotypic and intracellular cytokine profile of Indian patients with tuberculosis with and without human immunodeficiency virus co-infection.

BACKGROUND: Tuberculosis (TB) occurs in more than 50% of human immunodeficiency virus (HIV) infected Indian patients. This study was carried out to determine the immunophenotypic and intracellular cytokine profile of patients with HIV-TB co-infection. PATIENTS AND METHODS: Fifteen patients with HIV-TB co-infection and 15 each with TB alone and healthy individuals were studied. Immunophenotypic analysis and intracellular cytokines were measured using appropriate antibodies on a flowcytometer. RESULTS: Percentage of CD3+ did not differ significantly in the three groups. The ratio of CD4+ : CD8+ was reversed among patients with TB and HIV-TB. CD19+ and CD25+ were present on fewer cells of healthy individuals but this was not statistically significant. Significantly higher percentage of cells of patients with TB and HIV-TB were CD69 positive. Interferon-gamma (INF-gamma) and tumour necrosis factor-alpha (TNF-alpha) levels are significantly reduced in the CD4+ cells of patients with HIV-TB when compared with those with TB and healthy individuals. In CD8+ cells of patients with HIV-TB, levels of TNF-alpha are higher when compared with the other two groups. Interleukin-2 (IL-2) producing cells were not significantly different in any of the above subsets. Monocytes in individuals with HIV-TB had significantly higher interleukin-6 (IL-6) and TNF-alpha. CONCLUSIONS: T-helper cells among patients with HIV-TB have significantly lower cytokine production. T-suppressor cells and monocytes produce more TNF-alpha. These findings may be significant in view of recent attempts to treat HIV-TB coinfected patients with anti-TNF therapy.

Relationship between T lymphocyte subsets and cortisol in systemic lupus erythematosus.

BACKGROUND: Systemic Lupus Erythematosus (SLE) is a complex chronic immunological disease characterized by increased B cell activity and altered T cell function. OBJECTIVE: To investigate relationship between T lymphocyte subsets and cortisol with the disease activity of systemic lupus erythematosus patients in North India. MATERIALS AND METHODS: The percentage of CD4(+) and CD8(+) T cells in the lymphocyte of SLE patients and healthy controls were determined by flow cytometry. Serum cortisol of SLE patients and healthy controls was determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: A significant decrease in the percentage of CD4(+) T cells and increase in the percentage of CD8(+) T cells were found in patients with SLE compared to the healthy controls. Decrease in the ratio of CD4(+)/CD8(+) T cell and low level of serum cortisol were found in the patients with SLE. The ratio of CD4(+)/CD8(+) T cell was inversely correlated with systemic lupus erythematosus disease activity index (SLEDAI) score and erythrocyte sedimentation rate (ESR). A positive correlation was observed between CD8(+) T cells and SLEDAI score. Furthermore, CD8(+) T cells were positively correlated with ESR in the patients with SLE. CONCLUSION: The results showed that low level of cortisol and high percentage of CD8(+) T cells in the lymphocytes could be actively involved in the pathogenesis of SLE.

Relapsing polychondritis in North India: a report of 10 patients.

OBJECTIVE: Relapsing polychondritis (RP) is a rare autoimmune disorder characterized by recurrent episodes of inflammation and destruction of cartilaginous tissues. We describe the outcome of 10 patients followed up at the Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, over the past 10 years. METHODS: All the patients fulfilling the diagnostic criteria suggested by McAdam et al (Medicine (Baltimore) 1976;55:193-215) and modified by Damiani and Levine (Laryngoscope 1979;89;929-46) were included in the study. Detailed clinical features, investigations, treatment given, and outcome were recorded on file. RESULTS: Six women and four men, mean age 48.1 years (range 26-65 years), met the criteria for diagnosis. The mean duration of symptoms, before diagnosis, was 27 months (range 1-72 months). Clinical features included auricular chondritis (100%), arthritis (80%), fever (50%), constitutional symptoms (50%), eye involvement (50%), hearing loss (40%), collapsed bridge of nose (30%), laryngotracheal involvement (20%), aortic dilatation (10%), and nephrotic syndrome (10%). Two patients had the MAGIC (mouth and genital ulcers with inflamed cartilage) syndrome. The number of episodes of cartilaginous inflammation varied from one to eight. Treatment included oral prednisolone (n = 9), intermittent 'pulse' cyclophosphamide (n = 2), and azathioprine (n = 2). One patient required tracheostomy and died later. The others are doing well. Mean duration of follow-up was 35.5 months (range 1-79 months). CONCLUSIONS: The diagnosis of this potentially lethal condition is frequently delayed. Our series suggests that clinical manifestations of RP are similar in Caucasian, Oriental, and Asian populations. Laryngotracheal involvement was seen less frequently in our patients.

