Agranulocytosis Associated with Etodolac

1994 ◽  
Vol 28 (4) ◽  
pp. 458-460 ◽  
Author(s):  
Richard L. Cramer ◽  
Vivian C. Aboko-Cole ◽  
Richard J. Gualtieri
Keyword(s):  
Hemoglobin Concentration ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Blood Cell Count ◽  
Patient History ◽  
Antiinflammatory Drugs ◽  
Intravenous Antibiotic ◽  
Drug Induced ◽  
Case Summary ◽  
Case Assessment

OBJECTIVE: To report a case of probable etodolac-induced agranulocytosis. CASE SUMMARY: A 72-year-old woman who had been taking etodolac 300 mg bid for approximately six weeks presented to the emergency department with symptoms of urosepsis. She was found to be profoundly granulocytopenic. Etodolac was discontinued and broad-spectrum intravenous antibiotic therapy was administered for the next 17 days. Results of bone marrow biopsy revealed marked hypocellularity consistent with drug-induced agranulocytosis. Following etodolac withdrawal, the total white blood cell count reached a low value of 0.9 × 109L and then returned to a preetodolac baseline after 15 days. Her hemoglobin concentration also decreased significantly during hospitalization. DISCUSSION: Agranulocytosis has rarely been reported in association with nonsteroidal antiinflammatory drugs (NSAIDs), and there are no literature reports associating etodolac with agranulocytosis. This case involving etodolac is consistent with the pattern described with other NSAIDs. Factors correlating etodolac as the causative agent are identified. Details of patient history, treatment, follow-up, and assessment are discussed. CONCLUSIONS: Detailed case assessment demonstrated probable etodolac-induced agranulocytosis in our patient. Clinicians should be aware that etodolac, like other NSAIDs, has potential to cause agranulocytosis.

Oxaprozin-Induced Fulminant Hepatitis

1994 ◽  
Vol 28 (10) ◽  
pp. 1159-1161 ◽  
Author(s):  
Preston P. Purdum ◽  
Stacey L. Shelden ◽  
John W. Boyd ◽  
Mitchell L. Shiffman
Keyword(s):  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Fulminant Hepatitis ◽  
The Elderly ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Antiinflammatory Drugs ◽  
Drug Induced ◽  
Hepatic Transaminase ◽  
Long Acting ◽  
Work Up

OBJECTIVE: To report oxaprozin-induced fulminant hepatic failure. CASE SUMMARY: A 56-year-old woman was admitted with fulminant hepatic failure. Work-up for potential etiologies was negative except for the use of oxaprozin for the preceding two months. Results of premortem liver biopsy were consistent with drug-induced hepatic injury similar to that previously reported with diclofenac. DISCUSSION: Although the literature describes elevation in hepatic transaminase concentrations associated with oxaprozin, fulminant hepatic failure has not been described previously. CONCLUSIONS: Elevations in hepatic transaminase concentrations and now fulminant hepatic failure have been shown to occur with oxaprozin, as previously seen with other nonsteroidal antiinflammatory drugs (NSAIDs). Transaminitis is a known adverse effect of NSAID use, but is usually mild and reversible with discontinuation of drug. Transaminitis may be more likely to occur in the elderly, in patients receiving concurrent potentially hepatotoxic medications, and possibly with the newer long-acting NSAIDs. The existence of fulminant hepatitis, although rare, supports the need for monitoring liver function enzymes during NSAID therapy.

Angioedema Associated with Aspirin and Rofecoxib

2005 ◽  
Vol 39 (5) ◽  
pp. 944-948 ◽  
Author(s):  
Leisa L Marshall
Keyword(s):  
White Woman ◽  
Skin Testing ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Aspirin Therapy ◽  
Probability Scale ◽  
Antiinflammatory Drugs ◽  
Case Summary ◽  
Cox 2 ◽  
Cox 2 Inhibitors ◽  
Auto Injector

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.

