|Year : 2021 | Volume
| Issue : 2 | Page : 83-91
Novel infectious causes of acute pancreatitis: A comprehensive review
Saurabh Gaba1, Monica Gupta1, Ruchi Gaba2, Sarabmeet Singh Lehl1
1 Department of General Medicine, Government Medical College and Hospital, Chandigarh, India
2 Department of Paediatrics, All India Institute of Medical Sciences, New Delhi, India
|Date of Submission||27-Jan-2021|
|Date of Acceptance||25-Nov-2021|
|Date of Web Publication||24-Dec-2021|
Dr. Monica Gupta
Department of General Medicine, Level 4 D Block, Government Medical College and Hospital, Sector 32, Chandigarh - 160 030
Source of Support: None, Conflict of Interest: None
Acute pancreatitis can result from a variety of infections. The causative pathogens have been well established to be certain viruses and parasites. However, certain infections fail to find mention in standard literature and have been overlooked due to the trivial number of cases of pancreatitis that result from them. Among these are influenza, leptospirosis, acute viral hepatitis, and certain tropical infections such as dengue, chikungunya, scrub typhus, malaria, and typhoid. In this narrative review, we have conducted a literature search on PubMed and EMBASE databases for cases of pancreatitis occurring in these diseases and compiled the data. Most of these infections are prevalent in the developing world, and consequently, more cases are reported from these regions. The pathogenesis, predictors of outcome, and the response to antimicrobial therapy have not been studied extensively. The actual incidence is probably higher than what is reported, and this subject deserves more attention.
Keywords: Acute pancreatitis, chikungunya, coronavirus disease 2019, dengue, infections, influenza, leptospirosis, malaria, scrub typhus, viral hepatitis
|How to cite this article:|
Gaba S, Gupta M, Gaba R, Lehl SS. Novel infectious causes of acute pancreatitis: A comprehensive review. Indian J Community Fam Med 2021;7:83-91
|How to cite this URL:|
Gaba S, Gupta M, Gaba R, Lehl SS. Novel infectious causes of acute pancreatitis: A comprehensive review. Indian J Community Fam Med [serial online] 2021 [cited 2022 May 24];7:83-91. Available from: https://www.ijcfm.org/text.asp?2021/7/2/83/333666
| Introduction|| |
Acute pancreatitis (AP) is characterized by abrupt onset of inflammation that is often reversible and resolves with conservative management alone. The damage caused by the initial insult is propagated by activation of digestive proenzymes or zymogens within the pancreas, rather than the duodenum, leading to autodigestion. The diagnosis is made by the presence of any two of the following three criteria – the characteristic abdominal pain, elevation of serum amylase and/or lipase to more than three times the upper limit of normal, and imaging evidence of inflammation. The causes of AP are mentioned in [Table 1].
The classic clinical symptoms are nausea, vomiting, and epigastric pain that is continuous, radiates to the back, is exacerbated by food intake, and is partially relieved on bending forward. Third space fluid loss and systemic inflammation lead to hypotension. The clinical course can be complicated by certain local and systemic complications. The management involves bowel rest and early resuscitation with intravenous fluids. Early enteral feeding is preferred, and close monitoring for complications is needed. Antibiotics are indicated only when there is definite evidence of infection. Fluid collections may require drainage if they are infected or cause mass effects. This can be done by percutaneous, endoscopic, or surgical approach.
Among infections, the causes of AP have conventionally been started to include viruses such as Cytomegalovirus, mumps, coxsackievirus, and human immunodeficiency virus and parasites such as Toxoplasma and Ascaris. Apart from these, there are certain infections that have failed to find recognition in standard literature. These are mostly tropical infections, and occur predominantly in developing countries and in travelers who return from these regions. The data available is confined to isolated case reports or small series. We have provided an overview of the infectious causes of AP, which are mentioned in [Table 2].
| Material and Methods|| |
A search was conducted for articles indexed in PubMed and EMBASE databases using the keywords “specific infection + pancreatitis” and “specific infection + acute pancreatitis” to compile the available evidence of AP caused by influenza, chikungunya, viral hepatitis, dengue, malaria, fungi, leptospirosis, scrub typhus, typhoid, and coronavirus disease 2019 (COVID-19).
| Results|| |
People infected with HIV have a higher incidence of AP than the general population, and the risk is higher in advanced stages with lower CD4+ count. The etiology is diverse and may result from direct inflammation due to HIV itself, or from opportunistic infections such as Cytomegalovirus, Toxoplasma gondii, and Cryptosporidium. Drug-induced AP can result from antiretroviral drugs such as nucleoside reverse transcriptase inhibitors (didanosine, stavudine, and lamivudine) and nonnucleoside reverse transcriptase inhibitors (efavirenz and nevirapine). Didanosine has consistently been shown to confer the highest risk, among the antiretroviral drugs, in a dose-dependent manner. The mechanism is not completely identified, but it may be related to mitochondrial toxicity. The protease inhibitors are less commonly implicated. Drugs used in conjunction with antiretroviral therapy, such as corticosteroids, pentamidine, and trimethoprim-sulfamethoxazole, can also lead to AP. There are numerous case reports implicating herpes simplex, coxsackievirus, Epstein–Barr virus, and varicella-zoster virus in AP.,,
It has been shown that H5N1 influenza A can bind to pancreatic cells and induce apoptosis. The infected pancreatic cells also produce pro-inflammatory cytokines. Human H1N1 and H3N2 and avian H7N1 and H7N3 influenza virus can also infect human pancreatic islet cells. Damage to the pancreatic beta-cells by H1N1 influenza virus and precipitation of diabetes has also been documented., Baran et al. have reported the case of a 19-year-old male who presented with abdominal pain, fever, and upper respiratory symptoms. He was found to have H1N1 influenza, and no alternate cause of AP was found. He was treated with oseltamivir for 5 days and recovered quickly. Another case of AP has been reported in an 86-year-old male with untreated chronic lymphocytic leukemia. Severe AP with acute respiratory distress syndrome (ARDS) and acute kidney injury (AKI) has been reported in a 42-year-old woman. She was also treated with oseltamivir and recovered after a week. Possible association has also been reported by Sánchez Bautista et al. in a 12-year-old girl.
