ABSTRACT
BACKGROUND: Low dose methotrexate toxicity rarely occurs, but may present with severe complications, such as pancytopenia, hepatotoxicity, mucositis, and pneumonitis. Known risk factors for methotrexate toxicity include dosing errors, metabolic syndrome, hypoalbuminemia, renal dysfunction, lack of folate supplementation, and the concomitant use of drugs that interfere with methotrexate metabolism. Vitamin B12 deficiency leads to megaloblastic anemia and may cause pancytopenia, but its role in methotrexate toxicity has not been described. CASE PRESENTATION: We present a case of a patient with rheumatoid arthritis who was admitted with febrile neutropenia, pancytopenia, and severe mucositis, likely secondary to low dose methotrexate toxicity. She had multiple factors that potentially contributed to the development of toxicity, including concurrent sulfasalazine use for rheumatoid arthritis. An evaluation of the patient's macrocytic anemia revealed pernicious anemia. The patient's illness resolved with cessation of methotrexate and sulfasalazine, leucovorin treatment and vitamin B12 repletion. CONCLUSIONS: This case illustrates the multiple factors that may potentially contribute to low dose methotrexate toxicity and highlights the importance of testing for vitamin B12 deficiency in rheumatoid arthritis patients with macrocytic anemia. Addressing all the modifiable factors that potentially contribute to low dose methotrexate toxicity may improve outcomes.
ABSTRACT
Internal derangement of the knee secondary to a meniscal tear has been recently observed in patients with chondrocalcinosis. However, there is no data about the prevalence of meniscal tears associated to chondrocalcinosis. Therefore, the aim of this study was to know the rates of meniscal tear in patients with chondrocalcinosis. The study population was a cohort of 1031 consecutive outpatients who underwent arthroscopy of the knee. Meniscal tear was present in 322 patients and 709 patients had intact meniscus. The specific subgroup of interest included 58 knees from 58 patients (25 males and 33 females) with arthroscopic evidences of chondrocalcinosis. Patients with chondrocalcinosis had significantly higher rates of meniscal tear compared to those without chondrocalcinosis (74.1 versus 28.7%, p < 0.001). An absolute and attributable risk of tear was 74 and 8%, respectively, in knees with chondrocalcinosis. Relative risk of tear in patients with chondrocalcinosis versus without chondrocalcinosis was 2.58 (95% confidence interval 2.16-3.10). In patients with chondrocalcinosis and meniscal tear, the duration of the disease was about 5.3 (range 1-8) years versus 4.9 (range 3-7) years in those patients with chondrocalcinosis and an intact meniscus (p = 0.75). In conclusion, our findings support that chondrocalcinosis predispose meniscal tearing even in the absence of any traumatic event. Further longitudinal studies are needed to characterize the impact of chondrocalcinosis and meniscal vulnerability.
