Stevens‐Johnson Syndrome, Respiratory Distress and Acute Renal Failure Due to Synergic Bleomycin‐Cisplatin Toxicity

Brodsky, Andrés; Aparici, Ines; Argeri, Cecilia; Goldenberg, Daniel

doi:10.1002/j.1552-4604.1989.tb03426.x

Cited by 16 publications

(9 citation statements)

References 6 publications

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“…Stevens–Johnson syndrome has been reported in a patient receiving cisplatin and also has been noted more frequently in patients who are treated with corticosteroids. This patient was also taking tramadol, which has been associated with Stevens–Johnson syndrome, and the patient received 5‐fluorouracil, which has been associated with erythema multiforme 18–21…”

Section: Resultsmentioning

confidence: 99%

Establishing the dose of the oral NK₁ antagonist aprepitant for the prevention of chemotherapy‐induced nausea and vomiting

Chawla

Grunberg

Gralla³

et al. 2003

Cancer

208

147

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BACKGROUND The neurokinin‐1 antagonist aprepitant (EMEND™; Merck Research Laboratories, West Point, PA) has been shown to reduce chemotherapy‐induced nausea and vomiting when it is given with a 5‐hydroxytryptamine‐3 receptor antagonist and dexamethasone. The current study sought to define the most appropriate dose regimen of oral aprepitant. METHODS This multicenter, randomized, double‐blind, placebo‐controlled study was conducted in patients with cancer who were receiving initial cisplatin (≥ 70mg/m2) and standard antiemetic therapy (intravenous ondansetron plus oral dexamethasone). Patients were randomized to receive standard therapy plus either aprepitant 375 mg on Day 1 and 250 mg on Days 2–5, aprepitant 125 mg on Day 1 and 80 mg on Days 2–5, or placebo. Due to an apparent interaction with dexamethasone suggested by pharmacokinetic data obtained while the study was ongoing, the aprepitant 375/250 mg dose was discontinued and replaced with aprepitant 40 mg on Day 1 and 25 mg on Days 2–5, and a new randomization schedule was generated. Patients recorded nausea and emesis in a diary. The primary endpoint was complete response (no emesis and no rescue therapy), which was analyzed using an intent‐to‐treat approach with data obtained after the dose adjustment. Treatment comparisons were made using logistic regression models. Tolerability was assessed by reported adverse events and physical and laboratory assessments, and included all available data. RESULTS The percentages of patients who achieved a complete response in the overall study period were 71.0% for the aprepitant 125/80‐mg group (n = 131 patients), 58.8% for the aprepitant 40/25‐mg group (n = 119 patients), and 43.7% for the standard therapy group (n = 126 patients; P < 0.05 for either aprepitant regimen vs. standard therapy). Rates for Day 1 were 83.2% for the aprepitant 125/80‐mg group, 75.6% for aprepitant 40/25‐mg group, and 71.4% for the standard therapy group (P < 0.05 for aprepitant 125/80 mg vs. standard therapy), and rates on Days 2–5 were 72.7% for the aprepitant 125/80‐mg group, 63.9% for the aprepitant 40/25‐mg group, and 45.2% for the standard therapy group (P < 0.01 for either aprepitant group vs. standard therapy). The efficacy of the aprepitant 375/250‐mg regimen was similar to that of the aprepitant 125/80‐mg regimen. The overall incidence of adverse events was generally similar across treatment groups: 85% in the aprepitant 375/250‐mg group (n = 34 patients), 76% in the aprepitant 125/80‐mg group (n = 214 patients), 71% in the aprepitant 40/25‐mg group (n = 120 patients), and 72% in the standard therapy group (n = 212 patients), with the exception of a higher incidence of infection in the aprepitant 125/80‐mg group (13%) compared with the standard therapy group (4%). CONCLUSIONS When it was added to a standard regimen of intravenous ondansetron and oral dexamethasone in the current study, aprepitant reduced chemotherapy‐induced nausea and vomiting and was generally well tolerated, although increases in infection were noted that...

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Section: Resultsmentioning

confidence: 99%

Establishing the dose of the oral NK₁ antagonist aprepitant for the prevention of chemotherapy‐induced nausea and vomiting

Chawla

Grunberg

Gralla³

et al. 2003

Cancer

208

147

View full text Add to dashboard Cite

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“…One of the acute side effects of bleomycin is so‐called scratch dermatitis on the trunk and proximal extremities. To date, two cases of SJS induced by anticancer drugs containing bleomycin have been reported in Italy (9) and Argentina (10). The combination drugs were cisplatin and vinca alkaloids, and both of these patients died of lung fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Drug Eruption Due to Peplomycin: An Unusual Form of Stevens‐Johnson Syndrome with Pustules

