scholarly journals Drug-induced hypersensitivity syndrome caused by valproic acid as a monotherapy for epilepsy: First case report in Asian population

2017 ◽  
Vol 8 ◽  
pp. 108-110 ◽  
Author(s):  
X.T. Wu ◽  
P.W. Hong ◽  
D.J. Suolang ◽  
D. Zhou ◽  
H. Stefan
DICP ◽  
1989 ◽  
Vol 23 (3) ◽  
pp. 227-229 ◽  
Author(s):  
Patrick E. Nwakama ◽  
Harry J. Jenkins ◽  
Robert T. Bailey ◽  
John Pelligrino ◽  
Tom R. Demeester ◽  
...  

This is the first case report of esophageal injury caused by Percogesic. A 31-year-old healthy white woman presented with dysphagia and retrosternal pain following the ingestion of a Percogesic tablet. The patient felt the tablet lodge in her mid-esophagus even though she ingested it with a cupful of water and in the upright position. Additional fluid was taken to dislodge the tablet with no success. Past medical history was unremarkable for heartburn, regurgitation, or dysphagia. Upper gastrointestinal endoscopy revealed a well-circumscribed deep ulceration in the mid-esophagus. Hospitalization was required due to persistent dysphagia. Treatment consisted of a three-day regimen of liquid antacid, intravenous ranitidine hydrochloride, and metoclopramide. This case emphasizes that pill entrapment can occur in the esophagus in healthy individuals, even when taken in the upright position with plenty of fluid; and mucosal injury can be produced by drugs not generally reported to cause gastrointestinal adverse effects or mucosal injury.


2015 ◽  
Vol 53 (01) ◽  
pp. 92-96 ◽  
Author(s):  
Atsuko Shihyakugari ◽  
Akiko Miki ◽  
Natsue Nakamoto ◽  
Hiroki Satoh ◽  
Yasufumi Sawada

2017 ◽  
Vol 41 (S1) ◽  
pp. S254-S254
Author(s):  
S. Petrykiv ◽  
L. de Jonge ◽  
M. Arts

IntroductionBurning mouth syndrome (BMS) is characterized by an intraoral burning sensation for which no medical or dental cause can be found. Sporadic evidence suggests that drug induced conditions may evoke BMS. Intriguingly, we observed a patient who developed BMS after induction of citalopram.Objectives & aimsA case report of patient with BMS from our psychiatric ward will be presented here, followed by a literature review on drugs induced BMS.MethodsBased on a recent literature search, we present a first case report of BMS that was apparently induced in patient shortly after beginning of citalopram. We performed a systematic search through PubMed, EMBASE and Cochrane's Library to find more cases of psychotropic induced BMS.ResultsMs. A. was a 72-year old woman meeting DSM-IV diagnostic criteria for melancholic depression, who was observed in a clinical setting. We started citalopram 10 mg. 1dd1, with 10 mg. 1dd1 increase over 7 days to 20 mg, 1dd1. The following day, she displayed a persistent burning painful sensation in the mouth. Other than BMS oropharyngological syndromes were excluded after consultation with qualified medical specialists. Citalopram therapy was discontinued, and nortrilen treatment was initiated. BMS symptoms resolved over four days. Twelve case reports have linked BMS to the use antidepressants and anxiolytics.ConclusionContrasting the statement that no medical cause can be found for BMS, we found that psychotropics may evoke the syndrome. Compared to other psychotropic drugs, antidepressant medication has the strongest association with BMS.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2021 ◽  
Vol 14 (4) ◽  
pp. e241547
Author(s):  
Sandeep Pagali ◽  
Christopher Edquist ◽  
Nicholas O'Rourke

A 20-year-old woman presented following an intentional overdose of valproic acid. Use of valproic acid, either acute or chronic, can result in hyperammonaemia. Mild hyperammonaemia with chronic use is mostly asymptomatic but can also present with concern for encephalopathy. Acute valproic acid toxicity results in significant hyperammonaemia, which can contribute to encephalopathy. Levocarnitine is the treatment of choice in valproic acid toxicity-related hyperammonaemia. For severe cases of encephalopathy, intermittent haemodialysis can also be considered. To our knowledge, this is the first case report to clearly show symptom relapse and hyperammonaemia after discontinuing levocarnitine. We recommend levocarnitine therapy for at least 72 hours, followed by an additional 24 hours of monitoring for symptom relapse and hyperammonaemia after levocarnitine discontinuation.


