Tuberculosis and biologics in rheumatology: A special situation

India has a huge patient burden of rheumatic diseases (RDs) including rheumatoid arthritis. The use of biologics has transformed the treatment paradigm for RD; however, biologic treatment‐related infections (especially tuberculosis [TB]) are an area of potential concern for TB‐endemic nations like India. Anti‐tumor necrosis factor (TNF) therapy impairs the physiological TNF‐mediated signaling and may cause reactivation and dissemination of latent TB infection (LTBI). Careful screening is, thus, crucial in RD patients who are about to commence anti‐TNF treatment. To date, there is no consensus available for the screening, evaluation and treatment of LTBI as well as on the drug dosage and duration regimen (monotherapy or combination therapy) in the Indian population. An evidence‐based algorithm for LTBI screening and management in RD patients undergoing biologic disease‐modifying anti‐rheumatic drug therapy is suggested in this review for Indian rheumatologists. The proposed algorithm guides physicians through a step‐wise screening approach, including medical history, tuberculin skin test, interferon gamma release assay, chest radiograph and management of LTBI with isoniazid therapy or its combination with rifampicin. Further, the provided algorithm can aid the national bodies (such as National TB Control Program) in formulating recommendations for LTBI in this high‐risk population.     

Outcomes of Fecal Microbiota Transplantation for Clostridium difficile Infection in Patients with Inflammatory Bowel Disease

Digestive Diseases and Sciences - Fecal microbiota transplantation (FMT) has recently been shown to be a promising therapy for recurrent and refractory Clostridium difficile infections (CDI)...     

Multi-center prospective survey of inflammatory bowel diseases in Kerala: More than 2000 cases

Background

Inflammatory bowel disease (IBD) is considered uncommon in Asia. The aim of this study was to document the demographic characteristics and clinical aspects of ulcerative colitis (UC) and Crohn’s disease (CD) in Kerala, India.

Methods

A survey of IBD in Kerala was performed. All gastroenterologists in the region were invited. From May 2013 to October 2015, data were collected in a standardized pro-forma.

Results

Forty-seven doctors in 34 centers contributed data. A total of 2142 patients were analyzed. This is the largest state-wide survey of IBD in India. Ulcerative colitis was diagnosed in 1112 (38 new), Crohn’s disease in 980 (53 new), and 50 were unclassified (5 new). The district-wise distribution of IBD cases correlated with the District-wise Gross State Domestic Product (r =?0.69, p <?0.01). Three percent was below the age of 18. Patients with UC had more diarrhea (73% vs. 51%), bleeding PR (79% vs. 34%), and intermittent flares (35% vs. 13%) (all p <?0.01). Patients with CD had more abdominal pain (62% vs. 46%), weight loss (53% vs. 40%), fever (28% vs. 18%), and history of antituberculosis treatment (21% vs. 5%) (all p <?0.01). Compared to adults, children (below 18 years) were more likely to have extensive UC (58% vs. 34%, p <?0.01) and unclassified IBD (15% vs. 2%, p <?0.01).

Conclusion

Inflammatory bowel disease is common in Kerala, India. The disease characteristics of patients with IBD are almost similar to those from other parts of the country. Both UC and CD were seen in equal proportion in Kerala.

     

Comparison of platelet-lymphocyte ratio and CA 19-9 in differentiating benign from malignant head masses in patients with chronic pancreatitis

Introduction

Pancreatic head ductal adenocarcinoma (PDAC) and inflammatory head masses (IHM) related to chronic pancreatitis are often difficult to differentiate. PDAC produces significant inflammatory response with resultant lymphopenia and thrombocytosis. The prognostic role of platelet-lymphocyte ratio (PLR) as a tumor marker has been defined. We aimed to find the role of PLR as a diagnostic marker for PDAC in differentiating benign head mass comparing with carbohydrate antigen 19-9 (CA 19-9).

Methods

A prospective study of patients with biopsy-proven PDAC and benign IHM with underlying chronic pancreatitis from 1st November 2014 to 30th June 2016 was performed. Total blood count including platelet count and CA 19-9 were recorded and statistically analyzed.

Results

There was no significant difference in total leukocyte counts (7789±2027 vs. 7568±1289 cells/mm³) between PDAC (n = 34) and IHM (n = 27). However, the mean lymphocyte (2235±837 vs. 2701±631 cells/mm³) and platelet counts in mm³ (3.36±0.789) × 10⁵ vs. (2.45±0.598) × 10⁵ showed difference. The median PLR was 161.9 (IQR = 117.5–205.6) in PDAC and 91 (IQR = 77.2–106.6) in IHM. The median CA 19-9 (U/mL) in PDAC and IHM was 69.3 (IQR = 22.7–427.7) and 13.9 (IQR = 7.2–23.6), respectively. On plotting the receiver operator characteristic curve (ROC curve), area under the curve was maximum for PLR (88.7%) compared to CA 19-9 (77.8%) in diagnosing PDAC (p<0.0001). Using coordinates of ROC, PLR cutoff value was 113.5 (sensitivity—79.4%, specificity—92.6%, positive predictive value (PPV)—91.5%, negative predictive value (NPV)—99.7%) while CA 19-9 cutoff value was 25.3 U/mL (sensitivity—73.5%, specificity—77.8%, PPV—78.5%, NPV—74.6%).

Conclusion

PLR may be useful to differentiate PDAC from benign IHM in patients with chronic pancreatitis.

     

Haemolytic uraemic syndrome

Haemolytic uraemic syndrome (HUS) is defined by the simultaneous occurrence of nonimmune haemolytic anaemia, thrombocytopenia and acute renal failure. This leads to the pathological lesion termed thrombotic microangiopathy, which mainly affects the kidney, as well as other organs. HUS is associated with endothelial cell injury and platelet activation, although the underlying cause may differ. Most cases of HUS are associated with gastrointestinal infection with Shiga toxin‐producing enterohaemorrhagic Escherichia coli (EHEC) strains. Atypical HUS (aHUS) is associated with complement dysregulation due to mutations or autoantibodies. In this review, we will describe the causes of HUS. In addition, we will review the clinical, pathological, haematological and biochemical features, epidemiology and pathogenetic mechanisms as well as the biochemical, microbiological, immunological and genetic investigations leading to diagnosis. Understanding the underlying mechanisms of the different subtypes of HUS enables tailoring of appropriate treatment and management. To date, there is no specific treatment for EHEC‐associated HUS but patients benefit from supportive care, whereas patients with aHUS are effectively treated with anti‐C5 antibody to prevent recurrences, both before and after renal transplantation.