Umebayashi

Enomoto

Ogasawara

2004

The Journal of Dermatology

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A rare case of Stevens-Johnson syndrome (SJS) due to peplomycin in a 48-year-old man is described. The patient had squamous cell carcinoma on the scalp and underwent preoperative neoadjuvant chemotherapy with peplomycin. On the fifth day of the chemotherapy, he developed a fever and multiple dusky violaceous erythematous areas and pustules on his trunk, thighs, and palms. Erosive erythema and erosions also developed on his soles, scrotum, and oral mucosa. A biopsy specimen taken from the eruption on the thigh revealed marked liquefaction degeneration of the basal layer of the epidermis. Laboratory examinations demonstrated aggravation of liver function. Additionally, the patient developed conjunctivitis and corneal erosions. Although he had some subcorneal pustules, we diagnosed the case as an unusual form of SJS because of severe mucous membrane involvement. Oral prednisolone was administered, and the symptoms subsided. Then the patient underwent wide local excision. One month after surgery, we performed patch tests and a lymphocyte stimulation test with negative results. Then we re-administered peplomycin starting with 1/20 of a daily dose and gradually increasing the dose each day. After administration of the regular daily dose, the patient had a relapse of fever, eruptions, stomatitis, corneal erosions, and liver dysfunction. Therefore, a definite diagnosis of drug eruption due to peplomycin was made.

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“…Interestingly, bleomycin is also known to generate DNA breaks, and bleomycin treatment increased non-IPF fibroblast cell death while IPF fibroblasts were resistant to bleomycin-induced cell death via enhanced DNA repair activity (11). Since both cisplatin and bleomycin cause DNA breaks, the administration of combined bleomycincisplatin chemotherapy is known to worsen the outcomes (44,45). Radiation therapy is an additional example.…”

Section: Discussionmentioning

confidence: 99%

Fibroblasts from patients with idiopathic pulmonary fibrosis are resistant to cisplatin-induced cell death via enhanced CK2-dependent XRCC1 activity

Nho

2019

Apoptosis

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Idiopathic pulmonary fibrosis (IPF) is a deadly and progressive fibrotic lung disease, but the precise etiology remains elusive. IPF is characterized by the presence of apoptosis-resistant (myo)fibroblasts that relentlessly produce a collagen-rich extracellular matrix (ECM). Recent studies showed that an anti-cancer chemotherapy drug cisplatin is implicated in the development of pulmonary fibrosis, suggesting that the treatment of cancer patients with cisplatin may alter fibroblast viability. To address this possibility, we investigated the cisplatin-induced cell death mechanism in lung fibroblasts derived from IPF and non-IPF patients in response to a collagen matrix. IPF fibroblasts showed enhanced resistance to cisplatin-induced cell death compared to non-IPF fibroblasts in a time-and dose-dependent manner. Molecular study showed that the expression of γH2AX, PUMA and caspase-3/7 activity was abnormally reduced in IPF fibroblasts, suggesting that DNA damage-induced apoptosis caused by cisplatin was suppressed in IPF fibroblasts. Our study further revealed that DNA repair protein XRCC1 activity was aberrantly increased as a result of CK2 hyper-activation in cisplatin-treated IPF fibroblasts, and this alteration protected IPF fibroblasts from cisplatin-induced cell death. Our results showed that IPF fibroblasts residing in a collagen rich matrix are resistance to cisplatin-induced cell death due to the aberrantly high CK2/XRCC1-dependent DNA repair activity. This finding suggests that pulmonary fibrosis may develop and worsen due to the presence of apoptosis-resistant lung fibroblasts in cisplatin-treated cancer patients.

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Stevens‐Johnson Syndrome, Respiratory Distress and Acute Renal Failure Due to Synergic Bleomycin‐Cisplatin Toxicity

Cited by 16 publications

References 6 publications

Establishing the dose of the oral NK₁ antagonist aprepitant for the prevention of chemotherapy‐induced nausea and vomiting

Establishing the dose of the oral NK₁ antagonist aprepitant for the prevention of chemotherapy‐induced nausea and vomiting

Drug Eruption Due to Peplomycin: An Unusual Form of Stevens‐Johnson Syndrome with Pustules

Fibroblasts from patients with idiopathic pulmonary fibrosis are resistant to cisplatin-induced cell death via enhanced CK2-dependent XRCC1 activity

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Stevens‐Johnson Syndrome, Respiratory Distress and Acute Renal Failure Due to Synergic Bleomycin‐Cisplatin Toxicity

Cited by 16 publications

References 6 publications

Establishing the dose of the oral NK1 antagonist aprepitant for the prevention of chemotherapy‐induced nausea and vomiting

Establishing the dose of the oral NK1 antagonist aprepitant for the prevention of chemotherapy‐induced nausea and vomiting

Drug Eruption Due to Peplomycin: An Unusual Form of Stevens‐Johnson Syndrome with Pustules

Fibroblasts from patients with idiopathic pulmonary fibrosis are resistant to cisplatin-induced cell death via enhanced CK2-dependent XRCC1 activity

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Establishing the dose of the oral NK₁ antagonist aprepitant for the prevention of chemotherapy‐induced nausea and vomiting

Establishing the dose of the oral NK₁ antagonist aprepitant for the prevention of chemotherapy‐induced nausea and vomiting