Niraj Jani
University of Pittsburgh
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Featured researches published by Niraj Jani.
Gastroenterology Clinics of North America | 2002
Niraj Jani; Miguel Regueiro
Although newer therapeutic agents are being developed for the treatment of inflammatory bowel disease, aminosalicylates and corticosteroids remain the mainstay of treatment for UC (Tables 2-5). Patients who do not respond to these agents or become steroid dependent require immunomodulatory therapy or curative surgery. Cyclosporine represents the greatest treatment advance for UC in 10 years. The role of nicotine, heparin, antibiotics, probiotics, and SCFA in the treatment of UC is less clear, but these agents may offer an alternative therapeutic approach for patients intolerant or nonresponsive to standard therapy.
Digestive Diseases and Sciences | 2002
Niraj Jani; Sydney D. Finkelstein; David Blumberg; Miguel Regueiro
Diverticulosis is present in 35–50% of the population 60 years or older (1, 2). Inflammatory bowel disease (IBD) occurs most commonly in patients younger than 40 years of age, but does have a second peak in incidence over the age of 60 years (3, 4). Patients who present with IBD later in life more commonly have Crohn’s disease and tend to have left colon and rectal involvement (5). In the past 20 years there have been several reports of segmental colitis associated with diverticulosis, and although the exact etiology is unknown, it likely represents a distinct clinical and pathologic entity. Most of the reported cases of segmental colitis associated with diverticulosis have been successfully treated with the same medications used to treat IBD. We recently treated a patient with segmental colitis associated with diverticulosis that was refractory to medications and ultimately required surgery. We report this case and critically review the literature to address this entity.
The American Journal of Gastroenterology | 2017
James Buxbaum; Michael Quezada; Ben Da; Niraj Jani; Christianne J. Lane; Didi Mwengela; Thomas Kelly; Paul Jhun; Kiran Dhanireddy; Loren Laine
Objectives:Early aggressive intravenous hydration is recommended for acute pancreatitis treatment although randomized trials have not documented benefit. We performed a randomized trial of aggressive vs. standard hydration in the initial management of mild acute pancreatitis.Methods:Sixty patients with acute pancreatitis without systemic inflammatory response syndrome (SIRS) or organ failure were randomized within 4 h of diagnosis to aggressive (20 ml/kg bolus followed by 3 ml/kg/h) vs. standard (10 ml/kg bolus followed by 1.5 mg/kg/h) hydration with Lactated Ringer’s solution. Patients were assessed at 12-h intervals. At each interval, in both groups, if hematocrit, blood urea nitrogen (BUN), or creatinine was increased, a bolus of 20 ml/kg followed by 3 ml/kg/h was given; if labs were decreased and epigastric pain was decreased (measured on 0–10 visual analog scale), hydration was then given at 1.5 ml/kg/h and clear liquid diet was started. The primary endpoint, clinical improvement within 36 h, was defined as the combination of decreased hematocrit, BUN, and creatinine; improved pain; and tolerance of oral diet.Results:The mean age of the patients was 45 years and only 14 (23%) had comorbidities. A higher proportion of patients treated with aggressive vs. standard hydration showed clinical improvement at 36 h: 70 vs. 42% (P=0.03). The rate of clinical improvement was greater with aggressive vs. standard hydration by Cox regression analysis: adjusted hazard ratio=2.32, 95% confidence interval 1.21–4.45. Persistent SIRS occurred less commonly with aggressive hydration (7.4 vs. 21.1%; adjusted odds ratio (OR)=0.12, 0.02–0.94) as did hemoconcentration (11.1 vs. 36.4%, adjusted OR=0.08, 0.01–0.49). No patients developed signs of volume overload.Conclusions:Early aggressive intravenous hydration with Lactated Ringer’s solution hastens clinical improvement in patients with mild acute pancreatitis.
World Journal of Gastrointestinal Pharmacology and Therapeutics | 2015
Niraj Jani; James Buxbaum
Autoimmune pancreatitis (AIP) is part of a systemic fibrosclerotic process characterized by lymphoplasmacytic infiltrate with immunoglobulin G subtype-4 (IgG4) positive cells. It characteristically presents with biliary obstruction due to mass-like swelling of the pancreas. Frequently AIP is accompanied by extra-pancreatic manifestations including retroperitoneal fibrosis, thyroid disease, and salivary gland involvement. Auto-antibodies, hypergammaglobulemia, and prompt resolution of pancreatic and extrapancreatic findings with steroids signify its autoimmune nature. Refractory cases are responsive to immunomodulators and rituximab. Involvement of the biliary tree, termed IgG4 associated cholangiopathy, mimics primary sclerosing cholangitis and is challenging to manage. High IgG4 levels and swelling of the pancreas with a diminutive pancreatic duct are suggestive of autoimmune pancreatitis. Given similarities in presentation but radical differences in management and outcome, differentiation from pancreatic malignancy is of paramount importance. There is controversy regarding the optimal diagnostic criterion and steroid trials to make the diagnosis. Additionally, the retroperitoneal location of the pancreas and requirement for histologic sampling, makes tissue acquisition challenging. Recently, a second type of autoimmune pancreatitis has been recognized with similar clinical presentation and steroid response though different histology, serologic, and extrapancreatic findings.
Nature Clinical Practice Gastroenterology & Hepatology | 2006
Niraj Jani; Kevin McGrath
DESIGN AND INTERVENTION This retrospective study analyzed the inpatient and outpatient data from consecutive patients with clinically suspected pancreatic cancer who underwent EUS at the University of California Irvine Medical Center between January 1999 and August 2003. Exclusion criteria included evidence of chronic pancreatitis, focal pan creatic abnormality or pancreatic lesion on EUS, and previous EUS examination <6 months before the start of the study period. EUS was performed by one of three endosonographers using a radial echoendoscope. A linear echoendoscope was used if the pancreas could not be clearly seen using the radial device. All patients were under anesthesia or conscious sedation with midazolam and meperidine during EUS examination. Patients were followed up after EUS by telephone and/or clinic visits and/or CT scan >6 months later. EUS was considered to have excluded pancreatic cancer accurately if What is the negative predictive value of endoscopic ultrasonography in patients with suspected pancreatic cancer?
Endoscopy | 2007
Niraj Jani; John M. DeWitt; Mohamad A. Eloubeidi; Shyam Varadarajulu; V. Appalaneni; Brenda J. Hoffman; William R. Brugge; K. Lee; Ayesha N. Khalid; Kevin McGrath
Gastrointestinal Endoscopy | 2008
Niraj Jani; Asif Khalid; Neeraj Kaushik; Debra Brody; Kathy Bauer; Karen E. Schoedel; N. Paul Ohori; A. James Moser; Kenneth K. Lee; Kevin McGrath
Digestive Diseases and Sciences | 2002
Niraj Jani; Sydney D. Finkelstein; David Blumberg; Miguel Regueiro
Clinical Gastroenterology and Hepatology | 2006
Laurentia Nodit; Kevin McGrath; Maliha Zahid; Niraj Jani; Karen E. Schoedel; N. Paul Ohori; Sally E. Carty; Sydney D. Finkelstein; Asif Khalid
Gastrointestinal Endoscopy | 2008
Niraj Jani; Kevin McGrath