scholarly journals SAT-LB87 Golimumab Induced Thyroiditis

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Mo M Mai ◽  
Jocelyne G Karam ◽  
Nyein Lynn ◽  
Gurbaj Singh ◽  
Elizabeth Sedlis Singer
Keyword(s):  
Thyroid Nodules ◽  
Case Reports ◽  
Elevated Serum ◽  
Subacute Thyroiditis ◽  
Abnormal Behavior ◽  
Weight Changes ◽  
Drug Induced ◽  
Thyroid Cells ◽  
Patient Reported ◽  
History Of

Abstract Background: Subacute thyroiditis is caused by an inflammation and a destruction of the thyroid cells, leading to hyperthyroidism due to leakage of thyroid hormones, followed by possible hypothyroidism and/or full recovery of thyroid function. This is a case report describing a rare occurrence of drug-induced thyroiditis secondary to golimumab. Clinical Case: A 79-year-old female with HTN, hyperlipidemia, dementia and rheumatoid arthritis was brought to the ER for abnormal behavior including visual hallucinating and insomnia.Initial ER evaluation showed UTI for which antibiotic therapy was initiated. Dementia workup was performed including a negative head CT, nonreactive RPR, and borderline low vitamin B12 level. TFT obtained showed low TSH of 0.2mlU/L, elevated serum FT4 of 1.72ng/ml (n=0.58-1.64ng/ml) and elevated serum FT3 4.38pg/ml (n=2.5-3.9pg/ml), suggestive of hyperthyroidism. The patient reported no heat intolerance, hyperdefecation, or weight changes, but had intermittent palpitations. She denied any history of thyroid problem and did not take thyroid medication, amiodarone, biotin, or any new drug. She reported no fever or URI symptoms within the few weeks prior to admission. In addition to prednisone and methotrexate, she was taking golimumab 50mg every 30 days for the last 22 months for RA. The patient had a family history of hypothyroidism of two daughters and sister. She denied smoking, alcohol, or any other recreational drug use. Her home medications included prednisone 5mg daily, methotrexate, folic acid, lisinopril, simvastatin, and golimumab. On physical examination, she did not appear thyrotoxic and had no exophthalmos, thyroid tenderness, thyroid enlargement or thyroid nodules. Her HR range was 80bpm.Further analysis revealed normal TSI, TPO, and TgAb levels. The thyroglobulin level was very high at 2505ng/ml (n=1.6-59.9ng/ml). Her thyroid sonogram revealed bilateral thyroid nodules, largest at 1.9cm in the right mid pole. A 24-hr RAIU scan showed very low uptake (1.8%) consistent with thyroiditis (hyperthyroid phase).Endocrinology team did not recommend any antithyroid medications. In addition, she did not warrant NSAIDs or beta blockers as she was not symptomatic or tachycardic. In the absence of an autoimmune or an obvious viral process, her subacute thyroiditis was thought to be induced by golimumab. Conclusion: TNFɑ inhibitors used to treat chronic inflammatory diseases, have been rarely associated with subacute thyroiditis as described in case reports with adalimumab and etanercept use. We report the first subacute thyroiditis associated with golimumab use. We suggest that drug-induced subacute thyroiditis should be one of the differential diagnoses of thyroid dysfunction in patients treated with golimumab.

Suspected Lamotrigine-Induced Toxic Epidermal Necrolysis

1997 ◽  
Vol 31 (6) ◽  
pp. 720-723 ◽  
Author(s):  
Julie J Chaffin ◽  
Steven M Davis
Keyword(s):  
Valproic Acid ◽  
Toxic Epidermal Necrolysis ◽  
Case Reports ◽  
Stevens Johnson Syndrome ◽  
Complex Partial Seizures ◽  
Skin Reactions ◽  
Johnson Syndrome ◽  
Patient Reported ◽  
History Of ◽  
Relationship Of