During a chikungunya outbreak in French Guiana, two patients with underlying chronic pancreatitis developed AP. One was a 54-year-old man, and the other was a 55-year-old man who also developed Guillain–Barré syndrome and encephalitis.
AP can occur in acute viral hepatitis due to the hepatotropic viruses. The pathogenesis has been proposed to be related to the edema of the ampulla of Vater, which impedes the normal flow of pancreatic secretions into the duodenum. Direct injury of the pancreatic cells by virus is under investigation. The presence of hepatitis B DNA and surface antigen has been documented in the acinar cells of a patient of liver transplant suffering from AP due to acute-on-chronic hepatitis B. If viral hepatitis is associated with acute liver failure, AP may also result from sepsis or pancreatic ischemia due to hypotension and disseminated intravascular coagulation.
In their review, Haffar et al. have reported the incidence of AP in acute hepatitis A to be <0.1%. They found that 6% of the cases of AP were associated with acute liver failure. The median interval between appearance of clinical jaundice and the onset of abdominal pain was 4 days. Mostly young patients (median age of 16 years) were affected, and most of the documented cases were from Asia. The mortality rate was noted to be similar to other causes of AP. In a retrospective analysis of 790 cases of AP over 6 years at an institution in India, 16 cases (2.1%), with a mean age of 25 years, were attributed to acute hepatitis E. One patient had acute liver failure. From another center in India, Bhagat et al. have documented AP in four and three cases of acute hepatitis E and A, respectively. All of them recovered with conservative management. Jain et al. have documented the incidence of AP in acute viral hepatitis to be as high as 5.6% (7 cases out of 124). Hepatitis E, A, and B were implicated in four, two, and one case, respectively. The clinical course was uncomplicated, and all the patients recovered. The six cases of AP due to hepatitis E studied by Mishra et al. also recovered completely with conservative management. Severe AP complicated by multi-organ dysfunction and local complications has also been documented in hepatitis E., To the best of our knowledge, only one case of AP associated with hepatitis C (genotype 1b) has been published. The patient was a 70-year-old female from Brazil, and AP was mild.
After the mosquito bite, dengue virus enters the Langerhans cells via membrane receptors, and replicates using its cellular machinery. The new viruses are released by exocytosis, and they infect other cell types. Migration of the Langerhans cells to the lymph nodes accelerates the spread to other parts of the body. AP is a very rare complication since the number of reported cases is miniscule compared to the incidence of dengue. Most of the data are from India [Table 3]. The pathogenesis may involve direct invasion of the pancreatic acinar cells by the dengue virus, obstruction to bile flow due to edema of the ampulla of Vater, or as a part of multi-organ dysfunction in dengue shock syndrome (DSS). The clinical course is comprised of three phases. The febrile phase, which lasts for 3–7 days, is followed by the critical phase in which plasma leakage occurs that can lead to shock and organ dysfunction. The critical phase lasts for up to 2 days, but it can lead to certain complications that can be long lasting and determine the outcome of the illness. In the convalescent phase, complete defervescence occurs and the general well-being of the patient gradually improves. Clinically, dengue can present as dengue fever, dengue hemorrhagic fever (DHF), and DSS. DHF is characterized by thrombocytopenia, evidence of increased vascular permeability, and hemorrhagic manifestations. DHF complicated by shock results in DSS that is often refractory to treatment. There is no specific antimicrobial drug, and the treatment is supportive. It is worth noting that AP can develop during both the febrile and critical periods of illness.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the ongoing COVID-19 pandemic that has led to unprecedented health and social and economic desolation. It was first identified in the Wuhan city of China in December 2019 and quickly spread to the rest of the world. The coronavirus family consists of certain RNA viruses that have spikes on their surface and typically cause respiratory illness. The SARS and Middle East respiratory syndrome pandemics were also caused by coronaviruses. SARS-CoV-2 has a probable zoonotic origin (bats or pangolins), and human-to-human transmission occurs by respiratory droplets. Spread can also occur from a contaminated environment.,, Its entry into the host cells is mediated by the angiotensin-converting enzyme 2 (ACE2) receptors and facilitated by transmembrane protease serine 2. So far, only dexamethasone has been shown to reduce mortality in the severely ill patients. Well-designed randomized controlled trials have either failed to establish a clear-cut benefit, have not been conducted, or are underway with regard to other drugs such as hydroxychloroquine, ivermectin, azithromycin, tocilizumab, remdesivir, and favipiravir.,,,,, The use of convalescent plasma is also being tried. Supportive management and anticoagulation form the mainstay of therapy. Human trials for the vaccine are underway. In a retrospective study on 52 patients with COVID-19 pneumonia, evidence of pancreatic injury in the form of elevation of amylase and lipase was found in 17.3% of the cases. In their study on 121 patients, Liu et al. found that pancreatic injury was more common in patients with severe COVID-19 infection. Elevation of amylase or lipase was seen in 17.91% of the patients with severe disease, while it was seen in only 1.85% of those with mild disease. It might be related to the systemic inflammatory response or direct cell injury as the ACE-2 receptor is expressed both in the pancreatic islets and acinar glands. The reported cases of AP are compiled in [Table 4].
