scholarly journals Rash and cholestatic liver injury caused by methimazole in a woman with Turner syndrome and Graves’s disease: a case report and literature review

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jinhui Zeng ◽  
Fangtao Luo ◽  
Zhihua Lin ◽  
Yinghong Chen ◽  
Xiaoyun Wang ◽  
...  

Abstract Background Rash and cholestatic liver injury caused by methimazole (MMI) in patients with Turner syndrome (TS) and Graves’s disease (GD) are rarely reported, and there is a paucity of reports on the management of this condition. It is not clear whether propylthiouracil (PTU) can be used as a safe alternative in this case. Case presentation: A 37-year-old woman was admitted to our hospital with rash, severe pruritus and a change in urine colour after 2 months of GD treatment with MMI. Physical examination showed rash scattered over the limbs and torso, mild jaundice of the sclera and skin, short stature, facial moles, immature external genitals and diffuse thyroid gland enlargement. Liver function tests indicated an increase in total bilirubin, direct bilirubin, total bile acid, glutamic pyruvic transaminase, glutamic oxaloacetic transaminase and alkaline phosphatase. The level of sex hormones suggested female hypergonadotropic hypogonadism. The karyotype of peripheral blood was 46, X, i(X)(q10)/45, X. After excluding biliary obstruction and other common causes of liver injury, combined with rash and abnormal liver function following oral administration of MMI, the patient was diagnosed as having TS with GD and rash and cholestatic liver injury caused by MMI. MMI was immediately discontinued, and eleven days after treatment with antihistamine and hepatoprotective agents was initiated, the rash subsided, and liver function returned to nearly normal. Because the patient did not consent to administration of 131I or thyroid surgery, hyperthyroidism was successfully controlled with PTU. No adverse drug reactions were observed after switching to PTU. Conclusions While patients with TS and GD are undergoing treatment with MMI, their clinical manifestations, liver functions, and other routine blood test results should be closely monitored. When patients with TS and GD manifest adverse reactions to MMI such as rash and cholestatic liver injury, it is necessary to discontinue MMI and treat with antihistamine and hepatoprotective agents. After the rash subsides and liver function returns to nearly normal, PTU can effectively control hyperthyroidism without adverse drug reactions.

1993 ◽  
Vol 162 (5) ◽  
pp. 688-689 ◽  
Author(s):  
Christopher P. Alderman ◽  
Michelle M. Atchison ◽  
Janet I. McNeece

A 67-year-old man developed concurrent severe agranulocytosis and elevation of hepatic transaminases as a result of treatment with clomipramine. Although such adverse drug reactions can be considered rare events, the potentially serious nature of these reactions vindicate the routine monitoring of blood picture, and liver function tests, after initiation of treatment with tricyclic antidepressants.


2019 ◽  
Vol 6 (3) ◽  
pp. 1
Author(s):  
Kevin C. Kohm ◽  
Lauren Pioppo ◽  
Jack Xu ◽  
Preston Keiffer ◽  
Eric Pagan ◽  
...  

Methimazole (MMI) is a commonly used medication in the treatment of hyperthyroidism. The side effect profile is extensive and includes the rare but serious side effect of drug associated liver injury. We report the case of a 51-year-old female who presented with painless jaundice several weeks after initiating MMI therapy for treatment of hyperthyroidism complicated by Graves’ orbitopathy. Liver function tests on presentation showed alanine aminotransferase (ALT) 1366 IU/L, aspartate aminotransferase (AST) 853 IU/L, total bilirubin 26.2 mg/dl, alkaline phosphatase 954 IU/L. Workup of structural, infectious, and autoimmune causes of hepatic injury was negative. The patient was therefore found to have MMI associated liver injury. MMI was discontinued and the patient was started on ursodiol, resulting in resolution of her jaundice and improvement of her liver function tests.


2020 ◽  
Vol 49 (2) ◽  
pp. 20190214 ◽  
Author(s):  
Takahiro Maeda ◽  
Masafumi Oda ◽  
Shinji Kito ◽  
Tatsurou Tanaka ◽  
Nao Wakasugi-Sato ◽  
...  

