Current drug safety最新文献

Background: The Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) is a serious adverse reaction that occurs weeks after the onset of drug exposure. DRESS syndrome is commonly associated with antiseizure drugs, sulfa drugs, and antibiotics.

Case presentation: This was a case report of a 20-year-old female who suffered from DRESS due to vancomycin with symptoms similar to the Redman syndrome. The patient was a case of Infective endocarditis due to methicillin-resistant Staphylococcus aureus (MRSA), and vancomycin was intravenously administered. On the 18th day, during the administration of vancomycin, the patient developed sudden severe flushing over the face and trunk. The offending drug was suspended and treated with antihistamines in view of Redman syndrome. Later, the patient developed uncontrolled fever, desquamating rash all over the body, severe pruritis, and eosinophilia. On applying the RegiScar score, a probable case of DRESS was diagnosed. The patient was managed symptomatically and discharged.

Discussion: The clinical presentation of DRESS includes skin rash, fever, eosinophilia, and organ involvement. But, in this case, there was a varied initial presentation of DRESS with severe flushing, which mimics the Redman syndrome due to vancomycin. Difficulty in establishing organ involvement remained a challenge in diagnosing DRESS.

Conclusion: DRESS can have a varied clinical presentation. Careful monitoring of all vital parameters is important in preventing the misdiagnosis of DRESS syndrome.

Introduction: This case study presents a rare and fatal instance of Toxic Epidermal Necrolysis (TEN) and Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) syndrome in a 51-year-old male patient diagnosed with Rheumatoid Arthritis (RA).

Case presentation: The patient was initially treated with sulfasalazine, leflunomide, and hydroxychloroquine, following which he developed a rash, fever, and loose stools. Drug allergy was suspected, and the anti-rheumatic medications were withdrawn, following which, the patient improved. A subsequent attempt was made to treat the RA with methotrexate, prednisolone, and hydroxychloroquine, following which the rash returned along with an increase in severity, including detachment of the epidermis and mucosa, and systemic involvement, both hepatic and renal. The patient ultimately succumbed to multiple organ dysfunction syndrome and neutropenic sepsis.

Conclusion: This case highlights the possibility of DRESS syndrome and Stevens-Johnson Syndrome (SJS)/TEN following treatment with anti-rheumatic medications. Evidence of this is rare, with the exception of sulfasalazine. This case also considers that the signs of a moderately severe adverse drug reaction could be the early warning signs of DRESS syndrome, which can be difficult to manage and may turn fatal. Additionally, this case highlights the need for maintenance of quality health records in low- and middle-income countries due to the failure to identify hydroxychloroquine as a suspected drug inducing the initial adverse reaction that resulted in it being prescribed again, leading to a fatal outcome.

Background: Rifampicin is a first-line anti-tuberculosis drug, but it may cause severe allergic adverse reactions.

Case presentation: This case report describes an unusual and severe adverse reaction to rifampicin in a 53-year-old male patient with pulmonary tuberculosis. The patient developed intense systemic pain within 4 hours of rifampicin administration, affecting multiple organs and joints, without typical allergic manifestations, such as fever or rash. The pain progressively worsened over three consecutive days of treatment, reaching its peak intensity (NRS score 8/10) on the third day with pain duration extending from 3 to 8 hours. The severe pain was characterized as sharp and burning in nature, significantly impacting the patient's daily activities and mobility. A subsequent rifampicin challenge test (single dose 0.45g) confirmed the causal relationship by reproducing identical severe pain symptoms. The Naranjo adverse drug reaction probability scale yielded a score of 7, indicating a "probable" causal relationship. Notably, the patient exhibited underlying autoimmune abnormalities (positive ANA and elevated ESR), which may have contributed to the severity of the reaction through enhanced inflammatory responses and altered pain mechanisms. The symptoms completely resolved upon rifampicin discontinuation, and alternative treatment with levofloxacin proved successful with no pain recurrence during the fourmonth follow-up period.

Conclusion: This case highlights a previously unreported presentation of rifampicin hypersensitivity and emphasizes the importance of careful risk assessment in patients with autoimmune features before initiating rifampicin therapy.

Introduction: Prescribing cascade is a condition in which a drug administered to a patient causes an adverse reaction that is misinterpreted as a new condition, resulting in the addition of a new drug.

Case presentation: Here, we report the case of an elderly female patient who suffered from metabolic, neurologic, and urinary consequences of a prescribing cascade of antiemetic, antiepileptic, and dopaminergic drugs. While levosulpiride caused Parkinsonian symptoms, the dopaminergic drugs and valproate caused refractory hyponatremia followed by altered sensorium, and clidinium contributed to urinary retention.

Conclusion: The case highlights the need to be vigilant for adverse consequences of the prescribing cascade, especially for antiemetic drugs, such as levosulpiride, because of its propensity to induce extrapyramidal reactions in older patients. In cases of refractory hyponatremia, a trial of de-challenge of valproate and dopaminergic drugs should be considered. The identification and removal of the culprit drugs can rescue the patient from a disabling cycle of adverse drug reactions.

Background: The kidneys, intricate organs responsible for maintaining fluid and electrolyte balance, are susceptible to damage from diverse nephrotoxic insults, including drugs, toxins, and metabolic disorders. In recent years, flavonoids, bioactive compounds abundant in fruits, vegetables, and herbal extracts, have emerged as promising candidates for renal protection due to their potent antioxidant and anti-inflammatory properties.

Methods: We have collected the data that supported this idea to conduct a comprehensive review by using scientific databases, such as Pub Med ®, ScienceDirect ®, Google Scholar ®, and MEDLINE ®. An attempt was made to refer to all English-language articles published between 2000 to 2020 using keywords like flavonoids potential in nephrotoxicity and nephrotoxicity treatment approaches with herbal remedies.

