Eptifibatide-induced profound thrombocytopaenia: a rare complication

2021 ◽  
Vol 14 (6) ◽  
pp. e241594
Author(s):  
Pranav Mahajan ◽  
Fatima Ayub ◽  
Roxana Azimi ◽  
Naveed Adoni
Keyword(s):  
Platelet Count ◽  
Intracranial Haemorrhage ◽  
Rare Complication ◽  
Antiplatelet Agent ◽  
Cardiac Catheterisation ◽  
Beta Lactam ◽  
Drug Induced ◽  
Beta Lactam Antibiotics ◽  
Common Causes ◽  
The Common

Drug-induced immune thrombocytopaenia (DITP) is a type of thrombocytopaenia caused by medications. It is one of the common causes of unexplained thrombocytopaenia. It is caused by the formation of autoantibodies against a particular drug and is commonly observed with medications like heparin and beta-lactam antibiotics. One of the rare causes of DITP is eptifibatide, a widely used antiplatelet agent for pretreatment in cardiac catheterisation. These patients can be asymptomatic or develop complications like skin bruising, epistaxis and even intracranial haemorrhage. We present a case of a 64-year-old man who developed eptifibatide-induced profound thrombocytopaenia leading to extensive skin bruising. He was treated with platelet transfusions followed by prompt improvement in platelet count.

scholarly journals An unusual cause of edema in a child with congenital heart disease post Fontan procedure

2019 ◽  
Vol 7 (11) ◽  
pp. 4396
Author(s):  
Minal Wade ◽  
Shweta Shettiwar ◽  
Ankita Shah
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Congenital Heart ◽  
Rare Complication ◽  
Fontan Procedure ◽  
Protein Losing Enteropathy ◽  
Common Causes ◽  
Disease Protein ◽  
The Common ◽  
Fontan Palliation

Protein Losing Enteropathy Post Fontan procedure. Protein Losing Enteropathy (PLE) is an uncommon cause of edema in children with congenital heart disease. Protein-Losing Enteropathy may be defined as excessive loss of proteins across the intestinal mucosa and is due to either a primary gastrointestinal abnormality or secondary to cardiac disease. Protein-losing enteropathy (PLE) is a rare complication of the Fontan palliation for functional single-ventricle. Although PLE occurs in about 3.5% of patients post-Fontan, it confers marked morbidity and high mortality within 5 years of diagnosis. The pathogenesis of Fontan-related PLE is not completely understood, and it is unclear why it develops in some patients post-Fontan and not others. We describe a child with Double Inlet Right Ventricle who had undergone Fontan procedure, and presented to us with generalised oedema. The child had hypoproteinaemia, the common causes for which were ruled out and was diagnosed as Protein Losing Enteropathy (PLE) related to his surgical intervention. Though, not frequently encountered it should be kept in mind as one of the causes of anasarca.

Cloxacillin-Induced Acute Tubulo Interstitial Nephritis

1992 ◽  
Vol 26 (10) ◽  
pp. 1241-1242 ◽  
Author(s):  
Roberto García-Ortiz ◽  
Roberto S. Espinoza ◽  
Gonzalo R. Silva ◽  
Rodrigo K. Alonso ◽  
Hector S. Opazo ◽  
...  
Keyword(s):  
Renal Function ◽  
Interstitial Nephritis ◽  
Case Reports ◽  
Urinary Output ◽  
Lumbar Pain ◽  
Dramatic Improvement ◽  
Beta Lactam ◽  
Drug Induced ◽  
Beta Lactam Antibiotics ◽  
Sterile Pyuria

OBJECTIVE: To report a case of possible cloxacillin-induced acute tubulo interstitial nephritis (AIN). CASE SUMMARY: A 15-year-old male patient presented with hypertension, edema, lumbar pain, sterile pyuria, eosinophiluria (ten percent), and severe renal dysfunction three months after the ingestion of cloxacillin. A renal biopsy revealed diffuse edema and inflammatory infiltrate of the interstitium (five percent eosinophils). He received four sessions of peritoneal dialysis with dramatic improvement in urinary output and renal function. His biochemical parameters returned to normal values 21 days after admission, without the use of glucocorticosteroids. DISCUSSION: Published case reports on AIN induced by penicillin and related drugs are reviewed and compared. The role of interstitial edema in acute renal failure associated with drug-induced AIN is mentioned. CONCLUSIONS: AIN is a rare but significant complication of therapy with penicillin and related drugs. The clinical picture is similar for all of these drugs, but skin rash and fever are absent in AIN induced by cloxacillin and cloxacillin-related drugs. Dialysis improved the patient's urinary output and renal function. Beta-lactam antibiotics should be avoided in patients with cloxacillin-induced AIN.