Objective: The aim of this study was to examine whether a decreased occurrence rate of adverse drug reactions (ADRs) to contrast media in contrast-enhanced CT and MRI was attributable to appropriate criteria for patients with some diseases. A secondary aim was to elucidate safety profiles for contrast media and factors influencing the occurrence of ADRs. Methods: Clinical data of patients who underwent contrast-enhanced CT (5576 cases) or MRI (3357 cases) were retrospectively analyzed to evaluate rates of ADRs to contrast media, symptoms of ADRs, treatments for ADRs, and differences in medical history, blood test results, and other factors between patients with and without ADRs in a dental hospital. Results: The rate of ADRs to contrast media was 0.54% for CT and 0.09% for MRI. The most frequent ADRs in contrast-enhanced CT or MRI were nausea and vomiting as physiologic reactions. Two serious reactions were seen for CT, but none for MRI. Significant differences between patients with and without ADRs were seen in liver function according to blood tests for CT, and in digestive disorders elicited from medical interviews for MRI. Conclusion: The lower occurrence rate of ADRs to contrast media in dental hospitals could be due to the adoption of appropriate criteria for patients with some diseases undergoing enhanced CT or MRI. Complete suppression of ADRs to contrast media for CT or MRI is unrealistic, so attention is warranted for patients with decreased liver function when performing enhanced CT, and for patients with digestive disorders when performing enhanced MRI.


2002 ◽  
Vol 47 (4) ◽  
pp. 375-377 ◽  
Author(s):  
Donna E Stewart

Objective: Since 1999, international reports of hepatotoxicity associated with the antidepressant nefazodone (Serzone) have increased. In June 2001, a manufacturer's safety advisory notified Canadian physicians of “very rare reports of severe liver injury temporally associated with the use of nefazodone HC1.” We undertook this study to determine the prevalence of adverse drug reactions to nefazodone reported in a Canadian database. Method: We requested the Canadian Adverse Drug Reaction Monitoring Programme (CADRMP) database for nefazodone and analyzed it for suspected hepatic complications reported and entered from the time of marketing to June 30, 2001. Results: We found 32 cases of liver injury associated with nefazodone, with 26 (81.3%) classified as “severe.” Patients ranged in age from 30 to 69 years and took 100 to 600 mg of nefazodone daily. Most (68.8%) of the patients were women. Eleven patients were prescribed only nefazodone, and 20 took it concomitantly with other drugs. Of affected patients, 88% developed liver injury within 6 months of starting nefazodone. At the time of reporting, 17 patients recovered without sequelae, 12 patients had not yet recovered, and the outcomes for 3 were unknown. There were 3 cases of hepatic failure, 1 of hepatocellular degeneration, 1 of hepatic necrosis, and 1 of fulminant hepatitis. Conclusion: In common with similar databases, the CADRMP database includes only a small proportion of suspected drug reactions. In view of 32 reported cases of hepatotoxicity associated with nefazodone in Canada, 81.3% of which were severe, caution should be exercised if nefazodone is prescribed with other drugs, especially those metabolized by CYP4503A4. Nefazodone should not be prescribed to patients with preexisting liver disease. Baseline and regular liver function tests should be obtained in all patients on nefazodone therapy in the first 6 months, and the drug should be discontinued if abnormalities are found. Patients should be advised of symptoms of hepatotoxicity, and to report them immediately to their physician. Objectif: Depuis 1999, les rapports internationaux sur l'hépatotoxicité associée à l'antidépresseur néfazodone (Serzone) se sont multipliés. En juin 2001, l'avis de sécurité d'un fabricant avertissait les médecins canadiens de « très rares cas de lésion grave au foie associée dans le temps à l'utilisation de néfazodone HC1 ». Nous avons entrepris cette étude pour déterminer la prévalence des réactions indésirables à la néfazodone déclarées dans la base de données canadienne. Méthode: Nous avons interrogé la base de données du Programme canadien de surveillance des effets indésirables des médicaments (PCSEIM) à propos de la néfazodone, et avons analysé les données sur les complications hépatiques soupçonnées qui ont été déclarées et entrées depuis le moment de la mise en marché jusqu'au 30 juin 2001. Résultats: Nous avons trouvé 32 cas de lésions au foie associées à la néfazodone, dont 26 (81,3 %) étaient classés graves. l'âge des patients variait de 30 à 69 ans et ceux-ci prenaient entre 100 et 600 mg de néfazodone par jour. La plupart des patients (68,8 %) étaient des femmes. Onze patients n'avaient que de la néfazodone prescrite et 20 d'entre eux prenaient aussi d'autres médicaments. Parmi les patients affectés, 88 % ont développé une lésion au foie dans les 6 mois après avoir commencé à prendre de la néfazodone. Au moment de leur déclaration, 17 patients étaient rétablis sans séquelles, 12 patients n'étaient pas encore rétablis et les résultats n'étaient pas connus pour les 3 autres. Il y avait 3 cas d'insuffisance hépatique, 1 cas de dégénérescence hépatocellulaire, 1 cas de nécrose hépatique et 1 cas d'hépatite fulminante. Conclusion: Comme d'autres bases de données semblables, la base de données du PCSEIM n'inclut qu'une faible proportion des réactions aux médicaments soupçonnées. En fonction des 32 cas déclarés d'hépatotoxicité associée à la néfazodone au Canada, dont 81,3 % étaient des cas graves, il faut faire preuve de prudence en prescrivant la néfazodone avec d'autres médicaments, surtout ceux qui sont métabolisés par CYP4503A4. La néfazodone ne devrait pas être prescrite aux patients ayant des maladies du foie pré-existantes. Il faut obtenir des tests de base et de la fonction hépatique de tous les patients traités à la néfazodone dans les 6 premiers mois, et le médicament devrait être cessé si des anomalies sont découvertes. Les patients devraient être avertis des symptômes d'hépatotoxicité et de les déclarer immédiatement à leur médecin.