|Table 4: Cases of acute pancreatitis reported in Coronavirus disease 2019|
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Ascaris is a well-known cause of AP, and the burden is highest in developing countries. The pathogenesis involves obstruction of the bile flow when the worm enters the ampulla of Vater from the duodenum, or by irritating the Sphincter of Oddi More Details leading to its spasm. Cryptosporidium is a very rare cause of AP both in immunocompetent and immunodeficient individuals. Toxoplasmosis can cause AP in patients with HIV. Ahuja et al. and Hofman et al. have reported the presence of Toxoplasma cysts in the pancreatic acini on autopsy of patients with known AIDS., Similar finding has been reported by Garcia et al., but the patient was found to have HIV after presentation with AP.
Malaria is caused by five species of the parasite Plasmodium. These are Plasmodium falciparum, Plasmodium vivax, Plasmodium malariae, Plasmodium ovale, and Plasmodium knowlesi. It is transmitted by the bite of female Anopheles mosquitoes which transmit sporozoites to the host while taking blood meal. The parasite reproduces asexually in the liver and red blood cells (RBCs). The disease is a major public health problem in Sub-Saharan Africa and South Asia, and lower incidence is seen in some South American countries. It poses a significant danger to the travelers too, who are advised to take chemoprophylaxis when traveling to the endemic regions. Severe disease results from P. falciparum and less commonly P. vivax. Features of severe malaria are ARDS, shock, encephalopathy and seizures (cerebral malaria), AKI, hypoglycemia, acidemia, hemoglobinuria, severe anemia (hemoglobin <5 gm/dL), and hyperparasitemia (infection of >5% of RBCs). For sensitive vivax malaria, chloroquine is the drug of choice. Falciparum malaria, chloroquine-resistant vivax malaria, and complicated malaria are always treated with artemisinin-based therapy or quinine. AP is reported in falciparum, and less commonly in vivax malaria [Table 5]. It has not been included in the criteria for severe malaria, and the pathogenesis has not been elucidated yet, but it may involve cytoadherence of the infected RBCs to the endothelium of the pancreatic vasculature with resultant ischemia. It can be seen that AP occurs mostly in association with other complications.
AP can occur as a part of disseminated fungal disease. It has been reported in invasive aspergillosis. The mechanism may be related to direct invasion of the pancreas and its vasculature or microvascular thrombosis secondary to disseminated intravascular coagulation.
Cases of AP in Mycoplasma pneumoniae have been described in few studies., The pathogenesis may be multifactorial. There is hematogenous dissemination of the bacteria and production of inflammatory cytokines locally in the affected organs. Vasculitis and immune modulation due to the phagocytosed macrophages may play a role. Sporadic isolated reports of AP due to Campylobacter jejuni, Yersinia More Details enterocolitica, and Yersinia pseudotuberculosis More Details also exist., One author has suggested that AP in campylobacter disease may be due to direct invasion of the pancreatic duct, or due to the host immune response.
Leptospirosis is a zoonotic disease caused by spirochetal bacteria of the genus Leptospira. The disease is distributed worldwide, but the incidence in tropics is ten times higher than other regions. It can be controlled but not eradicated by improved sanitation. Humans are incidental hosts, and the infection is acquired by exposure of contaminated soil or excreta of infected animals to damaged skin, mucosa, or conjunctiva. Consequently, the disease is sporadic, and farmers, sewer workers, and animal handlers are at a higher risk. Less commonly, infection can also occur by ingestion of contaminated food or inhalation of aerosols. It commonly causes a mild and self-limiting febrile illness, but occasionally, it can be severe. Leptospirosis complicated by jaundice and AKI is commonly referred to as Weil's disease. High-quality literature is available on reports of AP from America, Europe, Asia, and Africa [Table 6]. AP is very rare and has been seen in severe disease with multiple complications, but the outcome is good. The possible mechanisms are ischemia and vasculitis.
Scrub typhus is caused by Orientia tsutsugamushi, a bacterium of the genus Rickettsia which comprises Gram-negative, obligate intracellular parasites. Humans are accidental end hosts for the pathogen, which is transmitted by the bite of Leptotrombidium mites. Scrub typhus is a resurging zoonotic infection occurring in parts of Asia and Oceania. Its pathogenesis involves infection of the endothelial cells which leads to a vasculitic type of reaction with microvascular injury and thrombosis. The same mechanism is probably responsible for AP. Many cases with AP have been reported from India [Table 7].
