Phenazopyridine-Induced Sulfhemoglobinemia

2005 ◽  
Vol 39 (6) ◽  
pp. 1128-1130 ◽  
Author(s):  
Anuradha S Gopalachar ◽  
Venita L Bowie ◽  
Parag Bharadwaj

OBJECTIVE: To report a case of sulfhemoglobinemia in a patient receiving phenazopyridine for a urinary tract infection. CASE SUMMARY: A 63-year-old white woman presented to the emergency department with complaints of fatigue and bluish discoloration of her body that had gradually progressed over the previous 6–8 weeks. About 4 months prior to presenting to the emergency department, she had started taking phenazopyridine, an over-the-counter medication for symptoms of dysuria. Because the cyanosis did not improve after the patient received oxygen and methylene blue, sulfhemoglobinemia was suspected and confirmed by spectrophotometer analysis. DISCUSSION: Sulfhemoglobin is a green-pigmented molecule containing a sulfur atom in one or more of the porphyrin rings. It is a rare cause of cyanosis, which is usually drug induced. Sulfhemoglobinemia is suspected when a cyanotic patient has normal to near-normal oxygen tension, laboratory reports of elevated methemoglobin, and does not respond to methylene blue therapy. Sulfhemoglobinemia is relatively rare, despite the widespread use of drugs that have been reported to cause it. Predisposing factors, such as chronic constipation, present in our patient, have been suggested as a source of hydrogen sulfide. CONCLUSIONS: This case of sulfhemoglobinemia, which occurred after the patient took phenazopyridine, is considered a probable adverse event according to the Naranjo probability scale.

2005 ◽  
Vol 39 (5) ◽  
pp. 944-948 ◽  
Author(s):  
Leisa L Marshall

OBJECTIVE: To report the probable association of angioedema with aspirin therapy and the selective cyclooxygenase-2 (COX-2) inhibitor rofecoxib. CASE SUMMARY: A 44-year-old white woman, previously tolerant to aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs), developed angioedema of the lips after ingesting two 325-mg aspirin tablets during one day. The reaction occurred 3 hours after taking the second aspirin and resolved within 3 hours. Two weeks later, the patient took a 25-mg rofecoxib tablet for a sore throat, and she developed angioedema 51/2 hours later. Although the woman took 50 mg of diphenhydramine, the swelling did not subside. She repeated the diphenhydramine dose in the evening and, by noon the next day, 261/2 hours after the angioedema began, it was resolved. The patient's internist prescribed an epinephrine auto-injector and advised her to consult an allergist. With skin testing and oral rechallenge with aspirin, but not rofecoxib, the allergist determined the cause of the reactions to be aspirin-induced angioedema and selective COX-2 inhibitor intolerance. The Naranjo probability scale indicated that aspirin was a highly probable cause and rofecoxib was a probable cause of this patient's angioedema. DISCUSSION: Aspirin-induced angioedema and NSAID intolerance have been well documented. There are reports of both tolerance and intolerance to selective COX-2 inhibitors in patients with documented allergy-like reactions to aspirin and NSAIDs. CONCLUSIONS: Patients with aspirin and NSAID intolerance may develop intolerance to COX-2 inhibitors, especially with repeated exposure.


2005 ◽  
Vol 39 (5) ◽  
pp. 966-969 ◽  
Author(s):  
Lydia ◽  
Nishan H Fernando ◽  
Hurbert I Hurwitz ◽  
Michael A Morse

