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Use of Dermatologics during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
Studies of rats and mice born to mothers exposed to etretinate had an increased frequency of congenital anomalies consistent with the human retinoic acid embryopathy, including limb, genitourinary, neural tube, and cloacal defects (Mesrobian et al., 1994). The implication of this with regard to human teratogenicity is unknown, but adds experimental support for the retinoic acid syndrome. Obviously, this drug should not be used for psoriasis during pregnancy.
Other Systemic Side Effects: Cardiovascular, Pulmonary, Otolaryngorhinologic, Genitourinary, Renal, and Immunologic
Published in Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish, Retinoids in Dermatology, 2019
Emin Ozlu, Akif Bilgen, Ayse Serap Karadag
The pulmonary side effects associated with retinoids other than oral isotretinoin are quite limited. A previous study on human patients with emphysema suggested that definitive clinical improvement could not be achieved with the administration of retinoids (26). To date, three cases have been reported, where patients developed retinoic acid syndrome due to the use of acitretin for treatment of psoriasis (27–29). Retinoic acid syndrome often develops in patients receiving all-trans-retinoic acid (ATRA) therapy for promyelocytic leukemia. It is characterized by fever, acute renal failure, respiratory distress, hypotension, pleural effusion, and weight gain (30). A 63-year-old patient with significant psoriasis who developed a drug fever attributed to acitretin was reported (31). The package insert also indicates that sinusitis, coughing, increased sputum, and laryngitis may occur (19).
Development of palliative medicine in the United Kingdom and Ireland
Published in Eduardo Bruera, Irene Higginson, Charles F von Gunten, Tatsuya Morita, Textbook of Palliative Medicine and Supportive Care, 2015
All-trans retinoic acid (ATRA) is used to treat acute promyelocytic leukemia. Approximately 10%-15% of patients develop the retinoic acid syndrome, which can cause fever, dyspnea, hypotension, pericardial effusions and myocardial ischemia/infarction.
Retinoic acid associates with mortality of patients on long-term hemodialysis
Published in Renal Failure, 2022
Marta Kalousová, Miroslava Zelenková, Aleš A. Kuběna, Sylvie Dusilová-Sulková, Vladimír Tesař, Tomáš Zima
ATRA is formed from retinol in a two-step oxidation: in the first, retinol is oxidized by alcohol dehydrogenase to retinal (retinaldehyde) and in the second catalyzed by retinal dehydrogenase, retinoic acid rises. ATRA serves as a lipophilic hormone, binding to the intracellular retinoic acid receptor (RAR), and transcriptionally regulating cell proliferation, differentiation, and immune response. ATRA and its isomers have been used for many years for the treatment of psoriasis, acne, acute promyelocytic leukemia, as well as some solid tumors [3,4]. Despite beneficial effects and general good tolerability, in some cases, the treatment may be accompanied by a complication known as retinoic acid syndrome (RAS) which also includes acute renal failure [5,6]. This syndrome was described in both adults [5] and children (a case with signs of nephrotic range proteinuria) [7]. On the other hand, tissue culture and animal studies show the protective effect of ATRA on the progression of kidney damage [8]. Additionally, the role of ATRA in the reduction of atherosclerotic plaques [9] and its dose-dependent effect on cardiac remodeling [10] was also demonstrated. As data on ATRA levels in patients with renal diseases are limited [11] and cardiovascular disease is the main reason for high mortality of patients with advanced renal diseases, our aim was to measure ATRA concentrations in serum from long-term HD patients and to determine their prognostic significance.
Heterogeneous Differentiation of Highly Proliferative Embryonal Carcinoma PCC4 Cells Induced by Curcumin: An In Vitro Study
Published in Nutrition and Cancer, 2021
Geetha Viswanathan, Lip Yong Chung, Usha K. Srinivas
Currently, the standard treatment option for GCT is chemotherapy in combination with etoposide, cisplatin, and bleomycin with or without surgical resection of the tumor. In addition, chemo-resistance is often a concern in GCT treatment. An alternative approach, referred to as differentiation therapy, employs a drug that reverses cell malignancy by inducing cell differentiation. A classic example of differentiation therapy is retinoic acid (RA) treatment for acute promyelocytic leukemia, an approach responsible for making this a curable form of cancer today (30). RA triggers differentiation of pluripotent cells to terminally differentiated and nonmalignant cells (31). However, RA treatment can cause retinoic acid syndrome in many patients, a syndrome characterized by symptoms that include fever, weight gain, respiratory distress, hypotension, and acute renal failure (32). Moreover, RA treatment is associated with developmental anomalies (33). Due to these potential severe side effects, the commonly used dosage of RA has been reduced from 45 to 25 mg/m2 per day (34); however, the dosage reduction reduces treatment efficacy.
Management of fever and neutropenia in the adult patient with acute myeloid leukemia
Published in Expert Review of Anti-infective Therapy, 2021
Andrew M. Peseski, Mitchell McClean, Steven D. Green, Cole Beeler, Heiko Konig
One such manifestation, the so-called ‘Differentiation syndrome’ (DS), has been a well-described complication of the treatment of acute promyelocytic leukemia (APL) for decades, and in fact has historically been referred to as ‘retinoic acid syndrome’ [187]. However, early clinical trials of oral FMS-like Tyrosine Kinase 3 (FLT3) and Isocitrate Dehydrogenase (IDH) inhibitors for the treatment of AML also unmasked this phenomenon. Specifically, DS has been noted with administration of the IDH1 inhibitor ivosidenib (FDA approved for newly diagnosed AML in patients 75 years and older or unfit for intensive chemotherapy, and for relapsed/refractory [R/R] disease), as well as the IDH2 inhibitor enasidenib and the FLT3 inhibitor gilteritinib (both approved for R/R disease) [188–191]. Together, these mutations may be found in up to 40% of cases of AML, and their inhibition results in the restoration of hematopoietic differentiation which can lead to DS [192–194]. Manifestations of DS can include fever, hypotension, leukocytosis, dyspnea/hypoxia, pulmonary infiltrates, pleural/pericardial effusions, peripheral edema, rash, tumor lysis syndrome, musculoskeletal pain, lymphadenopathy, and hepatic/renal failure [195–197]. The pathophysiology of DS for targeted AML agents has not been fully elucidated, but is thought to be like that implicated in APL; namely production of inflammatory cytokines, aggregation of leukemic cells, and tissue infiltration of maturing myeloid cells [198–200]. This is further bolstered by the fact that both APL and AML DS respond well to steroids, suggesting the involvement of inflammatory mediators.