OBJECTIVE: To describe a patient who developed toxic epidermal necrolysis (TEN) possibly secondary to lamotrigine use. CASE SUMMARY: A 74-year-old white man with a history of probable complex partial seizures was admitted to the neurology service for a prolonged postictal state. His antiepileptic regimen was changed while he was in the hospital to include lamotrigine. After 19 days of hospitalization and 14 days of lamotrigine therapy, the patient became febrile. The next day he developed a rash which progressed within 4 days to TEN, diagnosed by skin biopsy. All suspected drugs were discontinued, including lamotrigine. The patient was treated with hydrotherapy in the burn unit. His symptoms improved and he was discharged from the hospital 26 days after the rash developed. DISCUSSION: During lamotrigine's premarketing clinical trials, the manufacturer reported several cases of Stevens-Johnson syndrome and TEN. There are several published case reports of lamotrigine-induced severe skin reactions. All of these reports included patients being treated with both valproic acid and lamotrigine. Our patient was exposed to phenytoin, carbamazepine, clindamycin, and lamotrigine, but not valproic acid. The patient reported prior use of phenytoin with no skin rash. Carbamazepine was the antiepileptic drug the patient was maintained on prior to his hospital admission, and the symptoms of TEN resolved while he was still receiving carbamazepine. The patient received only two doses of clindamycin, which makes this agent an unlikely cause of TEN. CONCLUSIONS: Because of the temporal relationship of the onset of the patient's rash and several drugs that are known to cause severe rashes, it is not certain which drug was the definite culprit. However, based on the evidence from the literature, lamotrigine appears to be the causative agent.

Sudden Cardiac Arrest during Adenotonsillectomy in a Patient with Subclinical Duchenne's Muscular Dystrophy

1993 ◽  
Vol 72 (2) ◽  
pp. 130-131 ◽  
Author(s):  
Nick C. Benton ◽  
Robert A. Wolgat
Keyword(s):  
Cardiac Arrest ◽  
Muscular Dystrophy ◽  
General Anesthesia ◽  
Case Reports ◽  
Sudden Cardiac Arrest ◽  
Elevated Serum ◽  
Serum Creatine Kinase ◽  
Strong Family History ◽  
History Of ◽  
Duchenne's Muscular Dystrophy

We describe a four-year-old boy of Indian descent who had elective adenotonsillectomy for chronic sore throat and partial airway obstruction. About 10 minutes into the procedure, the patient suddenly developed cardiac asystole. After prolonged cardiac resuscitation, recovery was achieved. No permanent neurologic deficits resulted. The child was later found to have a strong family history of Duchenne's muscular dystrophy (DMD) and an elevated serum creatine kinase level documented since shortly after birth. We reviewed several case reports substantiating the risk for cardiac arrest during general anesthesia in DMD patients, and we concluded that DMD is a little-known risk for cardiac arrest during general anesthesia. The otolaryngologist must be aware of this potential complication, because tonsillectomy and adenoidectomy are commonly indicated for children at an age when DMD may be subclinical.

scholarly journals Drug-induced liver injury after switching from tamoxifen to anastrozole in a patient with a history of breast cancer being treated for hypertension and diabetes

2020 ◽  
Vol 11 ◽  
pp. 204062232096415
Author(s):  
Petr Potmešil ◽  
Radka Szotkowská
Keyword(s):  
Breast Cancer ◽  
Liver Injury ◽  
Early Stage ◽  
Case Reports ◽  
Cancer Resistance ◽  
Cytochrome P450 Enzymes ◽  
Drug Induced ◽  
Peripheral Tissues ◽  
History Of ◽  
Resistance Protein

Anastrozole is a selective non-steroidal aromatase inhibitor that blocks the conversion of androgens to estrogens in peripheral tissues. It is used as adjuvant therapy for early-stage hormone-sensitive breast cancer in postmenopausal women. Significant side effects of anastrozole include osteoporosis and increased levels of cholesterol. To date, seven case reports on anastrozole hepatotoxicity have been published. We report the case of an 81-year-old woman with a history of breast cancer, arterial hypertension, type 2 diabetes mellitus, hyperlipidemia, and chronic renal insufficiency. Four days after switching hormone therapy from tamoxifen to anastrozole, icterus developed along with a significant increase in liver enzymes (measured in the blood). The patient was admitted to hospital, where a differential diagnosis of jaundice was made and anastrozole was withdrawn. Subsequently, hepatic functions quickly normalized. The observed liver injury was attributed to anastrozole since other possible causes of jaundice were excluded. However, concomitant pharmacotherapy could have contributed to the development of jaundice and hepatotoxicity, after switching from tamoxifen to anastrozole since several the patient’s medications were capable of inhibiting hepatobiliary transport of bilirubin, bile acids, and metabolized drugs through inhibition of ATP-binding cassette proteins. Telmisartan, tamoxifen, and metformin all block bile salt efflux pumps. The efflux function of multidrug resistance protein 2 is known to be reduced by telmisartan and tamoxifen and breast cancer resistance protein is known to be inhibited by telmisartan and amlodipine. Moreover, the activity of P-glycoprotein transporters are known to be decreased by telmisartan, amlodipine, gliquidone, as well as the previously administered tamoxifen. Finally, the role of genetic polymorphisms of cytochrome P450 enzymes and/or drug transporters cannot be ruled out since the patient was not tested for polymorphisms.