OBJECTIVE: To report the successful desensitization of a patient to oxaliplatin utilizing an 8-hour desensitization regimen in a controlled environment. CASE SUMMARY: A 53-year-old white woman with metastatic colon cancer was receiving oxaliplatin, bevacizumab, and capecitabine every 2 weeks, with a partial response to therapy. On her fifth cycle of this regimen, she experienced diaphoresis, hypotension, nausea, abdominal cramping, and coryza. According to the Naranjo probability scale, oxaliplatin, and not bevacizumab, was the probable cause of the hypersensitivity reaction. The woman continued therapy with capecitabine and bevacizumab, resulting in stable disease. Due to her initial response to the oxaliplatin-based regimen, it was decided to attempt desensitization to oxaliplatin in a controlled, inpatient environment. An 8-hour desensitization schedule was employed, and the patient successfully completed an additional 3 cycles with full-dose oxaliplatin. DISCUSSION: Hypersensitivity reactions to platinum-containing compounds are well described and potentially life threatening. With expanded use of oxaliplatin in various malignancies, an increased number of hypersensitivity reactions will likely be reported. Patients with previous hypersensitivity reactions to carboplatin are at risk for similar reactions to oxaliplatin. We achieved successful desensitization for oxaliplatin using increased concentrations of the drug over an 8-hour period concomitant with oral and intravenous corticosteroids and histamine blockers. CONCLUSIONS: Hypersensitivity reactions to platinum compounds may result in discontinuation of active therapies in patients with metastatic disease. Desensitization to oxaliplatin is possible utilizing this approach.


BJPsych Open ◽  
2019 ◽  
Vol 5 (5) ◽  
Author(s):  
David Goldrich ◽  
Anita Sreedhar ◽  
Rehan Aziz ◽  
Kenneth R. Kaufman ◽  
Anthony Tobia ◽  
...  

Aspirin-use disorder is an underreported condition. Identification of the signs and symptoms of aspirin misuse are important in light of prevalent non-prescribed medicine/over-the-counter medication (NPM/OTC) misuse. We discuss here the case of a patient with a history of chronic aspirin misuse who presented to the emergency department with salicylate intoxication and described elation secondary to deliberate aspirin consumption. This case highlights the importance of screening for NPM/OTC medication misuse in at-risk populations.


2014 ◽  
Vol 2014 ◽  
pp. 1-2
Author(s):  
Marwan Sheikh-Taha ◽  
Pascale Frenn

Drug-induced autoimmune hemolytic anemia is a rare condition. We report the case of a 32-year-old white female who presented to the emergency department with generalized fatigue, fever, and jaundice. The patient reported using levofloxacin few days prior to presentation for urinary tract infection. The patient had evidence of hemolytic anemia with a hemoglobin of 6.7 g/dL which dropped to 5 g/dL on day 2, the direct Coombs test was positive, indirect bilirubin was 5.5 mg/dL, and LDH was 1283 IU/L. Further testing ruled out autoimmune disease, lymphoma, and leukemia as etiologies for the patient’s hemolytic anemia. Levofloxacin was immediately stopped with a gradual hematologic recovery within few days.


1996 ◽  
Vol 30 (11) ◽  
pp. 1251-1254 ◽  
Author(s):  
Gretchen M Tush ◽  
Robert J Kuhn

OBJECTIVE: To report a case of methemoglobinemia induced by benzocaine and resorcinol (Vagisil) cream, an over-the-counter medication that was used to treat diaper rash in a neonate. CASE REPORT: A 6-day-old, 3350-g white boy was found to be cyanotic with blue mucous membranes on presentation. He had a diaper rash that was red and irritated, which his mother had treated with Vagisil cream. Methemoglobinemia secondary to absorption of benzocaine and resorcinol (1,3-benzenediol) from the Vagisil was diagnosed, with a methemoglobin level of 35% on admission (normal 0.4–1.5). Intravenous methylene blue 3 mg (1 mg/kg) was given; the neonate's skin color returned to normal 45 minutes after the dose. DISCUSSION: Methemoglobinemia is a condition in which hemoglobin is oxidized to the ferric form. Oxidized hemoglobin, methemoglobin, is incapable of reversibly binding oxygen at the physiologic partial oxygen pressure. Main causes of methemoglobin formation are exposure to certain oxidizing agents and drugs, deficiency of one of the enzymes necessary for reduction of methemoglobin to hemoglobin, or the presence of an abnormal hemoglobin resistant to reduction. Clinical manifestations of methemoglobinemia include diffuse slate-gray cyanosis with low oxygen saturation in the absence of respiratory distress. A single intravenous dose of methylene blue 1–2 mg/kg is the treatment of choice. CONCLUSIONS: Newborn infants are at increased risk for methemoglobinemia due to diminished enzyme systems required to reduce ferrihemoglobin to ferrohemoglobin, as well as because fetal hemoglobin is more easily oxidized than is adult hemoglobin. It is important to recognize possible drug reactions and educate parents on the potential risks of treatment with over-the-counter medications, especially in neonates.