Prednisolone: role in amoxicillin–clavulanate-induced cholestatic liver injury

2021 ◽  
Vol 14 (4) ◽  
pp. e239488
Author(s):  
Melvin Qiyu Lee ◽  
Royale Chigozie ◽  
Irfan Khan ◽  
Gerard O'Mara
Keyword(s):  
Liver Injury ◽  
Liver Function Tests ◽  
Hepatocellular Injury ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
The Us ◽  
Common Causes ◽  
Amoxicillin Clavulanate ◽  
The Common ◽  
Cholestatic Liver Injury

A 68-year-old patient presented with symptoms of a urinary tract infection. A deterioration in the patient’s liver function tests (LFTs) was noted 1 week following completion of a course of amoxicillin–clavunalate. This progressively worsened, reaching its peak by day 30. Our investigations excluded other possible causes for deranged LFTs and there was no improvement of same despite reduced dosing of potentially hepatotoxic medications.A trial of 30 mg/day prednisolone was commenced, resulting in an immediate and progressive improvement in LFTs to baseline over a period of 22 days and an improvement in constitutional symptoms such as tiredness and poor appetite. Drug-induced liver injury (DILI) is one of the common causes of acute hepatitis and a leading cause of acute liver failure in the US and Europe. Patterns of DILI can be generally divided into: (1) hepatocellular injury, (2) cholestatic injury and (3) mixed injury.

Hematological Effects Associated with Beta-Lactam Use

1986 ◽  
Vol 20 (11) ◽  
pp. 833-836 ◽  
Author(s):  
Lesia M. Babiak ◽  
Michael J. Rybak
Keyword(s):  
Coagulation Cascade ◽  
Close Monitoring ◽  
Beta Lactam ◽  
Beta Lactams ◽  
Drug Induced ◽  
Antimicrobial Spectrum ◽  
Beta Lactam Antibiotics ◽  
Normal Platelet ◽  
Hematological Effects ◽  
Life Threatening

Beta-lactam antibiotics have continued to be the mainstay of antiinfective treatment. Newer agents, such as the third-generation cephalosporins or ureidopenicillins, have the advantage of a broader antimicrobial spectrum and improved pharmacokinetics. The beta-lactams are often promoted as alternatives to more toxic antibiotic regimens. However, several of the beta-lactams have been shown to produce hematological effects, some of which can be life threatening. The primary hematological effects appear to be inhibition of normal platelet function and the coagulation cascade, which is reflected by changes in bleeding times and increases in prothrombin time and activated partial thromboplastin time, respectively. Although not all patients will develop bleeding problems associated with these agents, close monitoring of patients with risk factors for bleeding and dosage adjustments may help to avert these drug-induced hematological problems.

scholarly journals Serologic Characterization of Antibodies in Patients Experiencing Piperacillin-Induced Immune Thrombocytopenia

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 1078-1078
Author(s):  
Mark Rasmussen ◽  
Daniel W. Bougie ◽  
Gregory H. Denomme ◽  
Richard H. Aster
Keyword(s):  
Conflicts Of Interest ◽  
Normal Subjects ◽  
Normal Serum ◽  
Beta Lactam ◽  
Drug Induced ◽  
Beta Lactam Antibiotics ◽  
Immune Hemolytic Anemia ◽  
Drug Dependent ◽  
High Concentrations ◽  
Optimized Conditions