Delayed Neutropenia with Ticlopidine

1994 ◽  
Vol 28 (12) ◽  
pp. 1344-1346 ◽  
Author(s):  
Debra K. Farver ◽  
Lori A. Hansen
Keyword(s):  
Blood Cell ◽  
Cell Count ◽  
Transient Ischemic Attack ◽  
Complete Blood Cell Count ◽  
Blood Cell Count ◽  
Drug Induced ◽  
Case Summary ◽  
Life Threatening ◽  
Ischemic Attack

OBJECTIVE: To report a case of ticlopidine-induced neutropenia occurring 18 days after discontinuation of the drug. CASE SUMMARY: A 68-year-old woman was placed on ticlopidine after a transient ischemic attack. Ten days later the drug was discontinued because the patient developed a rash. Eighteen days later she developed pneumonia and neutropenia, which were believed to be induced by ticlopidine. DISCUSSION: Drug-induced neutropenia is serious and at times life-threatening. Ticlopidine-induced neutropenia has been described in patients receiving the medication. We report neutropenia occurring 18 days after discontinuation of ticlopidine. CONCLUSIONS: Indications for prescribing ticlopidine must be closely followed. Complete blood cell count monitoring is imperative while the patient is receiving the medication. This case suggests that the duration of monitoring after the discontinuation of ticlopidine may need to be longer than the 14 days recommended by the manufacturer.

The Serum Level of Agalactosyl IgG in Rheumatoid Arthritis Patients Treated with Methotrexate

1996 ◽  
Vol 9 (1) ◽  
pp. 19-22
Author(s):  
J. K. Lacki ◽  
U. Mackiewicz ◽  
S. Mackiewicz ◽  
W. Muller
Keyword(s):  
Rheumatoid Arthritis ◽  
Serum Level ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Healthy Controls ◽  
Disease Course ◽  
Antiinflammatory Drugs ◽  
Significant Difference ◽  
One Year ◽  
Agalactosyl Igg

To verify the hypothesis that methotrexate may affect the serum level of agalactosyl IgG (IgG[0]) we followed the changes in IgG galactosylation patterns in a cohort of rheumatoid arthritis patients treated with either methotrexate (MTX) or nonsteroidal antiinflammatory drugs (NSAID). The average values of IgG[0] in RA patients at the beginning of the observation were significantly higher as compared to healthy controls (0.45 ± 0.39 vs. −0.03 ± 0.09, p<0.05). The findings of IgG[0] after one-year follow-up were also higher as compared to healthy controls (0.38 ± 0.39 vs. −0.03 ± 0.09, p<0.05). We did not notice any statistically significant difference in IgG[0] between MTX and NSAID treated patients at the beginning of the study (0.49 ± 0.42 vs. 0.42 ± 0.38, NS). However, during one-year MTX treatment IgG[0] significantly dropped (0.49 ± 0.42 vs. 0.25 ± 0.24, p<0.01). We did not establish any fluctuation in IgG[0] in the group of patients treated with NSAID (0.42 ± 0.38 vs. 0.46 ± 0.45, NS). The data thus far obtained suggest that IgG[0] may serve as an indicator for the disease course in patients with RA. Secondly, the clinical improvement and IgG[0] decrease after methotrexate implies, that the immunoregulatory abnormality in RA may be susceptible to correction by immunotherapy.

Nonsteroidal Antiinflammatory Drug-Induced Pseudoporphyria: A Case Series

2002 ◽  
Vol 6 (4) ◽  
pp. 320-326 ◽  
Author(s):  
Jeffrey R. LaDuca ◽  
Peter H. Bouman ◽  
Anthony A. Gaspari
Keyword(s):  
Clinical Symptoms ◽  
Porphyria Cutanea Tarda ◽  
Case Series ◽  
Antiinflammatory Drug ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Nonsteroidal Antiinflammatory Drug ◽  
Sustained Remission ◽  
Antiinflammatory Drugs ◽  
Drug Induced ◽  
Antibiotic Drugs