Typhoid or enteric fever is a bacterial infection caused by Salmonella More Details typhi. It is a specter of the developing countries that are battling with overcrowding and poor sanitation. Contrariwise, a single case in the affluent countries is sufficient to make the public health authorities vigilant. Most of the cases in the developed country have a history of travel to the endemic regions. The infection is acquired by oral route. Resistance to gastric acid enables the bacterium to establish infection in the Peyer's patches of the small intestine from where lymphatic and hematogenous dissemination occurs. Further replication occurs within the reticuloendothelial system. Carriers can release the bacilli via feces or urine for prolonged periods. The hypertrophy and necrosis of the Peyer's patches can lead to intestinal hemorrhage and subsequent perforation. The clinical features in an untreated patient follow a stereotypical timeline with fever, malaise, chills, nausea, abdominal pain, diarrhea, or constipation in the 1st week; hepatomegaly, spleenomegaly, salmon rash (rarely seen in dark-skinned individuals), and abdominal pain in the 2nd week; and intestinal bleeding, intestinal perforation, delirium, sepsis, and shock in the 3rd week. The mechanism of AP has been postulated to reflux of S. typhi containing bile into the pancreatic duct, leading to direct injury. The other possibilities include the effect of bacterial toxin and the host immune response. Patients with typhoid may have elevations of amylase and lipase without any clinical evidence of AP. This was confirmed by Hermans et al., who studied 14 adult patients and found that while seven patients had elevated serum enzyme levels, only four had AP, and this complication did not adversely affect the outcome. The data published on AP in culture-proven typhoid are mentioned in [Table 8].
We speculate that the true incidence of pancreatitis in the infections discussed in this review is higher than what is suggested by the available data. The reasons for this are manifold. Firstly, there may be significant under-reporting. Since most of the cases are from developing countries and a majority of the patients are treated at peripheral centers, there is little impetus for the clinicians to publish their experience. Secondly, the lack of diagnostic facilities at such centers can be an impediment. Thirdly, the symptoms of abdominal pain and vomiting may be attributed to the disease per se, or to other pathologies, such as gastritis, hepatitis, cholecystitis, or adverse drug reactions. The possibility of AP may not even be considered. Fourthly, the pancreatitis may be mild and have little symptoms, so the specific investigations required to diagnose it may not be done. Conversely, the patient may have severe pancreatitis and present in such sick condition that he is not able to give the history. Finally, pancreatitis may be attributed to other causes, such as gall stones, drugs, and alcohol, if there is a history of their intake. It is also possible that some patients in the endemic regions who present with a primary diagnosis of AP may have actually developed it as a complication of some infection. The antibiotics that they receive during their care resolve the underlying infection, precluding an accurate diagnosis.
| Conclusion|| |
The current understanding of the infectious etiology of AP is incomplete. Although some causes are well established, AP is also a rare complication of infections such as dengue, malaria, scrub typhus, leptospirosis, typhoid, chikungunya, influenza, acute viral hepatitis, and COVID-19. Physicians should be wary of its possibility before attributing the symptoms to another abdominal pathology. The data available are limited and confined to case reports or case series. An attempt to investigate the pathogenesis has not been made yet. Due to the dearth of data and absence of a well-planned study, no statistical conclusions can be drawn at the moment, and it is currently not possible to comment on how its severity compares to AP caused by other causes, the effect of antimicrobial treatment, and the long-term outcome. The subject provides an opportunity for future studies and research.
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| References|| |
Muniraj T, Gajendran M, Thiruvengadam S, Raghuram K, Rao S, Devaraj P. Acute pancreatitis. Dis Mon 2012;58:98-144.
Manfredi R, Calza L. HIV infection and the pancreas: Risk factors and potential management guidelines. Int J STD AIDS 2008;19:99-105.
Dassopoulos T, Ehrenpreis ED. Acute pancreatitis in human immunodeficiency virus-infected patients: A review. Am J Med 1999;107:78-84.
Oliveira NM, Ferreira FA, Yonamine RY, Chehter EZ. Antiretroviral drugs and acute pancreatitis in HIV/AIDS patients: Is there any association? A literature review. Einstein (Sao Paulo) 2014;12:112-9.
Konstantinou GN, Liatsos CN, Patelaros EG, Karagiannis SS, Karnesis LI, Mavrogiannis CC. Acute pancreatitis associated with herpes simplex virus infection: Report of a case and review of the literature. Eur J Gastroenterol Hepatol 2009;21:114-6.
Zhu Z, Yin SJ, Kong ZB, Li H, Hu LP, Zuo S, et al.
Pancreatitis combined with epstein-barr virus-induced infectious mononucleosis. Chin Med J (Engl) 2017;130:2001-2.
Wang Z, Ye J, Han YH. Acute pancreatitis associated with herpes zoster: Case report and literature review. World J Gastroenterol 2014;20:18053-6.
Huo C, Xiao K, Zhang S, Tang Y, Wang M, Qi P, et al.
H5N1 influenza a virus replicates productively in pancreatic cells and induces apoptosis and pro-inflammatory cytokine response. Front Cell Infect Microbiol 2018;8:386.
Capua I, Mercalli A, Pizzuto MS, Romero-Tejeda A, Kasloff S, De Battisti C, et al.
Influenza A viruses grow in human pancreatic cells and cause pancreatitis and diabetes in an animal model. J Virol 2013;87:597-610.