2020 ◽  
Vol 77 (7) ◽  
pp. 523-528
Author(s):  
Kwame Asare ◽  
Caroline Barone Gatzke

Abstract Purpose A case of mycophenolate mofetil (MMF)–induced oral ulceration in a kidney transplant recipient is reported. Summary A 54-year-old man who had received a kidney transplant 7 months previously reported to our outpatient clinic with severe oral ulcers with odynophagia and was admitted to the hospital. His maintenance immunosuppressive agents at the time of admission consisted of tacrolimus and mycophenolate. The patient had stable renal function, with all laboratory values within normal ranges. After various alternative etiologies were ruled out, drug-induced oral ulceration was suspected, and the patient’s tacrolimus dose was empirically reduced, resulting in reduction of the trough concentration from 10 ng/mL to 3.3 ng/mL without improvement of the ulceration. Mycophenolate-induced oral ulceration was suspected, and MMF was discontinued. Within 5 days of discontinuation, there was a remarkable improvement in both the size and severity of the ulceration, and the patient was discharged from the hospital. During the next clinic visit (a total of 12 days after MMF was discontinued), the patient’s mouth and esophageal ulcers had completely healed. Six weeks after complete resolution of the ulcer, MMF at a dosage of 250 mg twice daily was initiated; the dosage was subsequently increased to 500 mg twice daily without a recurrence of ulceration. Conclusion A 54-year-old man developed oral ulceration after 7 months of MMF therapy. Discontinuation of therapy resulted in prompt resolution of the patient’s ulcers, with no recurrence of ulceration at a lower MMF dose. This is the first case report indicating that mycophenolate-induced ulceration may be dose dependent.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yutaka Muto ◽  
Naoyuki Kuse ◽  
Minoru Inomata ◽  
Nobuyasu Awano ◽  
Mari Tone ◽  
...  

Abstract Background Drug-induced hypersensitivity syndrome (DIHS)/drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is an important adverse reaction caused by a few drugs. Reactivation of human herpesvirus 6 (HHV-6) is known to be associated with its pathogenesis. DIHS occasionally manifests as pulmonary lesions with a variety of imaging findings. Case presentation An 83-year-old woman started taking minodronic acid hydrate 5 years before admission. She noticed a generalized skin rash 44 days before admission and started oral betamethasone-d-chlorpheniramine maleate combination tablets for allergic dermatitis. She developed a fever and cough in addition to the rash, and was referred to our hospital. Laboratory data showed a high level of eosinophils and liver and biliary enzymes. Computed tomography (CT) studies revealed bilateral diffuse ground-glass opacities with ill-defined centrilobular nodules from the central to peripheral regions of the lungs. Transbronchial lung cryobiopsy specimens showed that lymphocyte infiltration was observed in the alveolar walls and fibrinous exudates and floating macrophages in the alveolar lumina. Immunohistochemistry of biopsy specimens showed more CD4+ lymphocytes than CD8+ lymphocytes, while few Foxp3+ lymphocytes were recognized. The serum anti-HHV-6 immunoglobulin G titer increased at 3 weeks after the first test. Based on these findings, we diagnosed her with DIHS. We continued care without using corticosteroids since there was no worsening of breathing or skin condition. Eventually, her clinical symptoms chest CT had improved. Minodronic acid hydrate was identified as the culprit drug based on the positive results of the patch test and drug-induced lymphocyte stimulation test. Conclusions We described the first case of DIHS caused by minodronic acid hydrate. Lung lesions in DIHS can present with bilateral diffuse ground-glass opacities and ill-defined centrilobular nodules on a CT scan during the recovery phase. Clinicians should be aware of DIHS, even if patients are not involved with typical DIHS/DRESS-causing drugs.


2015 ◽  
Vol 7 (1) ◽  
pp. 23-33 ◽  
Author(s):  
Jagoda Balaban ◽  
Đuka Ninković-Baroš

AbstractDrug-induced delayed multiorgan hypersensitivity syndrome, also known as drug rash (reaction) with eosinophilia and systemic symptoms (DRESS) syndrome, represents a drug-induced cluster of skin, hematologic and systemic symptoms. More than forty drugs have been associated with this syndrome. We present a case of DRESS syndrome suspecting that lamotrigine was directly responsible for the patient’s rash and other symptoms. A female patient presented with extensive skin rash, fever, hematologic abnormalities, organ involvement such as hepatitis, pancreatitis and respiratory symptoms. The symptoms developed four weeks after the initiation of the offending drug, and disappeared eight weeks after its discontinuation.


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