Beta lactam antibiotics (penicillins, cephalosporins, etc) are relatively common triggers for immune hemolytic anemia, neutropenia and drug-induced thrombocytopenia (DITP) but the mechanism(s) responsible for this side effect are not well understood. The ureidopenicillin, piperacillin, is one of the beta lactam drugs implicated most often as a trigger for immune cytopenia. We characterized drug-dependent reactions of antibodies (abs) identified in 18 patients with piperacillin-associated thrombocytopenia. Each of the 18 patients had an ab that reacted strongly (flow cytometry) with normal platelets but not RBC when soluble piperacillin was present. These reactions were not inhibited by the highest drug concentration that could be achieved in the reaction mixture and similar antibodies were not found in normal serum. These reactions are similar to those obtained with drug-dependent antibodies (DDAbs) found in patients sensitive to quinine, vancomycin, and many other drugs known to cause DITP. Evidence suggests that such drugs promote binding of DDAbs to their targets by reacting with antibody CDR3 and modifying its specificity (Blood 2015;126:2138). Beta-lactam drugs differ from most other medications in their ability to spontaneously link covalently to free amino groups on membrane proteins to produce potentially immunogenic haptens that could induce abs theoretically capable of contributing to thrombocytopenia in piperacillin-treated patients. We optimized conditions for "haptenization" of platelets and RBCs with piperacillin and tested patient and normal sera for abs that recognize piperacillin-coated cells. Complete inhibition of binding by excess soluble drug was a criterion for a "positive" reaction. As shown in Table 1, IgG and IgM abs reactive with piperacillin-coated RBCs were found in each of 18 patient and 20 normal sera tested; IgM abs reactive with piperacillin-coated platelets were found in nearly all of both groups and similar IgG abs were found in about half. Reaction strength of IgM abs against piperacillin-coated RBCs correlated closely with that against piperacillin-coated platelets The findings demonstrate two distinctly different types of piperacillin-specific abs in patients experiencing piperacillin-induced thrombocytopenia. The first is usually IgG, binds to platelets but not RBCs only when soluble drug is present, is not inhibited by excess drug, even at high concentrations, correlates with exposure to piperacillin and development of thrombocytopenia and is not found in normal persons. This behavior is similar to that of DDAbs induced by quinine, vancomycin and many other drugs. The second is commonly IgM and less often IgG, binds to piperacillin-coated platelets and RBCs, is inhibited by soluble drug and, as the IgM isoform, is found in nearly all normal subjects. Failure of abs that recognize piperacillin-coated cells to distinguish between platelets and RBCs in any consistent way argues against the possibility that they play a role in the pathogenesis of piperacillin-induced DITP. "Naturally-occurring" IgM abs that recognize piperacillin-coated RBC were previously described by Garratty et al (Transfusion 2008;48:2429) and could reflect widespread environmental exposure to beta-lactam antibiotics. Disclosures No relevant conflicts of interest to declare.

scholarly journals Etiology and Pattern of Drug Induced Liver Injury in a Tertiary Care Hospital of Nepal

2019 ◽  
Vol 21 (3) ◽  
pp. 220-223
Author(s):  
Anuj K.C. ◽  
S. Jha ◽  
S. Thapa
Keyword(s):  
Liver Injury ◽  
Liver Toxicity ◽  
Tertiary Care ◽  
Care Hospital ◽  
Drug Induced ◽  
Common Cause ◽  
Drug Induced Liver Injury ◽  
Common Causes ◽  
The Common ◽  
Mixed Pattern

Drug induced liver injury (DILI) is one of the common cause of liver toxicity. Most of the drugs used today are hepatotoxic. DILI accounts for approximately one-half of the cases of acute liver failure and mimics all forms of acute and chronic liver disease. It is the single most common adverse drug reaction leading to a halt in the development of new medication by pharmaceutical company, failure of new drug to obtain regulatory approval, and withdrawal or restriction of existing drug from the market. The aim of this study is to evaluate common causes and patterns of DILI in our setting. Twenty-seven patients were enrolled in the study. Ant tubercular drugs were most common cause of DILI, accounting for 48.2%. Other common causes of DILI were paracetamol (14.8%) and NSAID’s (11.1%). The most common pattern of liver injury seen was mixed pattern which was present in63%, followed by cholestatic and hepatocellular pattern. Hence, we should be very careful while prescribing these frequently used drugs.

scholarly journals Antibiotic‑associated drug‑induced liver damage with cholestasis: actualization of problem in COVID‑19 era

2021 ◽  
pp. 31-43
Author(s):  
O. D. Ostroumova ◽  
A. P. Pereverzev ◽  
E. E. Pavleeva ◽  
R. R. Romanovsky
Keyword(s):  
Liver Damage ◽  
Real Life ◽  
Beta Lactam ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Beta Lactam Antibiotics ◽  
Upper Limits ◽  
Daily Dose ◽  
Chronic Course