1992 ◽  
Vol 26 (7-8) ◽  
pp. 926-928 ◽  
Author(s):  
Sarah A. Spinier ◽  
Cheryl A. Elder ◽  
K. Elizabeth Kindwall

OBJECTIVE: To describe propafenone-induced liver injury. DESIGN: Retrospective case report. SETTING: Referred care in a large tertiary care center. Laboratory tests were performed at the auxiliary site and the tertiary care center. PATIENT: A 71-year-old woman with atrial fibrillation developed elevations of greater than two times the upper limit of normal in alkaline phosphatase (ALK), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma glutamyltransferase (GGT) after initiation of propafenone therapy. INTERVENTIONS: Studies included serial measurements of ALK, ALT, AST, and GGT. RESULTS: The patient developed elevations of greater than two times the upper limit of normal in ALK, ALT, and AST, one month after initiating propafenone therapy. The propafenone dose was decreased from 900 to 675 mg/d and, ten days later, the ALK, ALT, and AST were decreased slightly, but still above the upper limit of normal. One month later, serum transaminases had returned to baseline, but propafenone therapy was discontinued because of recurrent atrial fibrillation, persistent elevation in ALK, and elevation in GGT. Two months after discontinuing propafenone, serum aminotransaminase and ALK concentrations had normalized and GGT had decreased and remained only slightly elevated. CONCLUSIONS: The occurrence of liver injury secondary to propafenone therapy is rare. Reported cases appear to be secondary to hepatocellular injury, cholestasis, or a combination of the two. In this case, the pattern demonstrated by elevations in liver enzymes may be classified as acute cholestatic liver injury. Because the reported incidence is 0.1–0.2 percent and there are no known fatalities secondary to propafenone liver injury, routine monitoring of liver function tests in all patients receiving propafenone cannot be recommended at this time. Baseline liver function tests prior to initiating propafenone therapy with follow-up laboratory studies one month later are recommended in patients with known liver dysfunction. If elevations are noted, a reduction in dose may result in lower liver enzyme concentrations, although discontinuation of therapy may be required in some cases.


2000 ◽  
Vol 16 (2) ◽  
pp. 47-49 ◽  
Author(s):  
Matitiahu Lifshitz ◽  
Perez Kornmehl ◽  
Haim Reuveni

Objective: To determine the incidence of adverse drug reactions in patients with acetaminophen overdose following administration of intravenous acetylcysteine, and to evaluate the cost-benefit ratio of intravenous compared with oral acetylcysteine therapy. Methods: The incidence of adverse drug reactions to intravenous acetylcysteine therapy was studied retrospectively in all patients with acetaminophen overdose who were admitted to Soroka University Medical Center, Beer-Sheva, Israel, from 1994 to 1998. Data were obtained from hospital records. All patients were treated with a 20-hour intravenous regimen according to the Prescott protocol. Special attention was paid to the clinical manifestations of adverse reactions, time of onset, and history of patient allergy and asthma. Cost of therapy (drug prices, hospital per diems) for intravenous versus oral acetylcysteine administration was evaluated in accordance with average rates prevailing in Israel in December 1998. Results: Ninety-two patients, 32 adolescents aged 12–18 years (mean ± SD 14.2 ± 1.9) and 60 adults aged 18–52 years (28.2 ± 3.2), were treated with intravenous acetylcysteine for acetaminophen overdose during the study period. Three patients (3.2%) developed adverse reactions: one adult presented with a maculopapular rash and pruritus, and two adolescents developed mild urticaria; no other adverse reactions were reported. All adverse reactions occurred during administration of the loading dose, 15–20 minutes after initiation of therapy. The reactions subsided a few hours after the acetylcysteine infusion was stopped and did not require antiallergy therapy. None of the three patients had a history of allergy. The 20-hour intravenous acetylcysteine protocol is approximately three times less expensive than the recommended oral regimen in terms of drug cost and length of hospitalization. Conclusions: Intravenous acetylcysteine is a relatively safe antidote for acetaminophen poisoning. The incidence rate of adverse reactions is low, and they are mild and easily controlled by termination of the infusion. We recommend intravenous acetylcysteine therapy, particularly for patients with vomiting caused by the acetaminophen overdose or by oral acetylcysteine therapy. The 20-hour intravenous acetylcysteine therapy has a cost-benefit advantage over oral therapy; however, the oral formulation is not approved by the FDA.