2015 ◽  
Vol 54 (4) ◽  
pp. 395-399 ◽  
Author(s):  
Takao Watanabe ◽  
Masanori Abe ◽  
Fujimasa Tada ◽  
Kanako Aritomo ◽  
Hironori Ochi ◽  
...  

2005 ◽  
Vol 39 (5) ◽  
pp. 970-972 ◽  
Author(s):  
Agnès Henry ◽  
Bruno Charpiat ◽  
Thierry Vial ◽  
Serge Franchini ◽  
François J Cuilleret ◽  
...  

OBJECTIVE: To describe the unmasking of pheochromocytoma in a patient treated with amisulpride and tiapride. CASE SUMMARY: A 42-year-old white man developed acute hypertension with severe headache and vomiting 2 hours after the first doses of amisulpride 100 mg and tiapride 100 mg. Both drugs were immediately discontinued, and the patient recovered after subsequent nicardipine and verapamil treatment. Abdominal ultrasound showed an adrenal mass, and postoperative histologic examination confirmed the diagnosis of pheochromocytoma. DISCUSSION: Drug-induced symptoms of pheochromocytoma are often associated with the use of substituted benzamide drugs, but the underlying mechanism is unknown. In our case, use of the Naranjo probability scale indicated a possible relationship between the hypertensive crisis and amisulpride and tiapride therapy. CONCLUSIONS: As of March 24, 2005, this is the first reported case of amisulpride- and tiapride-induced hypertensive crisis in a patient with pheochromocytoma. Physicians and other healthcare professionals should be aware of this potential adverse effect of tiapride and amisulpride.


2002 ◽  
Vol 36 (5) ◽  
pp. 817-819 ◽  
Author(s):  
Raymond G Schlienger ◽  
Martin J Keller ◽  
Stephan Krähenbühl

OBJECTIVE: To report a patient with an acute mixed liver injury associated with tolterodine therapy. CASE SUMMARY: An 81-year-old white woman with urge incontinence experienced malaise, fever, and gastrointestinal disturbances 18 days after starting tolterodine 2 mg twice daily. The patient's concurrent medications included flunitrazepam, diclofenac, and dorzolamide/timolol eye drops. Laboratory examination was consistent with the presentation of an acute mixed liver injury with increased transaminase enzymes, alkaline phosphatase, λ-glutamyltransferase, and bilirubin. Additionally, she had mild leukocytosis with eosinophilia. After tolterodine was discontinued, the abnormal liver and hematologic parameters returned to normal within 4 weeks. DISCUSSION: Tolterodine, a muscarinic receptor antagonist, has predominantly anticholinergic effects. To our knowledge, this is the first case published describing tolterodine-associated acute mixed liver injury. However, some of the patient's additional symptoms can also be considered part of a drug-induced hypersensitivity syndrome. This is usually defined by the triad of fever, cutaneous reaction, and involvement of internal organs, mainly affecting the liver. The close temporal relationship between the start of tolterodine therapy and the first symptoms and the reversibility after dechallenge led us to conclude that the adverse reaction was possibly related to tolterodine exposure. CONCLUSIONS: Our case illustrates that tolterodine may rarely be associated with liver injury. This may have been an organ manifestation of tolterodine-induced hypersensitivity syndrome.


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