scholarly journals Lichen Planus Pemphigoides Induced by Enalapril: A Case Report and a Review of Literature

2017 ◽  
Vol 9 (3) ◽  
pp. 217-224 ◽  
Author(s):  
Woranit Onprasert ◽  
Kumutnart Chanprapaph
Keyword(s):  
Lichen Planus ◽  
Early Recognition ◽  
Case Reports ◽  
Direct Immunofluorescence ◽  
Drug Induced ◽  
First Case ◽  
Bullous Dermatosis ◽  
Culprit Drug ◽  
History Of ◽  
Hands And Feet

Lichen planus pemphigoides (LPP) is a rare autoimmune bullous dermatosis. The clinical presentation of LPP may mimic bullous pemphigoid making the diagnosis difficult. A thorough clinical, histopathological, and immunological evaluation is essential for the diagnosis of LPP. The etiology is largely idiopathic; however, there are several case reports of drug-induced LPP. We report an 81-year-old Thai woman with underlying hypertension and type 2 diabetes mellitus who presented with a 4-week history of multiple tense bullae initially on the hands and feet that subsequently expanded to the trunk and face. Enalapril was commenced to control hypertension. The histopathology and direct immunofluorescence were compatible with LPP. Circulating anti-basement antibodies BP180 was also positive. The patient was treated with topical corticosteroid with a modest effect. Enalapril was discontinued and complete resolution of LPP occurred within 12 weeks. There was no recurrence after a 1-year follow-up period. To the best of our knowledge, we present the first case of enalapril-induced LPP. Early recognition and prompt discontinuation of the culprit drug allow resolution of the disease. Medication given for LPP alone, without cessation of the offending drug, may not change the course of this condition.

scholarly journals Successful use of carbamazepine in a patient with drug rash with eosinophilia and systemic symptoms

2019 ◽  
Vol 9 (5) ◽  
pp. 331-335
Author(s):  
Alexandra L. Bixby ◽  
Sarah Goldsborough ◽  
Aaron Iuppa ◽  
Andrew LeBlanc ◽  
Heather E. Schultz ◽  
...  
Keyword(s):  
Case Reports ◽  
Elevated Serum ◽  
Primary Treatment ◽  
Cross Reactivity ◽  
Pathology Report ◽  
Medline Search ◽  
History Of ◽  
Drug Rash ◽  
Elevated Creatinine ◽  
Systemic Symptoms

Abstract Drug rash with eosinophilia and systemic symptoms (DRESS) is a serious adverse drug reaction with a high mortality rate. Discontinuation of the causative agent is the primary treatment. History of DRESS may put patients at higher risk of future episodes; however, cross-reactivity between various medications is not well established. An 18-year-old African American male with a history of bipolar I disorder with psychotic features was admitted for mania on his home dose of divalproex. After 1 week, olanzapine was added for refractory symptoms, but due to elevated creatinine phosphokinase (CPK), it was subsequently discontinued, and he was started on lorazepam and lithium. One week later, the patient was transferred to the intensive care unit with elevated CPK, fever, thrombocytopenia, elevated serum creatinine, hypotension, diarrhea, mild rigidity, bilateral inducible ankle clonus, and a rash. All medications were discontinued except for lorazepam. The skin pathology report was consistent with a drug eruption, and he was started on prednisone. Given continued symptoms of mania, carbamazepine was initiated. After clinical and laboratory improvement, the patient was discharged on hospital day 59 with instructions to continue carbamazepine and lorazepam. A MEDLINE search revealed no published case reports of the successful use of carbamazepine in a patient with a history of DRESS. Information regarding cross-reactivity between medications is limited primarily to aromatic antiepileptics. In our case report, carbamazepine was successfully used in a patient with a recent episode of DRESS during olanzapine, lithium, and valproate use.