Krishna SV, Sunil K, Prasad RD, Modi KD. Precipitation of new onset diabetes by H1N1 infection. Indian J Endocrinol Metab 2012;16:S438-40.
Watanabe N. Conversion to type 1 diabetes after H1N1 influenza infection: A case report. J Diabetes 2011;3:103.
Baran B, Karaca C, Soyer OM, Lacin S, Demir K, Besisik F, et al.
Acute pancreatitis associated with H1N1 influenza during 2009 pandemic: A case report. Clin Res Hepatol Gastroenterol 2012;36:e69-70.
Avalos C, Estifan E, Swyden S, Yuridullah R. Acute pancreatitis caused by complications of influenza A in the setting of chronic lymphocytic leukemia. Cureus 2020;12:e7067.
Habib A, Jain A, Singh B, Jamshed N. H1N1 influenza presenting as severe acute pancreatitis and multiorgan dysfunction. Am J Emerg Med 2016;34:1911.e1-2.
Sánchez Bautista A, Alcalá Minagorre PJ, Segura Sánchez S, Mira-Perceval Juan G. 2009 pandemic influenza A (H1N1) virus infection treated with oseltamivir and possible association with acute pancreatitis in a 12 years old patient. Enferm Infecc Microbiol Clin 2015;33:139-40.
Bonifay T, Prince C, Neyra C, Demar M, Rousset D, Kallel H, et al.
Atypical and severe manifestations of chikungunya virus infection in French Guiana: A hospital-based study. PLoS One 2018;13:e0207406.
Tsui CY, Burch GE, Harb JM. Pancreatitis in mice infected with coxsackievirus B1. Arch Pathol 1972;93:379-89.
Yuen MF, Chan TM, Hui CK, Chan AO, Ng IO, Lai CL. Acute pancreatitis complicating acute exacerbation of chronic hepatitis B infection carries a poor prognosis. J Viral Hepat 2001;8:459-64.
Raj M, Kumar K, Ghoshal UC, Saraswat VA, Aggarwal R, Mohindra S. Acute hepatitis E-associated acute pancreatitis: A single center experience and literature review. Pancreas 2015;44:1320-2.
Haffar S, Bazerbachi F, Prokop L, Watt KD, Murad MH, Chari ST. Frequency and prognosis of acute pancreatitis associated with fulminant or non-fulminant acute hepatitis A: A systematic review. Pancreatology 2017;17:166-75.
Bhagat S, Wadhawan M, Sud R, Arora A. Hepatitis viruses causing pancreatitis and hepatitis: A case series and review of literature. Pancreas 2008;36:424-7.
Jain P, Nijhawan S, Rai RR, Nepalia S, Mathur A. Acute pancreatitis in acute viral hepatitis. World J Gastroenterol 2007;13:5741-4.
Mishra A, Saigal S, Gupta R, Sarin SK. Acute pancreatitis associated with viral hepatitis: A report of six cases with review of literature. Am J Gastroenterol 1999;94:2292-5.
Karanth SS, Khan Z, Rau NR, Rao K. Acute hepatitis E complicated by acute pancreatitis and multiorgan dysfunction. BMJ Case Rep 2014;2014:bcr2014203875.
Somani SK, Ghosh A, Awasthi G. Severe acute pancreatitis with pseudocyst bleeding due to hepatitis E virus infection. Clin J Gastroenterol 2009;2:39-42.
Alvares-Da-Silva MR, Francisconi CF, Waechter FL. Acute hepatitis C complicated by pancreatitis: Another extrahepatic manifestation of hepatitis C virus? J Viral Hepat 2000;7:84-6.
Martina BE, Koraka P, Osterhaus AD. Dengue virus pathogenesis: An integrated view. Clin Microbiol Rev 2009;22:564-81.
Kumar P, Thapa BR, Himral H, Kapil V. Acute pancreatitis in dengue fever. Indian J Pediatr 2018;85:318-9.
Kularatne SA. Dengue fever. BMJ 2015;351:h4661.
Nawal CL, Meena PD, Chejara RS, Jain S, Marker S, Tuteja V. Dengue fever as a rare cause of acute pancreatitis. J Assoc Physicians India 2018;66:82-3.
Kumar KJ, Chandrashekar A, Basavaraja CK, Kumar HC. Acute pancreatitis complicating dengue hemorrhagic fever. Rev Soc Bras Med Trop 2016;49:656-9.
Correa R, Ortega-Loubon C, Zapata-Castro LE, Armién B, Culquichicón C. Dengue with hemorrhagic manifestations and acute pancreatitis: Case report and review. Cureus 2019;11:e4895.
Anam AM, Rabbani R, Shumy F, Polash MM. Subsequent pancreatitis and haemothorax in a patient of expanded dengue syndrome. Trop Doct 2016;46:40-2.
Jain V, Gupta O, Rao T, Rao S. Acute pancreatitis complicating severe dengue. J Glob Infect Dis 2014;6:76-8.
Simadibrata M. Acute pancreatitis in dengue hemorrhagic fever. Acta Med Indones 2012;44:57-61.
Lee CY, Tsai HC, Lee SS, Lin CK, Huang JS, Chen YS. Dengue hemorrhagic fever presenting with hemorrhagic pancreatitis and an intramural hematoma of the duodenal wall: A case report and review of the literature. Southeast Asian J Trop Med Public Health 2013;44:400-8.
