In spite of recent advances with experiments on animal models, strongyloidiasis, an infection caused by the nematode parasite Strongyloides stercoralis, has still been an elusive disease. Though endemic in some developing countries, strongyloidiasis still poses a threat to the developed world. Due to the peculiar but characteristic features of autoinfection, hyperinfection syndrome involving only pulmonary and gastrointestinal systems, and disseminated infection with involvement of other organs, strongyloidiasis needs special attention by the physician, especially one serving patients in areas endemic for strongyloidiasis. Strongyloidiasis can occur without any symptoms, or as a potentially fatal hyperinfection or disseminated infection. Th2 cell-mediated immunity, humoral immunity and mucosal immunity have been shown to have protective effects against this parasitic infection especially in animal models. Any factors that suppress these mechanisms (such as intercurrent immune suppression or glucocorticoid therapy) could potentially trigger hyperinfection or disseminated infection which could be fatal. Even with the recent advances in laboratory tests, strongyloidiasis is still difficult to diagnose. But once diagnosed, the disease can be treated effectively with antihelminthic drugs like Ivermectin. This review article summarizes a case of strongyloidiasis and various aspects of strongyloidiasis, with emphasis on epidemiology, life cycle of Strongyloides stercoralis, clinical manifestations of the disease, corticosteroids and strongyloidiasis, diagnostic aspects of the disease, various host defense pathways against strongyloidiasis, and available treatment options.
Warfarin is the most widely used oral anticoagulant and is indicated for many clinical conditions. Levofloxacin, a fluoroquinolone, is one of the most commonly prescribed antibiotics in clinical practice and is effective against Gram-positive, Gram-negative, and atypical bacteria. While small prospective studies have not revealed any significant drug-drug interaction between warfarin and levofloxacin, several case reports have indicated that levofloxacin may significantly potentiate the anticoagulation effect of warfarin. We report 3 cases of serious bleeding complications that appear to be the result of the interaction between warfarin and levofloxacin. Physicians should be aware of this potential interaction and use caution when prescribing levofloxacin to patients taking warfarin.
Strongyloidiasis can present with a wide variety of symptoms and can lead to a potentially fatal hyperinfection. Although any factors that suppress the host defense mechanisms can potentially trigger hyperinfection, prolonged steroid use has been quite well described. A patient with disseminated small cell lung cancer suffered a Strongyloides stercoralis hyperinfection syndrome complicating ectopic adrenocorticotropic hormone (Cushing syndrome). Evaluation revealed lymphopenia, elevated levels of adrenocorticotropic hormone in the setting of elevated cortisol levels, a normal pituitary, and metastatic malignancy. S. stercoralis larval forms were seen in the stool and sputum. At autopsy, S. stercoralis larval forms were seen in the lung along with evidence of metastatic small cell lung carcinoma.
Introduction: Vascular complications in pancreatitis generally occur in the form of hemorrhage or thrombosis. Pancreatitis resulting in splanchnic thrombosis has been well studied, but the cause of this correlation has not been studied in the current era of increasing anticoagulant use for deep venous thrombosis (DVT) prophylaxis. Hemorrhagic pancreatitis and peri-pancreatic bleeding are also known phenomena encountered in relation to pancreatitis, but these risks are not well established in the setting of chemical prophylaxis for DVT.
Objectives: Our objective was to identify whether chemical DVT prophylaxis in pancreatitis harms the patient by increasing the risk of hemorrhagic conversion of pancreatitis or peri-pancreatic hemorrhage or if it is beneficial by preventing splanchnic venous thrombosis in the abdominal vasculature that surrounds the pancreas.
Methods: We undertook a retrospective chart review with approval from the Institutional Review Board on patients who were hospitalized for or developed pancreatitis during their hospital stay from April 2014 to July 2015. We reviewed the charts for imaging suggestive of venous thrombosis or the development of intra-abdominal hemorrhage at admission during hospitalization and within 30 days after hospitalization. We also reviewed the methods of DVT prophylaxis to identify any correlation with the risk of hemorrhage or thrombosis. A bedside index of severity in acute pancreatitis score was used within 24 hours of admission to calculate the severity of the patients’ pancreatitis. The data collected were analyzed for descriptive statistics, correlation using Pearson’s coefficient, and multivariate regression analysis using Microsoft Excel and SPSS Inc. Released 2009. PASW Statistics for Windows, Version 18.0. Chicago: SPSS Inc.
Results: This study included 389 patients who met the inclusion criteria. Of these, 74.6% of patients received chemical prophylaxis, mostly low molecular weight heparin, and 18.5% of patients were not on chemical or mechanical means of DVT prophylaxis. Only 12 patients (3%) had complications related to thrombosis and hemorrhage. Seven patients had splanchnic venous thrombosis, one had a hemorrhagic conversion of pancreatitis, three had a peri-pancreatic hemorrhage, and one had both the hemorrhagic conversion of pancreatitis and peri-pancreatic hemorrhage. Ten patients out of 12 patients had complications before admission, and nine of the 12 patients were on chemical prophylaxis. Pearson’s coefficient showed no statistically significant correlation between the incidence of complications and the use of chemical DVT prophylaxis. Multivariate analysis showed no specific variable that increased the risk of complications.
Conclusions: Our study showed that chemoprophylaxis for DVT in patients hospitalized for acute pancreatitis is neither harmful by causing hemorrhagic conversion of pancreatitis, peri-pancreatic hemorrhage nor beneficial by preventing splanchnic venous thrombosis.
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