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.

Ambulatory Care: Medication Use Characteristics in an Ambulatory Elderly Population in Taiwan

1997 ◽  
Vol 31 (3) ◽  
pp. 308-314 ◽  
Author(s):  
Rou-Yee Chen Hsu ◽  
Min-Shung Lin ◽  
Mei-Huei Chou ◽  
Ming-Fang Lin
Keyword(s):  
Hormone Replacement ◽  
The Elderly ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Prescribing Patterns ◽  
Cross Sectional Survey ◽  
Antiinflammatory Drugs ◽  
Cross Sectional ◽  
Therapeutic Category ◽  
Prescribing Trends ◽  
Drug Expenditures

Objective To compare prescribing patterns between the elderly and nonelderly in 1994, to disclose prescribing trends in the elderly between 1992 and 1994, to explore whether drug utilization is in agreement with disease prevalence, and to identify suboptimal prescribing by drug category for ambulatory elderly patients. Design Cross-sectional survey at two separate time intervals. Setting All public group practice centers (GPCs) in Taiwan. Patients Ambulatory adults who visited GPCs during 1 random week. Those 65 years or over were classified as the elderly group, and those 20-64 years were the nonelderly group. Main Outcome Measures Mean diagnosis, drug use, and expenditure; frequency of diagnosis; and prescribing by therapeutic category. Results Data on 30 777 elderly and 38 184 nonelderly patients were collected in 1994. There was widespread use of antacids. Compared with nonelderly adults, the elderly were diagnosed with more diseases (1.3 vs. 1.2, respectively; p < 0.01), received more medications (4.7 vs. 4.1, respectively; p < 0.01), and had higher drug expenditures (5.4 vs. 4.6, respectively; p < 0.01). Chronic illness was more prevalent in the elderly, which accounted for the extensive use of cardiovascular drugs (32.1%), nonsteroidal antiinflammatory drugs (25.9%), and anxiolytics (15.9%). The upward trend in the elderly from 1992 to 1994 with hypertension (18.6% vs. 20.0%) or diabetes (9.2% vs. 10.9%) did not result in more cases of cerebrovascular disease (7.1% vs. 4.9%). There was a substantial increase in use of antispasmodic and gastroprokinetic agents (4.5% to 10.7%); the use of antacids decreased (73.6% to 63.4%) in the elderly. Conclusions Compared with the prevalence of disease, there was extensive nonspecific use of anxiolytics and antacids. However, lessened use of antidepressants and postmenopausal hormone replacement may have an impact on morbidity and mortality and deserves particular attention.

scholarly journals Reversible Fulminant Hepatitis Secondary to Cocaine in the Setting of β-Blocker Use

2020 ◽  
Vol 8 ◽  
pp. 232470962092420 ◽  
Author(s):  
Rohan Sharma ◽  
Nidhi Kapoor ◽  
Kaustubh Suresh Chaudhari ◽  
Robert Hal Scofield
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Fulminant Hepatitis ◽  
Viral Infections ◽  
Hepatic Function ◽  
Cocaine Use ◽  
Β Blocker ◽  
Acute Hypoglycemia

Background. Fulminant hepatitis is acute hepatic injury with severe decline in hepatic function manifested by encephalopathy, hypercoagulable state, jaundice, renal failure, hypoglycemia, or a constellation of these symptoms in patients without preexisting liver disease. Etiologies include viral infections, hepatotoxic drugs, autoimmune diseases, vaso-occlusive diseases, sepsis, and malignant infiltration. Case Report. A 56-year-old man presented with acute heart failure in the setting of cocaine use. The patient subsequently developed fulminant hepatic failure manifested by acute hypoglycemia, elevated liver enzyme, and worsening liver function, which resolved over 1 week with supportive care. The patient was on β-blocker, which was stopped during the admission. He was again admitted on several different occasion for cocaine-induced acute heart failure but did not develop hepatic failure as his β-blocker was discontinued. Discussion. Cocaine has been known to cause hepatotoxicity in humans. However, our patient developed fulminant hepatic failure in the setting of concomitant cocaine and β-blocker use likely secondary to unopposed α-adrenergic activity and ischemic hepatopathy. The patient did not develop hepatic failure on subsequent admissions with cocaine use after discontinuation of β-blockers.

scholarly journals Gap junction inhibition prevents drug-induced liver toxicity and fulminant hepatic failure

2012 ◽  
Vol 30 (2) ◽  
pp. 179-183 ◽  
Author(s):  
Suraj J Patel ◽  
Jack M Milwid ◽  
Kevin R King ◽  
Stefan Bohr ◽  
Arvin Iracheta-Vellve ◽  
...  
Keyword(s):  
Gap Junction ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Liver Toxicity ◽  
Drug Induced ◽  
Gap Junction Inhibition

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.

Fulminant hepatic failure as the presenting form of type 1 autoimmune hepatitis in the elderly

2002 ◽  
Vol 97 (5) ◽  
pp. 1265-1266 ◽  
Author(s):  
Eduardo Redondo-Cerezo ◽  
Flor Nogueras-Lopez ◽  
Rafael Martin-Vivaldi ◽  
Esperanza Egea Simon
Keyword(s):  
Autoimmune Hepatitis ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
The Elderly

Fulminant hepatic failure in the elderly: A clinicopathological study of autopsy cases aged over 65 years

2000 ◽  
Vol 50 (2) ◽  
pp. 98-105 ◽  
Author(s):  
Motoji Sawabe ◽  
Tomio Arai ◽  
Yukiyoshi Esaki ◽  
Toshio Fukazawa ◽  
Kaiyo Takubo ◽  
...  
Keyword(s):  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
The Elderly ◽  
Clinicopathological Study

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.

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