Karoli R, Fatima J, Singh G, Maini S. Acute pancreatitis: An unusual complication of dengue fever. J Assoc Physicians India 2012;60:64-5.
Wijekoon CN, Wijekoon PW. Dengue hemorrhagic fever presenting with acute pancreatitis. Southeast Asian J Trop Med Public Health 2010;41:864-6.
Seetharam P, Rodrigues G. Dengue fever presenting as acute pancreatitis. Eurasian J Med 2010;42:151-2.
Zhu N, Zhang D, Wang W, Li X, Yang B, Song J, et al.
A novel coronavirus from patients with pneumonia in China, 2019. N Engl J Med 2020;382:727-33.
Lam TT, Jia N, Zhang YW, Shum MH, Jiang JF, Zhu HC, et al.
Identifying SARS-CoV-2-related coronaviruses in Malayan pangolins. Nature 2020;583:282-5.
Zhou P, Yang XL, Wang XG, Hu B, Zhang L, Zhang W, et al
. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature 2020;579:270-3.
Kampf G, Todt D, Pfaender S, Steinmann E. Persistence of coronaviruses on inanimate surfaces and their inactivation with biocidal agents. J Hosp Infect 2020;104:246-51.
Hoffmann M, Kleine-Weber H, Schroeder S, Krüger N, Herrler T, Erichsen S, et al.
SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell 2020;181:271-80.e8.
RECOVERY Collaborative Group, Horby P, Lim WS, Emberson JR, Mafham M, Bell JL, et al
. Dexamethasone in hospitalized patients with covid-19 – Preliminary report. N Engl J Med 2021;384:693-704.
Tang W, Cao Z, Han M, Wang Z, Chen J, Sun W, et al
. Hydroxychloroquine in patients with mainly mild to moderate coronavirus disease 2019: Open label, randomised controlled trial. BMJ 2020;369:m1849.
Cai Q, Yang M, Liu D, Chen J, Shu D, Xia J, et al.
Experimental treatment with favipiravir for COVID-19: An open-label control study. Engineering (Beijing) 2020;6:1192-8.
Rosenberg ES, Dufort EM, Udo T, Wilberschied LA, Kumar J, Tesoriero J, et al.
Association of treatment with hydroxychloroquine or azithromycin with in-hospital mortality in patients with COVID-19 in New York State. JAMA 2020;323:2493-502.
Heidary F, Gharebaghi R. Ivermectin: A systematic review from antiviral effects to COVID-19 complementary regimen. J Antibiot (Tokyo) 2020;73:593-602.
Campochiaro C, Della-Torre E, Cavalli G, De Luca G, Ripa M, Boffini N, et al.
Efficacy and safety of tocilizumab in severe COVID-19 patients: A single-centre retrospective cohort study. Eur J Intern Med 2020;76:43-9.
Wang Y, Zhang D, Du G, Du R, Zhao J, Jin Y, et al.
Remdesivir in adults with severe COVID-19: A randomised, double-blind, placebo-controlled, multicentre trial. Lancet 2020;395:1569-78.
Piechotta V, Chai KL, Valk SJ, Doree C, Monsef I, Wood EM, et al.
Convalescent plasma or hyperimmune immunoglobulin for people with COVID-19: A living systematic review. Cochrane Database Syst Rev 2020;7:CD013600.
Wang F, Wang H, Fan J, Zhang Y, Wang H, Zhao Q. Pancreatic injury patterns in patients with coronavirus disease 19 pneumonia. Gastroenterology 2020;159:367-70.
Liu F, Long X, Zhang B, Zhang W, Chen X, Zhang Z. ACE2 expression in pancreas may cause pancreatic damage after SARS-CoV-2 infection. Clin Gastroenterol Hepatol 2020;18:2128-30.e2.
Aloysius MM, Thatti A, Gupta A, Sharma N, Bansal P, Goyal H. COVID-19 presenting as acute pancreatitis. Pancreatology 2020;20:1026-7.
Meireles PA, Bessa F, Gaspar P, Parreira I, Dias Silva V, Mota C, et al
. Acalculous acute pancreatitis in a COVID-19 patient. Eur J Case Rep Intern Med 2020;7:001710.
Hadi A, Werge M, Kristiansen KT, Pedersen UG, Karstensen JG, Novovic S, et al.
Coronavirus Disease-19 (COVID-19) associated with severe acute pancreatitis: Case report on three family members. Pancreatology 2020;20:665-7.
Miao Y, Lidove O, Mauhin W. First case of acute pancreatitis related to SARS-CoV-2 infection. Br J Surg 2020;107:e270.
Schepis T, Larghi A, Papa A, Miele L, Panzuto F, De Biase L, et al.
SARS-CoV2 RNA detection in a pancreatic pseudocyst sample. Pancreatology 2020;20:1011-2.
Karimzadeh S, Manzuri A, Ebrahimi M, Huy NT. COVID-19 presenting as acute pancreatitis: Lessons from a patient in Iran. Pancreatology 2020;20:1024-5.
Szatmary P, Arora A, Thomas Raraty MG, Joseph Dunne DF, Baron RD, Halloran CM. Emerging phenotype of severe acute respiratory syndrome-coronavirus 2-associated pancreatitis. Gastroenterology 2020;159:1551-4.