scholarly journals Collapsing Focal Segmental Glomerulosclerosis in a Patient with Acute Malaria

2015 ◽  
Vol 2015 ◽  
pp. 1-4 ◽  
Author(s):  
Najamus Sehar ◽  
Emad Gobran ◽  
Suzanne Elsayegh
Keyword(s):  
Focal Segmental Glomerulosclerosis ◽  
Case Reports ◽  
Left Kidney ◽  
Elevated Serum ◽  
Segmental Glomerulosclerosis ◽  
Acute Distress ◽  
Night Sweats ◽  
History Of ◽  
Secondary Form ◽  
Collapsing Fsgs

Introduction. Collapsing focal segmental glomerulosclerosis (FSGS) is most commonly seen in association with HIV infection. Rare data is available about the association between collapsing FSGS and malaria.Case Description. A 72-year-old African male patient presented to the hospital for generalized body aches, fatigue, fever, and night sweats for three days. He had history of recent travel to Ghana. Patient looked in acute distress and was shivering. Laboratory tests showed elevated serum creatinine (Cr) of 2.09 mg/dL (baseline was 1.5 mg/dL in 2012). Hospital course was significant for rapid elevation of Cr to 9.5 mg/dL and proteinuria of 7.9 grams. Autoimmune studies resulted negative. Blood smear resulted positive forPlasmodium falciparumand patient was treated with Artemether/Lumefantrine. Patient’s fever and pain improved, but kidney function continued to deteriorate and he became oliguric. On day seven, he was started on Hemodialysis. Tests for different causes of glomerular pathology were also negative. He underwent left kidney biopsy which resulted in findings consistent with severe collapsing glomerulopathy.Discussion. This case illustrates a biopsy proven collapsing FSGS likely secondary to malarial infection requiring renal replacement therapy. Literature review revealed only few case reports that suggested the possible association of malaria with secondary form of FSGS.

scholarly journals Diphenhydramine as a Cause of Drug-Induced Liver Injury

2017 ◽  
Vol 2017 ◽  
pp. 1-4 ◽  
Author(s):  
Yunseok Namn ◽  
Yecheskel Schneider ◽  
Isabelle H. Cui ◽  
Arun Jesudian
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Chromosomal Translocation ◽  
Altered Mental Status ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Patient Reported ◽  
History Of ◽  
Concomitant Medications ◽  
Unites States

Drug-induced liver injury (DILI) is the most common cause of acute liver failure in the Unites States and accounts for 10% of acute hepatitis cases. We report the only known case of diphenhydramine-induced acute liver injury in the absence of concomitant medications. A 28-year-old man with history of 13/14-chromosomal translocation presented with fevers, vomiting, and jaundice. Aspartate-aminotransferase and alanine-aminotransferase levels peaked above 20,000 IU/L and 5,000 IU/L, respectively. He developed coagulopathy but without altered mental status. Patient reported taking up to 400 mg diphenhydramine nightly, without concomitant acetaminophen, for insomnia. He denied taking other medications, supplements, antibiotics, and herbals. A thorough workup of liver injury ruled out viral hepatitis (including A, B, C, and E), autoimmune, toxic, ischemic, and metabolic etiologies including Wilson’s disease. A liver biopsy was consistent with DILI without evidence of iron or copper deposition. Diphenhydramine was determined to be the likely culprit. This is the first reported case of diphenhydramine-induced liver injury without concomitant use of acetaminophen.

Recurrent Limb Pain and Migraine: Case Reports and A Clinical Review

Cephalalgia ◽  
2009 ◽  
Vol 29 (8) ◽  
pp. 898-905 ◽  
Author(s):  
S Prakash ◽  
ND Shah ◽  
SY Dholakia
Keyword(s):  
Migraine Headache ◽  
Temporal Relationship ◽  
Preventive Measures ◽  
Case Reports ◽  
Limb Pain ◽  
Patient Reported ◽  
History Of ◽  
Clinical Profiles ◽  
Relationship Of ◽  
Close Temporal Relationship

