Chronic Diseases and Translational Medicine最新文献

Cytarabine is one of the most used drugs for the treatment of hematological malignancies such as leukemia and non-Hodgkin's lymphoma. In cells, cytarabine is activated into ara-CTP, which can replace deoxycytidine triphosphate (dCTP) and become incorporated into the DNA of proliferating cells. Thus, it can block DNA synthesis, resulting in proliferation arrest and cell death.¹ High doses of cytarabine usually induce dermatological toxicity commonly reported as morbilliform eruptions, acral erythema, neutrophilic eccrine hidradenitis, vasculitis, toxic epidermal necrolysis, and eccrine squamous syringome taplasia.^2-5 Of these toxicity effects, violaceous erythema is especially rare.^{6, 7} Herein, we present a case of delayed generalized violaceous erythema associated with cytarabine and discuss its necessary treatment.

An 11-year-old boy came to the hospital complaining of an ache in the lower limb. Bone marrow puncture results confirm that he has acute lymphoblastic leukemia. He received a chemotherapy with cyclophosphamide, cytarabine, and 6-mercaptopurine (according to the Chinese Children Cancer Group [CCCG]-Acute lymphoblastic leukemia [ALL]-2015) for induction chemotherapy. The treatment course lasted 7 days, with cytarabine (100 mg/m²) and 6-mercaptopurine (60 mg/m²) given daily. Cyclophosphamide (1 g/m²) was given on the first day. On the seventh day of chemotherapy, he developed a high fever (39.8°C). The next day, a florid, diffuse, nonpruritic erythematous macule eruption appeared on his face, ears, and scalp. Antihistamines have no effect on the erythematous macule. Over the next 24 h, erythematous macules spread over his neck, arms, chest, abdomen, and back (Figure 1A). The percentage of eosinophils (6%; reference value, 0–5%) increased transiently on the eighth day of chemotherapy. On the ninth day of chemotherapy, erythematous macules coalesced into purpuric plaques and spread throughout the body (Figure 1B). The color of the erythema turned to bright red as well as a growing facial edema was observed. Histopathological examination of skin biopsy tissue demonstrated neutrophilic, lymphocytic infiltration and erythrocytic extravasation (Figure 2). C-reactive protein (CRP) level (56.7 mg/L; reference value, 0–8 mg/L) and D-dimer (2860 µg/L; reference value, 0–550 µg/L) were high throughout the period of erythema. Meanwhile, anti-infective therapy showed no effect on the progression of erythema or the reduction of CRP. On the 12th day of initial cytarabine exposure, dry desquamation was noted (Figure 1C), with complaints of slight pruritus. Then, the eruption faded away and disappeared on the 17th day after initial exposure to cytarabine (Figure 1D). However, in the later stage of erythema, the patient developed a liver injury and lasted for 13 days. After 28 days of initial exposure to cytarabine, the patient recovered. Subs

Immunoglobulin A nephropathy (IgAN) is the most common primary glomerular disease, and the “four-hit” theory represents its currently accepted pathogenic mechanism. Mucosal immunity triggered by infections in the respiratory tract, intestines, or other areas leads to antigen presentation, T cell stimulation, B cell maturation, and the production of IgA-producing plasma cells. The proteins B-lymphocyte stimulator (BLyS) and a proliferation-inducing ligand (APRIL) are involved in this process, and alternative complement and lectin pathway activation are also part of the pathogenic mechanism. Kidney Disease Improving Global Outcomes guidelines indicate that a specific effective treatment for IgAN is lacking, with renin–angiotensin–aldosterone system inhibitors being the primary therapy. Recent research shows that biological agents can significantly reduce proteinuria, stabilize the estimated glomerular filtration rate, and reverse some pathological changes, such as endocapillary proliferation and crescent formation. There are four main categories of biological agents used to treat IgA nephropathy, specifically anti-CD20 monoclonal antibodies, anti-BLyS or APRIL monoclonal antibodies, monoclonal antibodies targeting both BLyS and APRIL (telitacicept and atacicept), and monoclonal antibodies inhibiting complement system activation (narsoplimab and eculizumab). However, further research on the dosages, treatment duration, long-term efficacy, and safety of these biological agents is required.