2017 ◽  
Vol 11 (3) ◽  
pp. 564-568 ◽  
Author(s):  
Qin Rao ◽  
Isaiah Schuster ◽  
Talal Seoud ◽  
Kevin Zarrabi ◽  
Nirvani Goolsarran

Nafcillin-induced acute liver injury is a rare and potentially fatal complication that has been known since the 1960s but inadequately studied. At this time, the only proven treatment is early discontinuation of the drug. Because of the high prevalence of nafcillin class antibiotic use in the United States, it is important for clinicians to have a high clinical suspicion for this diagnosis. We present a case of liver failure attributable to nafcillin use in a 68-year-old male with a history methicillin-sensitive Staphylococcus and L3/L4 osteomyelitis. After starting long-term antibiotic therapy, he presented with painless jaundice which necessitated discontinuation of the drug. At the time of presentation, the patient’s lab work exhibited a bilirubin/direct bilirubin of 9.4/8.2 mg/dL, alkaline phosphatase of 311 IU/L, and aspartate transaminase/alanine transaminase of 109/127 IU/L. The patient was switched to i.v. vancomycin given the concern for drug-induced liver injury. Imaging did not show obstruction of the hepatobiliary or pancreaticobiliary trees. Serology was unremarkable for viral etiology, autoimmune processes, Wilson disease, and hemochromatosis. A liver biopsy showed findings consistent with drug-induced liver injury. The patient’s liver function tests peaked at day 7 of admission and trended towards normal levels with cessation of nafcillin therapy. The patient was discharged with a diagnosis of nafcillin-induced acute liver injury. Our case highlights the importance of early recognition of the diagnosis and careful monitoring of liver function when nafcillin is employed in the clinical setting.


2021 ◽  
Vol 14 (4) ◽  
pp. e239488
Author(s):  
Melvin Qiyu Lee ◽  
Royale Chigozie ◽  
Irfan Khan ◽  
Gerard O'Mara

A 68-year-old patient presented with symptoms of a urinary tract infection. A deterioration in the patient’s liver function tests (LFTs) was noted 1 week following completion of a course of amoxicillin–clavunalate. This progressively worsened, reaching its peak by day 30. Our investigations excluded other possible causes for deranged LFTs and there was no improvement of same despite reduced dosing of potentially hepatotoxic medications.A trial of 30 mg/day prednisolone was commenced, resulting in an immediate and progressive improvement in LFTs to baseline over a period of 22 days and an improvement in constitutional symptoms such as tiredness and poor appetite. Drug-induced liver injury (DILI) is one of the common causes of acute hepatitis and a leading cause of acute liver failure in the US and Europe. Patterns of DILI can be generally divided into: (1) hepatocellular injury, (2) cholestatic injury and (3) mixed injury.


Author(s):  
Anooja Thampi

 Acute liver failure is a clinical entity associated with a high mortality rate and majority of these patients may require liver transplantation. N-Acetylcysteine (NAC), an antioxidant agent that replenishes mitochondrial and cytosolic glutathione stores, is an antidote for acetaminophen poisoning. But their role in non–acetaminophen-related acute liver failure is still not proven. Here, we discuss about a 67 year old male patient diagnosed with hepatitis with acute liver injury who was admitted in Emergency Medicine. He was treated with N- Acetylcysteine infusion for an average of 48 hours and later it was found that his liver function tests improved. In this study, we could find that N-Acetylcysteine plays a major role in improving the liver function test of patients with non–acetaminophen-related acute liver failure.


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