Background: Pseudoporphyria is a diagnosis that is used when porphyria-like clinical lesions arise in the setting of normal porphyrin levels. This condition was first described in the 1960s and was initially related to the use of certain antibiotic drugs. In 1985, pseudoporphyria was first attributed to the use of nonsteroidal antiinflammatory drugs (NSAIDs). Subsequently, a host of NSAIDs and other drugs have been found to elicit the same clinical entity. The exact mechanism by which certain drugs create clinical lesions resembling porphyria cutanea tarda or erythropoietic protoporphyria is still unknown. A phototoxic mechanism is hypothesized. Objective: We describe six patients diagnosed with pseudoporphyria and detail the diagnostic tests leading to the eventual diagnosis. Results: The patients ranged in age from 27 to 59 years and had a female:male predominance of 2:1. The offending NSAID was DayPro (oxaprozin) for three of the patients, Relafen (nabumetone) for two of the patients, and Aleve (naproxen) for one patient. For each patient, histology and immunofluorescence was either consistent with the diagnosis of porphyria cutanea tarda or nonspecific, while serum, stool, and urine porphyrins did not support that diagnosis. Withdrawal of the offending agent provided relief from the clinical symptoms for each patient. None of our patients were rechallenged with the putative offending drug. However, prolonged avoidance has provided a sustained remission from symptoms in all six patients. Conclusions: Pseudoporphyria is a relatively rarely reported condition. Clinical suspicion with appropriate laboratory and histopathologic findings help to make this diagnosis, and exclude true porphyrias. Rechallenge with the offending drug to produce symptom relapse has been proposed to be helpful in confirming this diagnosis of exclusion. Since all 6 patients with drug-induced pseudoporphyria experienced resolution of their symptoms after discontinuing the offending agent, we propose that this clinical correlation alone is sufficient to confirm this diagnosis. Our observation of six new cases of NSAID-induced pseudoporphyria over a two-year interval suggests that this is not a rare entity.

Nonsteroidal Antiinflammatory Drug-Induced Renal Dysfunction Related to Inhibition of Renal Prostaglandins

1987 ◽  
Vol 21 (12) ◽  
pp. 954-960 ◽  
Author(s):  
Richard G. D'Angio
Keyword(s):  
Renal Dysfunction ◽  
Antiinflammatory Drug ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Nonsteroidal Antiinflammatory Drug ◽  
Antiinflammatory Drugs ◽  
Drug Induced ◽  
Frequent Use ◽  
The Face ◽  
Patients At Risk

This article reviews the role of prostaglandins (PG) in maintaining renal function in the face of vasoconstrictive substances and decreased renal blood flow. Inhibition of the synthesis of renal PG by nonsteroidal antiinflammatory drugs (NSAID) may lead to the development of hemodynamically induced renal dysfunction in patients with a decreased effective plasma volume or chronic renal insufficiency. The importance of stimulation of renal PG activity to the action of diuretics and a pharmacodynamic mechanism for NSAID-induced diuretic resistance are presented. Evidence for the relative selectivity of sulindac in inhibiting systemic PG without inhibiting renal PG is also reviewed. Inhibition of renal PG synthesis has been postulated to be a contributing factor for other forms of NSAID-induced renal dysfunction (interstitial nephritis, analgesic-associated nephropathy). The relationship between renal PG inhibition by NSAID and these syndromes is briefly discussed. Considering the frequent use of NSAID, it is important that practitioners are aware of the mechanisms whereby patients may develop NSAID-induced renal dysfunction and that they are able to identify patients at risk.

Patellar Tendinopathy in Athletes

2000 ◽  
Vol 28 (3) ◽  
pp. 392-397 ◽  
Author(s):  
Alfredo Schiavone Panni ◽  
Mario Tartarone ◽  
Nicola Maffulli
Keyword(s):  
Operative Management ◽  
Clinical Results ◽  
Symptomatic Improvement ◽  
Rehabilitation Program ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Patellar Tendinopathy ◽  
Mucoid Degeneration ◽  
Tendon Tissue ◽  
Antiinflammatory Drugs