Mazrouei SS, Saeed GA, Al Helali AA. COVID-19-associated acute pancreatitis: A rare cause of acute abdomen. Radiol Case Rep 2020;15:1601-3.
Brikman S, Denysova V, Menzal H, Dori G. Acute pancreatitis in a 61-year-old man with COVID-19. CMAJ 2020;192:E858-9.
Kataria S, Sharif A, Ur Rehman A, Ahmed Z, Hanan A. COVID-19 induced acute pancreatitis: A case report and literature review. Cureus 2020;12:e9169.
Khuroo MS, Rather AA, Khuroo NS, Khuroo MS. Hepatobiliary and pancreatic ascariasis. World J Gastroenterol 2016;22:7507-17.
Leitch GJ, He Q. Cryptosporidiosis – An overview. J Biomed Res 2012;25:1-16.
Parenti DM, Steinberg W, Kang P. Infectious causes of acute pancreatitis. Pancreas 1996;13:356-71.
Ahuja SK, Ahuja SS, Thelmo W, Seymour A, Phelps KR. Necrotizing pancreatitis and multisystem organ failure associated with toxoplasmosis in a patient with AIDS. Clin Infect Dis 1993;16:432-4.
Hofman P, Michiels JF, Mondain V, Saint-Paul MC, Rampal A, Loubière R. Acute toxoplasmic pancreatitis. An unusual cause of death in AIDS. Gastroenterol Clin Biol 1994;18:895-7.
Garcia LW, Hemphill RB, Marasco WA, Ciano PS. Acquired immunodeficiency syndrome with disseminated toxoplasmosis presenting as an acute pulmonary and gastrointestinal illness. Arch Pathol Lab Med 1991;115:459-63.
Basu S, Sahi PK. Malaria: An update. Indian J Pediatr 2017;84:521-8.
Abhilash KP, Ahmed AS, Sathyendra S, Abraham OC. Acute pancreatitis due to malaria: A case report of five patients and review of literature. J Family Med Prim Care 2016;5:691-4.
] [Full text]
Singh J, Dinkar A, Singh RG, Kapoor S. Successful management of necrotizing pancreatitis in mixed malaria and review of literature. Trop Parasitol 2018;8:8-11.
] [Full text]
Barman B, Bhattacharya PK, Lynrah KG, Ete T, Issar NK. Acute pancreatitis in a patient with complicated falciparum malaria. J Clin Diagn Res 2016;10:OD18-20.
Lakhotia M, Pahadiya HR, Kumar H, Singh J, Sangappa JR, Choudhary PK. Acute pancreatitis, ascites, and acute renal failure in Plasmodium vivax
malaria infection, a rare complication. Trop Parasitol 2015;5:120-2.
] [Full text]
Reoyo Pascual JF, Cartón-Hernández C, Valero-Cerrato X, León-Miranda R, García Plata-Polo E, Martínez-Castro RM, et al.
Acute hemorrhagic necrotizing pancreatitis in falciparum malaria. Rev Esp Enferm Dig 2016;108:285-7.
Atam V, Singh AS, Yathish BE, Das L. Acute pancreatitis and acute respiratory distress syndrome complicating Plasmodium vivax
malaria. J Vector Borne Dis 2013;50:151-4.
] [Full text]
Ghosh S, Das SK, Sharma A. Unusual presentation of acute pancreatitis in falciparum malaria. Trop Parasitol 2014;4:56-7.
] [Full text]
Mahdi AS, Molai M, Chandwani J, Khalili HA, Ibrahim H, Pandak N, et al.
Late onset acute pancreatitis in P. falciparum
malaria – An adverse reaction to intravenous artesunate? IDCases 2018;12:124-6.
Guice KS, Lynch M, Weatherbee L. Invasive aspergillosis: An unusual cause of hemorrhagic pancreatitis. Am J Gastroenterol 1987;82:563-5.
Yang A, Kang B, Choi SY, Cho JB, Kim YJ, Jeon TY, et al.
Acute necrotizing pancreatitis associated with Mycoplasma pneumoniae
infection in a child. Pediatr Gastroenterol Hepatol Nutr 2015;18:209-15.
Benzaquen M, Lebowitz D, Belenotti P, Durand JM, Serratrice J. Acute pancreatitis and pneumonia due to Mycoplasma pneumoniae
: A case report. BMC Res Notes 2016;9:397.
Kobayashi R, Matsumoto S, Yoshida Y. Case of acute pancreatitis associated with Campylobacter
enteritis. World J Gastroenterol 2014;20:7514-7.
Hartskeerl RA, Collares-Pereira M, Ellis WA. Emergence, control and re-emerging leptospirosis: Dynamics of infection in the changing world. Clin Microbiol Infect 2011;17:494-501.
Dupont H, Dupont-Perdrizet D, Perie JL, Zehner-Hansen S, Jarrige B, Daijardin JB. Leptospirosis: Prognostic factors associated with mortality. Clin Infect Dis 1997;25:720-4.
Maier A, Kaeser R, Thimme R, Boettler T. Acute pancreatitis and vasoplegic shock associated with leptospirosis – A case report and review of the literature. BMC Infect Dis 2019;19:395.
Mazhar M, Kao JJ, Bolger DT Jr. A 23-year-old man with leptospirosis and acute abdominal pain. Hawaii J Med Public Health 2016;75:291-4.
