Case Report: Baricitinib as an Alternative in the Maintenance Therapy for Macrophage Activation Syndrome Secondary to Nodular Panniculitis.

Background: Macrophage activation syndrome (MAS) is a severe complication of autoimmune diseases with high mortality. We report the effectiveness of baricitinib as an option for the maintenance therapy in MAS secondary to nodular panniculitis. Case summary: A 24-year-old female came to our hospital with repeated fever and a skin nodule on right tibial tuberosity. Results were notable for raised serum ferritin (SF), triglycerides (TG), elevated liver function enzymes, interleukin-6 (IL-6), interferon-γ (IFN-γ), soluble interleukin-2 receptor (sIL-2R) and decreased activity of NK cells. The pathological biopsy of the subcutaneous nodules indicated nodular panniculitis. Hemophagocytic cells were found in bone marrow aspiration. She was diagnosed as MAS secondary to nodular panniculitis. With the treatment of methylprednisolone (MP) and immunoglobulin, her symptoms and laboratory data gradually improved. Nevertheless, her disease relapsed when the MP dose was tapered. Regarding the usage of JAK inhibitors in MAS, we used baricitinib (JAK1/2 inhibitor) to treat MAS and her symptom and abnormal laboratory findings returned to normal. During follow-up, though the MP dose was tapered, she was stable without a MAS recurrence. Conclusion: The case report suggested baricitinib is an option for MAS in the maintenance therapy phase and is potentially beneficial to prevent recurrence.

Phytoecdysteroids from Ajuga iva act as potential antidiabetic agent against alloxan-induced diabetic male albino rats.

The present study investigated the protective effect of phytoecdysteroids extracted from the Ajuga iva plant on body weight changes, blood glucose, insulin total protein, blood urea nitrogen (BUN), creatinine, triglycerides (TG), cholesterol, lipid peroxidation, antioxidant enzymes, pancreatic histopathology and hexokinase-I expression in the alloxan-induced diabetic rats. Experimental diabetes was induced following 15day intraperitoneal administration of alloxan. The rats were divided into four groups. Group I served as a sham group, and group II served as the diabetic control. Group III served as a treatment for phytoecdysteroids (10mg/kg), and group IV served as a treatment for phytoecdysteroids (20mg/kg). Phytoecdysteroids restored body weight loss to its antihyperglycemic effect. Blood glucose was reduced 19.2 and 52.9% in group III and IV respectively. Blood insulin (54.9 and 105.88%) and total protein (25 and 72.2%) was increased in group III and IV respectively. BUN, creatinine, TG, cholesterol and lipid peroxidation was significantly reduced following treatment. Catalase, superoxide dismutase (SOD), and glutathione peroxidase activity were significantly increased following treatment. Islet ß-cells are lost in alloxan-induced diabetic rats. Regeneration of islets and reduced atrophy of acinar cells were noted. The number of insulin-secreting cells was tremendously reduced in alloxan-induced diabetic rats. Insulin-secreting cells were increased 48 and 61% in group III and IV respectively. Hexokinase-I mRNA (28.3 & 93.5%) and protein (27.9 and 55.3%) expression were significantly increased following treatment. Taking all these data together, it is suggested that the phytoecdysteroid could be a potential therapeutic agent against experimental diabetes.

Glutathione S-transferases T1 null genotype is associated with susceptibility to aristolochic acid nephropathy.

OBJECTIVES: This study aims to determine whether six polymorphisms of the genes involved in drug metabolism are associated with susceptibility to the development and progression of aristolochic acid nephropathy (AAN). METHODS: In the study, 91 aristolochic acid nephropathy (AAN) cases and 152 healthy controls of Chinese Han population were examined. Six common polymorphisms of genes, including multidrug resistance gene 1 (MDR1), cytochrome P450 (CYP1A1), NAD(P)H quinone oxidoreductase 1 (NQO1), glutathione S-transferase (GST) T1 and M1, were determined. Associations between their genotypes with AAN risk were calculated using an unconditional logistic regression model. RESULTS: Among the six candidate polymorphisms, only the distribution frequency of GSTT1 null genotype was significantly higher among AAN cases compared with controls (P = 0.041, 62.6% vs. 48.7%) and was associated with a 1.7-fold increased risk (OR = 1.728, 95%CI: 1.013-2.948, P = 0.045) of developing AAN, after adjustment for age and gender. The stratified analysis further showed that the GSTT1 null genotype was dominant in slow progressive AAN patients (OR = 2.497, 95%CI: 1.028-6.064, P = 0.043). The GSTM1 genotypes were not shown to influence the development of AAN. CONCLUSION: This study supports the hypothesis that polymorphisms related to drug metabolism such as GSTT1 may be an important factor influencing the development of AAN in the Chinese Han population exposed to AA.