tretinoin and Alcoholism

BACKGROUND Acute promyelocytic leukemia (APL) is a rare subtype of acute myeloid leukemia (AML) and is characterized by a genetic translocation affecting the retinoic acid receptor-alpha gene, leading to blockage in the differentiation of granulocytic cells. The accumulation of promyelocytes in bone marrow leads to cytopenias and life-threatening coagulopathies. Definitive diagnosis is made with bone marrow biopsy. Differentiation of APL from other leukemias is important to appropriately treat with all-trans retinoic acid (ATRA) and arsenic trioxide. Patients with HIV are at a higher risk to develop AML. This article identifies how multiple comorbidities and social factors can contribute to difficulties in diagnosing AML. CASE REPORT We present a 67-year-old man with a past medical history of hypertension and substance use disorder who presented with progressive exertional dyspnea and was found to have HIV, chronic hepatitis C, and APL with pancytopenia. His bone marrow biopsy confirmed AML. This was a case of co-existing HIV and aleukemic leukemia. CONCLUSIONS APL can present with pancytopenia, weakness, failure to thrive, or bleeding complications, which can be similar to presentations of those diagnosed with HIV. Diagnosis of APL can be differentiated between hypergranular and hypogranular; our patient demonstrated APL with only 52% blasts, which can make for a challenging diagnosis. Given increased mortality of APL, immediate ATRA therapy is warranted. Aleukemic leukemia is a rare presentation typically accompanied by skin manifestations. Our case highlights the importance of having high clinical suspicion for malignancy in patients with comorbidities that can interfere with the classic presentation of leukemia.

Topics: Aged; Alcoholism; Hepatitis C; HIV Infections; Humans; Leukemia, Promyelocytic, Acute; Male; Pancytopenia; Tretinoin

Fetal alcohol spectrum disorder (FASD) is an umbrella term used to describe the craniofacial dysmorphic features, malformations, and disturbances in growth, neurodevelopment and behavior occurring in individuals prenatally exposed to alcohol. Fetal alcohol syndrome (FAS) represents the severe end of this spectrum. Many pathophysiological mechanisms have hitherto been proposed to account for the disrupted growth and morphogenesis seen in FAS. These include impaired cholesterol-modification of the Sonic hedgehog morphogen, retinoic acid deficiency, lipoperoxidative damage due to alcohol-induced reactive oxygen species combined with reduced antioxidant defences, and malfunctioning cell adhesion molecules. In this report, we propose a completely novel concept regarding the pathogenesis of FAS. Based on our observation that transferrin isoelectric focusing (TIEF) - the most widely used screening tool for congenital disorders of glycosylation (CDG) - was transiently abnormal in a newborn with FAS and a confirmed maternal history of gestational alcohol abuse, we came to believe that FAS exemplifies a congenital disorder of glycosylation secondary to alcohol-inflicted disruption of (N-linked) protein glycosylation. Various pieces of evidence were found in the literature to substantiate this hypothesis. This observation implies, among others, that one might need to consider the possibility of maternal alcohol consumption in newborns with transient glycosylation abnormalities. We also present an integrated pathophysiological model of FAS, which incorporates all existing theories mentioned above as well as our novel concept. This model highlights the pivotal role of disrupted isoprenoid metabolism in the origination of FAS.

Topics: Alcohol Drinking; Alcoholism; Antioxidants; Cholesterol; Dolichols; False Positive Reactions; Female; Fetal Alcohol Spectrum Disorders; Glycosylation; Hedgehog Proteins; Humans; Infant; Infant, Newborn; Isoelectric Focusing; Male; Models, Theoretical; Pregnancy; Reactive Oxygen Species; Transferrin; Tretinoin; Vitamin A Deficiency

Topics: Alcoholism; Etretinate; Humans; Male; Middle Aged; Psoriasis; Tretinoin