Case Presentation: 46 year old male with history of hypertension on losartan, gastroesophageal reflux disease on omeprazole and history of gout (not on medications) presents to his primary care provider for a new onset skin rash. Examination revealed a non-pruritic, petechial rash on his anterior chest and upper extremities that started 5 days ago. He denied any other prodromal symptoms of cough, sore throat, fever, myalgias or sick contact exposure. Laboratory evaluation revealed a platelet count of 5 x10(9)/L (normal range 150-350 x 10(9)/L). Hemoglobin, white blood cell count and renal function were within normal range. Liver enzymes were mildly elevated with aspartate aminotransferase at 104 U/L (8-43 U/L) and alanine aminotransferase at 154 U/L (7-45 U/L). Peripheral smear revealed no clumping of platelets or schistocytes. Given severe thrombocytopenia and petechial rash he was admitted to the hospital for further work up. Infectious work up including Hepatitis B and C, HIV, Epstein Barr Virus, Cytomegalovirus and SARS COVID 19 were negative. Autoimmune panel for vasculitis revealed weakly positive antinuclear antibody, but normal otherwise. He consumes 6 drinks of alcohol/week along with nightly use of cannabidiol (CBD) oil for sleep. Given progressive petechial rash and severe thrombocytopenia the diagnosis of severe Immune Thrombocytopenic Purpura (ITP) was considered and he was initiated on oral prednisone (1mg/kg/day) and Intravenous Immunoglobulin (IVIG) of 1g/kg/day. Given the critically low platelets, he also received a one-time platelet transfusion. Following initiation of steroids his platelets improved to 56 x10(9)/L on Day 2, 80 x10(9)/L on Day 3 and 148 x10(9)/L on Day 4. On further discussion he mentioned that one week prior to rash initiation, he switched to a new brand of synthetic CBD oil. Given the temporal relationship, this presentation was deemed to be drug induced ITP secondary to synthetic CBD oil use. He was recommended to stop using synthetic CBD oil. He was discharged home with a dose of 60 mg daily of prednisone with close follow up.
Discussion: CBD and tetrahydrocannabinol (THC) are the two common chemical compounds of cannabis. Some CBD compounds are synthetically derived in the laboratory and are not FDA approved, but still used for medicinal purposes. ITP is a diagnosis of exclusion and drug induced ITP secondary to synthetic CBD needs to be in the differential for thrombocytopenia. Only two case reports of ITP related to synthetic CBD use are noted in literature. In both these scenarios, ITP promptly responded to oral prednisone therapy. This could either be an uncommon clinical presentation or more likely an underdiagnosed clinical presentation as cannabinoid use history is not explicitly and accurately obtained by providers or voluntarily shared by patients. Management includes discontinuation of the synthetic CBD product and initiation of oral steroids. This case highlights the need for clinicians to consider synthetic CBD use as a differential for ITP. Given increased CBD use due to legalization, specific questioning about CBD use should be a routine similar to alcohol and tobacco use history. Reporting of these case scenarios will augment medical literature on the possible complications due to synthetic CBD use.
Conclusions: Synthetic CBD use can cause ITP. Recreational and medicinal CBD use needs to be elicited promptly in medical history. Management includes discontinuation of the CBD product and initiation of oral steroids.