Conclusion: This comprehensive review delves into the molecular mechanisms underlying the reno-protective effects of flavonoids. By scavenging reactive oxygen species, inhibiting inflammatory mediators, and modulating intracellular signalling pathways, flavonoids can mitigate oxidative stress and inflammation, thereby preserving renal function and integrity. Preclinical studies have demonstrated the potential of specific flavonoids in ameliorating drug-induced nephrotoxicity, renal ischemia-reperfusion injury, diabetic nephropathy, and other kidney diseases. Furthermore, epidemiological evidence highlights the inverse relationship between flavonoid intake and the risk of developing kidney diseases. Nevertheless, understanding the molecular mechanisms of flavonoids in nephroprotection offers exciting prospects for developing novel therapeutic strategies to combat kidney diseases and promote kidney health.

Introduction: It is essential to exclude other causes, such as autoimmune diseases and bacterial infections, before attributing cutaneous/systemic vasculitis to drug use.

Case study: This report discusses the case of a young man who developed multi-organ failure and cutaneous vasculitis following the use of antifungal medications (terbinafine and itraconazole) for dermatophyte infections. Tests for autoimmune diseases and infections were negative. Given his drug history and a skin biopsy indicating leukocytoclastic vasculitis, it was inferred that the vasculitis was likely drug-induced. Despite treatment with steroids, intravenous immunoglobulins, and plasmapheresis, the patient did not survive, possibly due to delayed diagnosis and treatment.

Conclusion: In community practice, Drug-induced Vasculitis (DIV) is frequently overlooked. When patients present with skin rash, fever, and multi-organ dysfunction, DIV should be considered, particularly in the context of recent drug use. Over-the-counter antifungals, like terbinafine or itraconazole, can cause DIV and may be fatal if not promptly diagnosed and treated.

Depression, a pervasive mental health disorder, affects millions worldwide, necessitating the widespread use of synthetic anti-depressant medications. While these pharmaceutical interventions have demonstrated efficacy in alleviating depressive symptoms, they are not without their associated side effects. This review provides a comprehensive overview of the side effects of synthetic anti-depressants, aiming to enhance the understanding of their clinical implications. Common side effects explored include gastrointestinal disturbances, sexual dysfunction, insomnia, weight gain, and cognitive impairments. Additionally, this review delves into less frequent but potentially severe adverse events, such as serotonin syndrome, hyponatremia, and cardiac complications associated with specific classes of synthetic anti-depressants. Moreover, the review examines the interplay between side effects and treatment adherence, emphasizing the importance of monitoring and managing these effects in clinical practice. It also discusses strategies to mitigate side effects, including dose adjustments, combination therapy, and alternative treatment approaches. In conclusion, this comprehensive review sheds light on the multifaceted landscape of side effects associated with synthetic anti-depressants. By providing clinicians with a nuanced understanding of these effects, it aims to facilitate informed decision-making, personalized treatment plans, and improved patient outcomes in managing depression.

Background: Acute Pancreatitis (AP) is an uncommon complication that rarely occurs during Rheumatoid Arthritis (RA). Among the varied etiologies of AP, Drug-induced Pancreatitis (DIP) remains a rare entity and a rather challenging condition. A large panel of drugs have been reported to cause pancreatitis; however, there are no cases of tofacitinib-induced pancreatitis reported in the literature.

Case presentation: We have, herein, reported the case of a Tunisian 58-year-old woman with a four-year history of RA who experienced two episodes of AP; the first one occurred on the second day of a 3-day series of methylprednisolone intravenous injections, and the second episode occurred on the sixth-day of tofacitinib administration. Each time, she presented acute abdominal pain with characteristic radiation to the back. Symptoms resolved spontaneously once the suspected drug was discontinued. In the event of a negative investigation, including abdominal ultrasonography and magnetic resonance imaging, and assessment of albumin, calcemia, triglyceridemia, serum ferritin, and IgG4 levels, DIP was the most likely diagnosis.

Conclusion: Although DIP is still a rare condition, it remains serious with an increased risk of mortality. We intended to alert clinicians that in addition to the known side effects of tofacitinib, pancreatitis may be induced by this drug, especially in predisposed patients.

Introduction: Serotonin syndrome is a potentially life-threatening condition that can occur as a result of the therapeutic use of serotonergic medications or drug interaction. In this study, we describe two cases of serotonin syndrome-associated hypertensive crisis following linezolid use.

Case presentation: The first patient was a 52-year-old female who was admitted due to a diabetic foot infection and pneumonia associated with a decreased consciousness level. Serotonin syndrome occurred 24 hours after starting the linezolid use. Resistant hypertension was the main hemodynamic finding. It could not be controlled with amlodipine, valsartan, prazosin, and nitroglycerin infusion. Resistant hypertension and other symptoms of serotonin syndrome were resolved about 48 hours after discontinuation of linezolid use. The second case was a man with a history of kidney transplant, diabetes, and hypertension. He was admitted to the ICU due to severe COVID-19. Broad-spectrum antibiotics [linezolid, cefepime], and remdesivir was initiated. Following intubation, continuous infusion of fentanyl was used for sedation. Within 24 hours after fentanyl and linezolid initiation, severe agitation, eye clonus, hyperreflexia, hypertension [160-186 /90-110 mmHg], and tachycardia [>100/min] were noted. With the possible diagnosis of serotonin syndrome, fentanyl was discontinued, and morphine was initiated. The patient's symptoms improved 48 hours after discontinuation of fentanyl.

Conclusion: Both patients had a history of well- controlled hypertension. Hypertensive crisis has occurred after recent or concurrent use of serotonergic agents with linezolid. A thorough evaluation of the patient's medical history and current condition can help clinicians prevent this syndrome in critically ill patients.