Successful treatment of severe gastrointestinal involvement in adult-onset Henoch-Schönlein purpura.

Henoch-Schönlein purpura is a small vessel vasculitis which is uncommon in adults. The presentations of adult-onset disease are different from those seen in childhood. The commonly-recognised serious gastrointestinal complications of childhood are less well-documented in adults. We report three cases of adult-onset Henoch-Schönlein purpura with severe gastrointestinal involvement. All were men, aged 22, 35 and 42 years, respectively. Two of these patients had evidence of mesenteric ischaemia on computed tomography of the abdomen. All three patients were successfully treated with steroids.

Polymorphism in the CCR5 gene promoter and HIV-1 infection in North Indians.

The clinical course and outcome of human immunodeficiency virus-1 (HIV-1) infection are highly variable among individuals. CCR5 is the primary coreceptor that mediates entry of HIV-1 (R5) into permissive host cells. In this study, five SNPs (59029G/A, 59353T/C, 59356C/T, 59402A/G, and 59653C/T) in the promoter region and a deletion of 32 bp (Delta32) in the CCR5 gene were evaluated in 180 chronically HIV-1-infected North Indians. The study showed the following: (1) the protective CCR5 Delta32 allele was absent; (2) the frequency of CCR5*59402A allele in the HIV-infected people (66.4%) was higher than in healthy subjects (57.1%, p = 0.027) and in the CDC stage C patients (76%) versus stages A and B patients together (60%; p = 0.002); (3) homozygous CCR5*59402 AA genotype was significantly increased in the seropositive subjects (46.1%) compared with healthy control subjects (30.2%; p = 0.008) and in the CDC stage C patients (59.2%) compared with stage A and B subjects (37.6%, p = 0.007); and (4) an increased frequency of homozygous ACCAC haplotype was present in the seropositive stage C patients (32.4%) versus 15.6% in patients in stages A plus B (p = 0.013). These observations suggest an association of CCR5*59402A with increased likelihood of acquisition of HIV-1 and development of AIDS in the Asian Indian population. Further studies are required to confirm these findings and understand the effect of CCR5 polymorphisms on the outcome of HIV-1 infection.

Adherence to generic reverse transcriptase inhibitor-based antiretroviral medication at a Tertiary Center in North India.

At least 95% adherence to medications is required for sustained response to antiretroviral therapy (ART). In resource constraint restrained settings it is not possible to use electronic methods to determine adherence. We determined adherence during the previous 4 weeks by the recall method in 200 patients (138 males) receiving generic triple drug reverse transcriptase inhibitor-based antiretroviral medications. They were administered a uniform questionnaire to determine the number of time they forgot or were unable to take their medications and the reasons thereof. One hundred and fifty received two and 50 took three pills daily. One hundred and forty-seven did not miss any dose. Fifty-three (26.5%) missed at least one dose during the preceding 4 weeks. Thirty-one took treatment on and off. Seven missed a dose in the preceding 3 days, nine more between the last 3 and 7 days, and six from 1 to 4 weeks. The major reasons for non-adherence were financial constraints, forgetting to take the medication, drug toxicity, lack of access to the drug, fear of getting immune to the benefit of the drug, and to avoid adverse effects. Non-adherence in 26.5% individuals could be an additional factor that can increase the risk of drug resistance.

Chemokines and chemokine receptors in HIV infection: role in pathogenesis and therapeutics.