We report the results of nonoperative and operative management of patellar tendinopathy in 42 athletes with Blazina stage 2 (26 patients) or stage 3 (16 patients) patellar tendinopathy. All patients were initially managed nonoperatively with nonsteroidal antiinflammatory drugs, physical therapy, and a progressive rehabilitation program based on isometric exercises, stretching, and eccentric exercises. After 6 months, 33 patients showed symptomatic improvement and were able to resume their sports. In nine patients with Blazina stage 3 tendinopathy, nonoperative measures failed, and surgery was performed. Operative treatment consisted of removal of the degenerated areas of the tendon, multiple longitudinal tenotomies, and drilling of the lower pole of the patella at the site of tendon attachment. Histologic examination of the excised tendon tissue showed areas of necrosis and mucoid degeneration, and alterations of the bone-tendon junction. After a mean follow-up of 4.8 years, clinical results were excellent or good in all patients. In the group treated nonoperatively, results were better in the patients who had stage 2 tendinopathy than in those with stage 3.

scholarly journals Postoperative nonsteroidal antiinflammatory drugs and the prevention of heterotopic ossification after cervical arthroplasty: analysis using CT and a minimum 2-year follow-up

2015 ◽  
Vol 22 (5) ◽  
pp. 447-453 ◽  
Author(s):  
Tsung-Hsi Tu ◽  
Jau-Ching Wu ◽  
Wen-Cheng Huang ◽  
Hsuan-Kan Chang ◽  
Chin-Chu Ko ◽  
...  
Keyword(s):  
Heterotopic Ossification ◽  
Clinical Outcomes ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Antiinflammatory Drugs ◽  
Cervical Arthroplasty ◽  
Arm Pain ◽  
Nsaid Group ◽  
Number Of Patients ◽  
Cox 2

OBJECT Heterotopic ossification (HO) after cervical arthroplasty is not uncommon and may cause immobility of the disc. To prevent HO formation, study protocols of clinical trials for cervical arthroplasty undertaken by the US FDA included perioperative use of nonsteroidal antiinflammatory drugs (NSAIDs). However, there are few data supporting the use of NSAIDs to prevent HO after cervical arthroplasty. Therefore, this study aimed to evaluate the efficacy of NSAIDs in HO formation and clinical outcomes. METHODS Consecutive patients who underwent 1- or 2-level cervical arthroplasty with a minimum follow-up of 24 months were retrospectively reviewed. All patients were grouped into 1 of 2 groups, an NSAID group (those patients who had used NSAIDs postoperatively) and a non-NSAID group (those patients who had not used NSAIDs postoperatively). The formation of HO was detected and classified using CT in every patient. The incidence of HO formation, disc mobility, and clinical outcomes, including visual analog scale (VAS) scores of neck and arm pain, neck disability index (NDI) scores, and complications were compared between the two groups. Furthermore, a subgroup analysis of the patients in the NSAID group, comparing the selective cyclooxygenase (COX)-2 to nonselective COX-2 NSAID users, was also conducted for each of the above-mentioned parameters. RESULTS A total of 75 patients (mean age [± SD] 46.71 ± 9.94 years) with 107 operated levels were analyzed. The mean follow-up duration was 38.71 ± 9.55 months. There were no significant differences in age, sex, and levels of arthroplasty between the NSAID and non-NSAID groups. There was a nonsignificantly lower rate of HO formation in the NSAID group than the non-NSAID group (47.2% vs. 68.2%, respectively; p = 0.129). During follow-up, most of the arthroplasty levels remained mobile, with similar rates of immobile discs in the NSAID and non-NSAID groups (13.2% and 22.7%, respectively; p = 0.318). Furthermore, there was a nonsignificantly lower rate of HO formation in the selective COX-2 group than the nonselective COX-2 group (30.8% vs 52.5%, respectively; p = 0.213). The clinical outcomes, including VAS neck, VAS arm, and NDI scores at 24 months postoperatively, were all similar in the NSAID and non-NSAID groups, as well as the selective and nonselective COX-2 groups (all p > 0.05). CONCLUSIONS In this study there was a trend toward less HO formation and fewer immobile discs in patients who used postoperative NSAIDs after cervical arthroplasty than those who did not, but this trend did not reach statistical significance. Patients who used selective COX-2 NSAIDs had nonsignificantly less HO than those who used nonselective COX-2 NSAIDs. The clinical outcomes were not affected by the use of NSAIDs or the kinds of NSAIDs used (selective vs nonselective COX-2). However, the study was limited by the number of patients included, and the efficacy of NSAIDs in the prevention of HO after cervical arthroplasty may need further investigation to confirm these results.