Panagopoulos P, Terzi I, Karanikas M, Galanopoulos N, Maltezos E. Myocarditis, pancreatitis, polyarthritis, mononeuritis multiplex and vasculitis with symmetrical peripheral gangrene of the lower extremities as a rare presentation of leptospirosis: A case report and review of the literature. J Med Case Rep 2014;8:150.
Popa D, Vasile D, Ilco A. Severe acute pancreatitis – A serious complication of leptospirosis. J Med Life 2013;6:307-9.
Ranawaka N, Jeevagan V, Karunanayake P, Jayasinghe S. Pancreatitis and myocarditis followed by pulmonary hemorrhage, a rare presentation of leptospirosis – A case report and literature survey. BMC Infect Dis 2013;13:38.
Maier A, Kaeser R, Thimme R, Boettler T. Acute pancreatitis and vasoplegic shock associated with leptospirosis – A case report and review of the literature. BMC Infect Dis 2019;19:395.
Monno S, Mizushima Y. Leptospirosis with acute acalculous cholecystitis and pancreatitis. J Clin Gastroenterol 1993;16:52-4.
Afzal I, Thaker R, Weissman S, Kothari M. Leptospirosis as an unusual culprit of acute pancreatitis and portal vein thrombosis in a New Yorker. Clin Case Rep 2020;8:690-5.
Diyas S, Lezreg M, Badsi S, Housni B. Leptospirosis revealed by acute pancreatitis. Pan Afr Med J 2019;34:83.
Rajapakse S, Rodrigo C, Fernando D. Scrub typhus: Pathophysiology, clinical manifestations and prognosis. Asian Pac J Trop Med 2012;5:261-4.
Sv PD, Aruna M, Kumar AC, Krishna Reddy H, Bl S, Siva Kumar V. Acute pancreatitis associated with scrub typhus. Trop Doct 2017;47:65-7.
Chaturvedi A, Gupta M, Bhardwaj S, Handa D. Scrub typhus masquerading as acute pancreatitis. BMJ Case Rep 2016;2016:bcr2015213929.
Ahmed AS, Kundavaram AP, Sathyendra S, Abraham OC. Acute pancreatitis due to scrub typhus. J Glob Infect Dis 2014;6:31-4.
Dhakal M, Dhakal OP, Bhandari D. Pancreatitis in scrub typhus: A rare complication. BMJ Case Rep 2014;2014:bcr2013201849.
Iqbal N, Viswanathan S, Remalayam B, Muthu V, George T. Pancreatitis and MODS due to scrub typhus and dengue co-infection. Trop Med Health 2012;40:19-21.
Wang NC, Ni YH, Peng MY, Chang FY. Acute acalculous cholecystitis and pancreatitis in a patient with concomitant leptospirosis and scrub typhus. J Microbiol Immunol Infect 2003;36:285-7.
Waddington CS, Darton TC, Woodward WE, Angus B, Levine MM, Pollard AJ. Advancing the management and control of typhoid fever: A review of the historical role of human challenge studies. J Infect 2014;68:405-18.
Stuart BM, Pullen RL. Typhoid; clinical analysis of 360 cases. Arch Intern Med (Chic) 1946;78:629-61.
Hearne SE, Whigham TE, Brady CE 3rd
. Pancreatitis and typhoid fever. Am J Med 1989;86:471-3.
Hermans P, Gerard M, van Laethem Y, de Wit S, Clumeck N. Pancreatic disturbances and typhoid fever. Scand J Infect Dis 1991;23:201-5.
Cho JH. Successful endoscopic hemoclipping and conservative management for typhoid fever complicated by massive intestinal bleeding and acute pancreatitis: Case report. Medicine (Baltimore) 2019;98:e16521.
Khan FY, Al-Ani A, Ali HA. Typhoid rhabdomyolysis with acute renal failure and acute pancreatitis: A case report and review of the literature. Int J Infect Dis 2009;13:e282-5.
Ali M, Abdalla H. Salmonella typhi
infection complicated by rhabdomyolysis, pancreatitis and polyneuropathy. Arab J Nephrol Transplant 2011;4:91-3.
Rombolà F, Bertuccio SN. Typhoid fever and acute pancreatitis: Two cases. Infez Med 2007;15:63-5.
Martinez-Roig A, Bonet-Alcaina M, Casellas-Montagut M, Ymbert-Pellejà L. Pancreatitis in typhoid fever relapse. Pediatr Infect Dis J 2009;28:74.
Adhikari S, Shrestha AL, Thapa SR, Ghimire A. A rare cause of acute hepatopancreatitis in a Nepalese teen. Case Rep Pediatr 2018;2018:8456503.
Snelling PJ, Moriarty P, Vaska VL, Levitt D, Nourse C. Rhabdomyolysis complicating typhoid fever in A child and review of the literature. Pediatr Infect Dis J 2017;36:915-6.
Basak DK, Gomes RR, Ahmed MA, Alam AS. Mysterious looks of typhoid fever: A new experience. Bangladesh Crit Care J 2015;3:36-8.
Roy S, Majumdar SD, Chakrabartty S, Chakravarti S. Typhoid fever with acute pancreatitis in a five-year-old child. Pediatr Infect Dis J 2017;13:240-1.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8]