Chemokines are known to function as regulatory molecules in leukocyte maturation, traffic, homing of lymphocytes and in the development of lymphoid tissues. Besides these functions in the immune system, certain chemokines and their receptors are involved in HIV pathogenesis. In order to infect a target cell, the HIV envelope glycoprotein gp120 has to interact with the cellular receptor CD-4 and co-receptor, CC or CXC chemokine receptors. Genetic findings have yielded major insights into the in vivo roles of individual co-receptors and their ligands in providing resistance to HIV infection. Mutations in chemokine receptor genes are associated with protection against HIV infections and also involved in delayed progression to AIDS in infected individuals. Blocking of chemokine receptors interrupts HIV infection in vitro and this offers new options for therapeutic strategies. Approaches have been made to study the CCR-5 inhibitors as antiviral therapies and possibly as components of a topical microbicide to prevent HIV-1 sexual transmission. Immune strategies aimed at generating anti-CCR-5 antibodies at the level of the genital mucosa might be feasible and represent a strategy to induce mucosal HIV- protective immunity. It also remains to be seen how these types of agents will act in synergy with existing HIV-1 targeted anti viral or those currently in developments. Beyond providing new perspectives in fundamental aspects of the HIV-1 transmission and pathogenesis, chemokines and their receptors suggest new areas for developing novel therapeutic and preventive strategies against HIV infections. Studies in this review were identified through a search for relevant literature in the pubmed database of the national library of medicine. In this review, some developments in chemokine research with particular focus on their roles in HIV pathogenesis, resistance and therapeutic applications have been discussed.

Prevention of opportunistic infections in HIV infection by pentoxiphylline.

BACKGROUND & OBJECTIVES: Levels of tumour necrosis factor (TNF) are increased in patients with HIV infection leading to increased apoptosis and reduced CD4 cell life. Pentoxiphylline is a TNF inhibitor with properties that might make it useful for the treatment of HIV infection. These include improved cell mediated immunity and inhibition of viral replication. We carried out this study to determine the therapeutic utility of pentoxiphylline in improving constitutional manifestations, preventing opportunistic infections and sustaining CD4 counts among asymptomatic HIV infected individuals (i.e., those with no opportunistic infection). METHODS: Individuals with HIV infection who were over 18 yr of age and free of opportunistic infections were recruited in the study and followed up 4 weekly. CD4 counts were measured using a flowcytometer using anti-human CD4 intervals. Pentoxiphylline was prescribed in a dose of 400 mg thrice daily. RESULTS: Thirty three (18 males) patients with HIV infection were studied. During their follow up (mean 12.5 +/- 5.6 months) one patient each developed cryptococcal meningitis and fibrocavitary tuberculosis. Weight increased from 51.3 +/- 7.4 kg at baseline to 55.3 +/- 7.4 kg (P<0.05). Malaise, fatigue and appetite improved in all those with these complaints, except the two with opportunistic infections. Mean CD4 counts were 184 +/- 36.4/microl at baseline and increased to 210 +/- 28.6/microl3 at four weeks (P<0.05). The patients had stable CD4 counts over the follow up period since then, i.e., within 25 per cent of the previous levels. INTERPRETATION & CONCLUSION: Pentoxiphylline therapy in HIV infected individuals, who were free of opportunistic infections, improved their body weight, minimized opportunistic infections, increased and sustained CD4 counts. Given the low cost of the drug it could be recommended for the use in individuals who are at a high risk of developing opportunistic infections.

Caspase 1 and caspase 8 in HIV infected patients with and without tuberculosis.

