tretinoin and Pancreatitis

Topics: Acute Disease; Humans; Leukemia, Promyelocytic, Acute; Pancreatitis; Tretinoin

A 55-year-old woman developed acute promyelocytic leukaemia during treatment with all-trans-retinoic acid and arsenic trioxide. Initially, she presented with symptoms of epigastric pain, vomiting, and nausea, and she developed acute pancreatitis. She was treated with parenteral nutritional supplementation for 20 days. However, the patient continued to develop refractory hyponatraemia, hypotension, and apathy. Finally, the patient was diagnosed with Wernicke encephalopathy (WE) using head magnetic resonance imaging. The patient underwent high-dose intravenous thiamine administration, and her symptoms were alleviated. WE is a rare adverse event during acute pancreatitis therapy. Acute pancreatitis that is caused by all-trans-retinoic acid and arsenic trioxide is a rare complication of acute promyelocytic leukaemia during chemotherapy. Further study is essential to improve our comprehension of the risk factors for complications in patients with acute promyelocytic leukaemia, considering that the associated complications were potentially caused by multiple etiological factors. A better understanding of these risk factors may help to improve the prognosis of patients with acute promyelocytic leukaemia at an early stage.

Topics: Acute Disease; Arsenic Trioxide; Arsenicals; Female; Humans; Leukemia, Promyelocytic, Acute; Middle Aged; Oxides; Pancreatitis; Tretinoin; Wernicke Encephalopathy

The Wilms' tumor suppressor gene (Wt1) encodes a zinc finger transcription factor that plays an essential role in the development of kidneys, gonads, spleen, adrenals and heart. Recent findings suggest that WT1 could also be playing physiological roles in adults. Systemic deletion of WT1 in mice provokes a severe deterioration of the exocrine pancreas, with mesothelial disruption, E-cadherin downregulation, disorganization of acinar architecture and accumulation of ascitic transudate. Despite this extensive damage, pancreatic stellate cells do not become activated and lose their canonical markers. We observed that pharmacological induction of pancreatitis in normal mice provokes de novo expression of WT1 in pancreatic stellate cells, concomitant with their activation. When pancreatitis was induced in mice after WT1 ablation, pancreatic stellate cells expressed WT1 and became activated, leading to a partial rescue of the acinar structure and the quiescent pancreatic stellate cell population after recovery from pancreatitis. We propose that WT1 modulates through the RALDH2/retinoic acid axis the restabilization of a part of the pancreatic stellate cell population and, indirectly, the repair of the pancreatic architecture, since quiescent pancreatic stellate cells are required for pancreas stability and repair. Thus, we suggest that WT1 plays novel and essential roles for the homeostasis of the adult pancreas and, through its upregulation in pancreatic stellate cells after a damage, for pancreatic regeneration. Due to the growing importance of the pancreatic stellate cells in physiological and pathophysiological conditions, these novel roles can be of translational relevance.

Topics: Aldehyde Oxidoreductases; Animals; Cell Lineage; Ceruletide; Disease Models, Animal; Epithelium; Gene Expression; Genes, Wilms Tumor; Homeostasis; Humans; Mice; Mice, Knockout; Mice, Transgenic; Pancreas; Pancreatic Stellate Cells; Pancreatitis; Regeneration; Repressor Proteins; Tissue Distribution; Translational Research, Biomedical; Tretinoin; WT1 Proteins

We report a rare case of hypercalcemia and acute pancreatitis in a subject with acute promyelocytic leukemia (APL) and pulmonary tuberculosis, during all-trans-retinoic acid (ATRA) treatment. Both associated complications were potentially due to several causes. A careful monitoring and exclusion of all causative factors must be addressed. Further research is necessary to improve our understanding of risk factors for these complications in patients with (APL). Studying these patterns may help us to improve outcomes for all children and young adults with hematologic malignancies.

Topics: Acute Disease; Antineoplastic Combined Chemotherapy Protocols; Asparaginase; Causality; Febrile Neutropenia; Humans; Hypercalcemia; Leukemia, Promyelocytic, Acute; Male; Mercaptopurine; Methotrexate; Middle Aged; Models, Biological; Pancreatitis; Pleural Effusion; Prednisone; Pulmonary Aspergillosis; Risk Factors; Tretinoin; Tuberculosis, Pulmonary; Vincristine

Topics: Acute Disease; Antineoplastic Agents; Humans; Hypertriglyceridemia; Pancreatitis; Tretinoin

Topics: Acute Disease; Adolescent; Antineoplastic Agents; Female; Humans; Hypertriglyceridemia; Leukemia, Promyelocytic, Acute; Pancreatitis; Tretinoin

All-trans-retinoic acid (ATRA) has been successfully used in the treatment of acute promyelocytic leukemia (APL). One of its adverse effects is acute pancreatitis. In the literature, a proposed cause of acute pancreatitis is hypertriglyceridemia. Here, we present the case of a 45-year-old male with APL, treated with ATRA combined with induction chemotherapy (cytarabine and idarubicin), who developed acute pancreatitis without overt hypertriglyceridemia. This finding suggests that hypertriglyceridemia might not be the sole contributing factor in the pathogenesis of ATRA-induced acute pancreatitis and that attention should be paid to the possibility that ATRA treatment causes acute pancreatitis in the absence of overt hypertriglyceridemia.

Topics: Acute Disease; Antineoplastic Combined Chemotherapy Protocols; Cytarabine; Humans; Hypertriglyceridemia; Idarubicin; Leukemia, Promyelocytic, Acute; Male; Middle Aged; Pancreatitis; Tretinoin

Topics: Antineoplastic Combined Chemotherapy Protocols; Humans; Leukemia, Promyelocytic, Acute; Male; Middle Aged; Pancreatitis; Tretinoin; Triglycerides

Topics: Acute Disease; Humans; Leukemia, Promyelocytic, Acute; Lipid Metabolism; Male; Middle Aged; Pancreatitis; Tretinoin

Topics: Acute Disease; Adult; Female; Humans; Hypertriglyceridemia; Leukemia, Promyelocytic, Acute; Pancreatitis; Tretinoin

Cytosolic retinoic acid receptor in carcinoma, chronic pancreatitis, and normal pancreatic tissue were examined using sucrose density gradient centrifugation, isoelectric focussing on agarose gel and saturation analysis. Thirteen patients were studied. Cytosolic retinoic acid binding protein (cRABP) was detected in all the samples with chronic pancreatitis and pancreatic carcinoma, but not in the normal tissue. Using sucrose gradient centrifugation, the highest concentrations of cRABP were found in pancreatic carcinoma tissues, ranging from 5.5-23.9 pmol/mg protein. These concentrations were markedly different than in chronic pancreatitis tissue (0.7-2.7 pmol/mg protein). Saturation analysis of cRABP showed a mean dissociation constant of 21.5 nM and maximum binding sites of 5.2 pmol/mg protein. Cytosolic retinoic acid binding protein was separated at an isoelectric point of 4.5 on agarose gel. The presence of cRABP suggest that retinoic acid may have a role to play in the function of the pancreas.

Topics: Adult; Aged; Aged, 80 and over; Carrier Proteins; Chronic Disease; Cytosol; Humans; Middle Aged; Neoplasm Proteins; Pancreas; Pancreatic Neoplasms; Pancreatitis; Receptors, Retinoic Acid; Tretinoin

Topics: Adult; Estrogens, Conjugated (USP); Female; Humans; Hyperlipidemias; Isotretinoin; Pancreatitis; Plasmapheresis; Tretinoin; Triglycerides