Drug-induced liver injury (DILI) is a fairly frequent adverse drug reaction, which accounts for about half (40–50 %) of cases of acute liver damage. The cholestatic variant of DILI is characterized by an increase in the activity of alkaline phosphatase (ALP) above the two upper limits of the norm (ULN) or the ratio of alanine aminotransferase (ALT) / ALP ≤ 2 in chronic course. A common cause of the cholestatic variant of DILI is a use of drugs for the treatment of infectious diseases, such as beta-lactam antibiotics, Aminoglycosides, Amphenicol, Lincosamides, macrolides, fluoroquinolones, antituberculosis drugs, etc. This problem has acquired particular urgency during the COVID-19 pandemic. The widespread use of azithromycin, hydroxychloroquine, interferons, lopinavir, and other drugs for the treatment of COVID-19 also contributed to an increase in the incidence of DILI. In accordance with clinical guidelines in case of suspicion of a drug-induced liver damage, one should stop use of suspected drug and, if necessary, prescribe hepatoprotectors, for example, ursodeoxycholic acid (UDCA). The effectiveness of the use of UDCA in patients with DILI, including those caused by the intake of antibacterial drugs, has been confirmed by randomized placebo-controlled clinical trials. The effectiveness of UDCA -drug Ursosan® has been confirmed in real life clinical practice. This drug can be used for long-term (up to several months), or lifelong treatment with hepatotoxic drugs like antituberculosis and antirheumatic drugs. The daily dose of Ursosan® is 12–15 mg/kg, if necessary – 20 mg / kg (with a weight of a patient about 75–100 kg, daily dose will be equal to two tablets of Ursosan Forte®, 500 mg).

scholarly journals The Odd Couple(s): An Overview of Beta-Lactam Antibiotics Bearing More Than One Pharmacophoric Group

2021 ◽  
Vol 22 (2) ◽  
pp. 617
Author(s):  
Margherita De Rosa ◽  
Anna Verdino ◽  
Annunziata Soriente ◽  
Anna Marabotti
Keyword(s):  
Antimicrobial Resistance ◽  
Large Family ◽  
Biological Properties ◽  
Beta Lactam ◽  
Chemical Modifications ◽  
Novel Weapons ◽  
Beta Lactam Antibiotics ◽  
The Common ◽  
Bifunctional Compound

β-lactam antibiotics are among the most important and widely used antimicrobials worldwide and are comprised of a large family of compounds, obtained by chemical modifications of the common scaffolds. Usually these modifications include the addition of active groups, but less frequently, molecules were synthesized in which either two β-lactam rings were joined to create a single bifunctional compound, or the azetidinone ring was joined to another antibiotic scaffold or another molecule with a different activity, in order to create a molecule bearing two different pharmacophoric functions. In this review, we report some examples of these derivatives, highlighting their biological properties and discussing how this strategy can lead to the development of innovative antibiotics that can represent either novel weapons against the rampant increase of antimicrobial resistance, or molecules with a broader spectrum of action.

scholarly journals COVID-19—A Trigger Factor for Severe Immune-Mediated Thrombocytopenia in Active Rheumatoid Arthritis

Life ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 77
Author(s):  
Anca Bobircă ◽  
Florin Bobircă ◽  
Ioan Ancuța ◽  
Anca Florescu ◽  
Mihai Bojincă ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Platelet Count ◽  
Viral Infections ◽  
Molecular Mimicry ◽  
Rare Complication ◽  
Antigen Expression ◽  
Trigger Factor ◽  
Drug Induced ◽  
Immune Mediated ◽  
Prognosis Indicator

Thrombocytopenia is defined as a platelet count below 150,000/mm3 for adults. There is still controversy about whether individuals with platelet counts of 100,000/mm3 to 150,000/mm3 should be classified as having genuine thrombocytopenia or borderline thrombocytopenia. Thrombocytopenia is considered mild when the platelet count is between 70,000 and 150,000/mm3 and severe if the count is less than 20,000/mm3. Thrombocytopenia in rheumatoid arthritis is a rare complication, with an incidence estimated between 3 and 10%. The main etiological aspects include drug-induced thrombocytopenia and immune thrombocytopenic purpura. The most common hematological abnormalities in SARS-CoV-2 infection are lymphopenia and thrombocytopenia. It has been observed that the severity of thrombocytopenia correlates with the severity of the infection, being a poor prognosis indicator and a risk factor for mortality. COVID-19 can stimulate the immune system to destroy platelets by increasing the production of autoantibodies and immune complexes. Autoimmunity induced by viral infections can be related to molecular mimicry, cryptic antigen expression and also spreading of the epitope. During the COVID-19 pandemic, it is of great importance to include the SARS-CoV-2 infection in differential diagnoses, due to the increased variability in forms of presentation of this pathology. In this review, our aim is to present one of the most recently discovered causes of thrombocytopenia, which is the SARS-CoV-2 infection and the therapeutic challenges it poses in association with an autoimmune disease such as rheumatoid arthritis.

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