BACKGROUND: Caspase 8 is involved in apoptosis mediated by Fas and p55 tumor necrosis factor receptor ligation in HIV infection. Apoptosis is partially mediated by interleukin-1beta-converting enzyme (caspase-1). AIMS: We determined apoptosis, using caspase-1 and caspase-8, among patients with HIV infection, with and without tuberculosis (TB), those with TB alone and healthy individuals. SETTING AND DESIGN: Cross-sectional analysis of caspase-1 and caspase-8 among patients with HIV infection, with and without TB, those with TB alone and healthy individuals. MATERIALS AND METHODS: Nineteen HIV infected patients with TB (HIV+/TB+) and 20 with HIV infection without TB (HIV+/TB-) were studied. Fifteen individuals with TB alone were disease controls (HIV-/TB+) and 20 were healthy controls (HIV-/TB-). Caspases were measured by single-step ELISA using commercially available monoclonal antibodies. STATISTICAL ANALYSIS: Two-way ANOVA and Pearson's correlation coefficient. RESULTS: Mean CD4 counts of HIV+/TB+ were lower than HIV+/TB- (p<0.05). OD value of caspase 1 in HIV+/TB+ was 0.295+0.05, while that in HIV+/TB- it was 0.302+0.18. It was 0.293+0.07 in HIV-/TB+ and in HIV-/TB- the values were 0.287+0.06. OD value of caspase 8 in HIV+/TB+ was 0.307+ 0.07, lower than HIV+/TB- (0.927+0.25). It was 0.008+0.03 in HIV-/TB+ and in HIV-/TB-, 0.074+0.004. Values of caspase 8 in patients with HIV infection (with/without TB) were higher than those with TB alone or healthy individuals (p<0.01). Levels of caspase 8 in HIV+/TB- were higher than patients with HIV+/TB+ (p<0.01). CONCLUSION: Levels of caspase-1 are not different irrespective of presence or otherwise of TB and HIV infection. Fas-related apoptosis is higher in HIV infection. With concomitant TB, levels of caspase 8 were lower as compared with those without TB.

Beta2 microglobulin as a surrogate marker for HIV infection: good correlation with CD4 counts.

To determine if beta-2 microglobulin (beta2M) levels were elevated in our HIV infected patient population and if it could be used as a surrogate marker for disease progression. Thirty-eight HIV infected individuals and 26 age and sex-matched controls were studied. Measurement of CD4 cell count was carried out on a flowcytometer using anti-human CD4 monoclonal antibody and beta2M was measured by an enzyme immunoassay. Mean levels of HIV infected individuals were 1.29 +/- 0.52 mg/L and were significantly higher than 0.74 +/- 0.07 mg/L, the value of controls (p value <0.01). There was a negative correlation between CD4 counts and beta2M levels (r-value-0.79, p value <0.001). Beta2M levels in HIV infected individuals who have no opportunistic infection are elevated and these levels correlate with the CD4 counts. Beta2M can be used for the clinical follow-up of patients with HIV infection.

Acute pancreatitis following propoxyfur (Baygon) ingestion.

Elevation of serum amylase and blood glucose is not uncommon following anticholinesterase poisoning. We report a young male who developed acute cholinergic crisis and acute pancreatitis following propoxyfur (Baygon) ingestion and recovered completely with conservative management.

Reduced apoptosis by pentoxiphylline among patients with HIV infection.

BACKGROUND: Apoptosis is a significant cause of CD4(+) T cell death. Caspase 8 (FLICE) is involved in apoptosis mediated by Fas and p55 tumor necrosis factor (TNF) receptor ligation. It is also partially mediated by interleukin-1beta (IL-1beta)-converting enzyme (ICE; caspase 1). We and others have shown that pentoxiphylline inhibits TNF-alpha. We used it among patients with HIV infection to determine if 24 weeks of therapy altered the levels of caspase 1 and caspase 8. PATIENTS AND METHODS: Nineteen HIV-infected patients having no opportunistic infection at the time of recruitment were administered pentoxiphylline 400 mg thrice daily for 24 weeks. Caspase levels were measured using a single-step ELISA using commercially available monoclonal antibodies against caspase 1 and caspase 8. RESULTS: Mean CD4 counts of the patients were 202.6+/-111.6 (/mm(3)). Mean OD value of caspase 1 among patients before therapy was 0.302+/-0.197 and was higher than that of controls (0.287+/-0.064), but this was not statistically significant. Following 24 weeks of therapy with pentoxiphylline, the OD value declined significantly to 0.164+/-0.028 among patients (p<0.001). Mean OD value of caspase 8 among patients prior to therapy was 0.927+/-0.249. This was significantly higher than that of controls, whose level was 0.0074+/-0.004 (p<0.001). Following 24 weeks of therapy with pentoxiphylline, the OD value declined to 0.199+/-0.064 among patients and this was significantly lower than the value at the start of treatment (p<0.001). CONCLUSION: Therapy with pentoxiphylline for 24 weeks is associated with a decline in the levels of caspase 1 and caspase 8. Since the drug is known to produce TNF inhibition, this might result in reduced apoptosis and an improved CD4 lymphocyte survival.