Drug-Induced Photosensitivity: A Clinical Review

1996 ◽  
Vol 12 (2) ◽  
pp. 52-57
Author(s):  
Stacey Beasley ◽  
Oscar E Araujo ◽  
Franklin P Flowers
Keyword(s):  
English Language ◽  
Data Extraction ◽  
Treatment Options ◽  
Coal Tar ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Hypoglycemic Agents ◽  
Thiazide Diuretics ◽  
Antiinflammatory Drugs ◽  
Drug Induced ◽  
Study Selection

Objective: To provide an overview of drug-induced phototoxic and photoallergy reactions, the mechanism involved, and the most common classes of drugs causing these reactions. Data Source: Pertinent English-language literature (1987–1993). Study Selection: Representative articles documenting mechanisms and types of drug-induced photosensitivity reactions, as well as treatment options. Data Extraction: Data were extracted only from articles that documented relevant and substantive information backed by clinical studies. Data Synthesis: Drug-induced photosensitivity can be acute or chronic. The chromophore that absorbs the radiation and activates the process of photosensitivity results in color within the longer ultraviolet wavelength. The primary classes of drugs causing phototoxic reactions include nonsteroidal antiinflammatory drugs, thiazide diuretics, tetracycline, and quinolone antibiotics, tricyclic antidepressants, and amiodarone. Those causing photoallergic reactions include antihistamines, thiazide diuretics, sulfonamides, griseofulvin, sulfonylurea hypoglycemic agents, benzocaine, and coal tar preparations. Conclusions: The importance of understanding the mechanism of photosensitivity is stressed as well as the difficulty in determining whether a phototoxic or photoallergic reaction has occurred. Established classes of each type of photosensitivity are identified and the importance of recognizing treatment options is emphasized. Patients prone to photosensitizing reactions should be advised concerning how to manage these problems.

Neurologic Adverse Effects during Concomitant Treatment with Ciprofloxacin, Nsaids, and Chloroquine: Possible Drug Interaction

1993 ◽  
Vol 27 (9) ◽  
pp. 1058-1059 ◽  
Author(s):  
Jan Rollof ◽  
Ellen Vinge
Keyword(s):  
Drug Interaction ◽  
Adverse Effects ◽  
Alternative Explanation ◽  
Signs And Symptoms ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Concomitant Treatment ◽  
Gamma Aminobutyric Acid ◽  
Antiinflammatory Drugs ◽  
Case Summary ◽  
Toxic Concentrations

OBJECTIVE: To report a case of neurologic adverse effects that developed during concomitant treatment with ciprofloxacin, nonsteroidal antiinflammatory drugs (NSAIDs), and chloroquine. Possible mechanisms for a drug interaction are discussed. CASE SUMMARY: A 68-year-old woman who was receiving chronic treatment with NSAIDs and chloroquine developed dizziness, anxiety, and tremors when ciprofloxacin 500 mg twice daily was begun for Salmonella osteitis. When she discontinued the antirheumatic treatment, there was a prompt relief of symptoms. After indomethacin was reintroduced, the patient developed signs and symptoms of peripheral neuropathy, which partially subsided when ciprofloxacin was discontinued. DISCUSSION: Enhanced neurologic adverse effects of ciprofloxacin when taken together with NSAIDs or chloroquine may result from reduced effects of gamma-aminobutyric acid. An alternative explanation could be that NSAIDs and chloroquine impair the elimination of ciprofloxacin, thereby contributing to toxic concentrations of the antibiotic. CONCLUSIONS: The possibility of interactions between ciprofloxacin and antirheumatic drugs should be considered.

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