Recurrent limb pain (RLP) is a well-known entity in childhood. It is considered a precursor of migraine. The temporal relationship of RLP with headache in childhood is lacking in the literature. However, there are many cases with limb pain in a close temporal relationship with migraine headache in adults. We report six female patients with RLP and migraine and delineate the temporal relationship between the two. Three patients had a history of RLP in childhood and developed migraine headache after many years. Conversely, two patients had a long history of migraine headache and later developed RLP. One patient developed RLP and migraine headache at the same age. Isolated limb pain was frequent in all six patients. It was mild to severe, for a few minutes to a few days, and predominantly located in the upper extremities. Only one patient reported allodynia. The patients showed response to preventive measures (all six patients) and abortive therapies (four patients), even in those attacks of RLP that were not associated with headache episodes. We also review the clinical profiles of the patients in whom RLP and migraine were related to each other, and speculate on the possible mechanisms for RLP in the patients with migraine.

scholarly journals Spontaneous Nasal Polypectomy Proceeded by Fluticasone Propionate (XHANCE®) and Zileuton (Xyflo®) Application

2020 ◽  
Vol 1 (2) ◽  
pp. 8-12
Author(s):  
Marija Rowane ◽  
Kelsey Graven ◽  
Robert Hostoffer
Keyword(s):  
Fluticasone Propionate ◽  
Treatment Regimen ◽  
Nasal Polyposis ◽  
Case Reports ◽  
Subcutaneous Immunotherapy ◽  
Intranasal Corticosteroids ◽  
Patient Reported ◽  
Oral Corticosteroids ◽  
History Of ◽  
New Treatment

Abstract Background: Nasal polyps (NPs) are inflammatory outgrowths of paranasal sinus mucosa that occur in one to four percent of the population and most commonly cause congestion, obstruction, or hyposmia. Intranasal corticosteroids, along with short courses of oral corticosteroids, are most often recommended for symptomatic nasal polyposis, prior to consideration of surgical intervention. We present the first reported case of spontaneous nasal polypectomy, occurring after use of fluticasone propionate (XHANCE®) and zileuton (Xyflo®). Methods: A 43-year-old Asian-Indian male with history of allergic rhinitis, asthma, and nasal polyposis had been prescribed subcutaneous immunotherapy for five years without effectiveness before another polypectomy was scheduled. After the polyps resurfaced, the patient was prescribed prednisone and underwent another polypectomy. He later presented with persistent NPs and congestion, as well as diffuse lymphadenopathy and pruritic eyes and ears. Fluticasone Propionate was continued as maintenance therapy and Zileuton was prescribed in place of Montelukast (Singulair®). Results: After several weeks of the new treatment regimen, the patient reported polyp irritation and movement, as well as influenza-like symptoms. Epistaxis soon occurred, followed by a spontaneous polypectomy. Three more polyps were expelled with bloody discharge. The patient reported resolved hyposmia and reduced symptoms thereafter. The treatment regimen was continued without change or further episodes of epistaxis and polypectomy. Conclusion: Few case reports in the literature describe polyp autoamputation. We report the first instance of spontaneous nasal polypectomy in the literature, induced by Fluticasone Propionate and Zileuton.

scholarly journals Acute Ascending Muscle Weakness Secondary to Medication-Induced Hyperkalemia

2014 ◽  
Vol 2014 ◽  
pp. 1-3 ◽  
Author(s):  
Lauren A. Kimmons ◽  
Justin B. Usery
Keyword(s):  
Chronic Kidney Disease ◽  
Serum Potassium ◽  
Potassium Concentration ◽  
Close Monitoring ◽  
Drug Induced ◽  
Lower Extremity Weakness ◽  
Serum Potassium Concentration ◽  
Patient Reported ◽  
Life Threatening ◽  
History Of

Secondary hyperkalemic paralysis is an uncommon but potentially life-threatening consequence of drug-induced disease. We report a case of a 53-year-old female with history of chronic kidney disease presenting to the emergency department with a one-day history of upper and lower extremity weakness and paresthesias. Serum potassium concentration on admission was greater than 8 mEq/L, and serum creatinine was elevated above baseline. Electrocardiogram showed first-degree atrioventricular block with peaked T waves. The patient reported compliance with daily lisinopril 10 mg, spironolactone 25 mg, and 40 mEq twice daily of potassium chloride. Symptoms and electrocardiogram returned to baseline within 24 hours of presentation and serum potassium returned to 4.2 mEq/L at approximately 36 hours without the need for dialysis. This case emphasizes the importance of including such a condition in the differential diagnosis of patients with ascending paralysis and the importance of close monitoring of patients placed on potassium-elevating agents.

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