To the editor: A 31-year-old previous healthy male patient was admitted to the hospital with fever (Tmax 41°C) and nonproductive cough for seven days and dyspnea for three days. On day 4 after disease onset, his chest X-ray showed right upper lung small opacity and left lung large opacity (Figure 1A). The patient has been administrated levofloxacin for two days before he came into our hospital. Upon physical examination, blood pressure was 76/45 mmHg, pulse rate was 110/minute, respiratory rate was 35 breaths/min and temperature was 39.0°C. Chest examination showed bilateral fine moist rales and sporadic dry rales. Lab results showed that white blood cell (WBC) count was 8.86×109 with 82.7% neutrophils, platelet count 127×109/mm3 and hemoglobin 133 g/dl. Blood chemistry including liver profile, kidney profile, and coagulation studies were within normal limits. The chest X-ray showed progressive infiltration with left lung extensive consolidation (Figure 1B). Artery blood gas on non-rebreath oxygen face mask with 10 L/min oxygen flow rate showed PH 7.457, PaO2 77.8 mmHg, PaCO2 29.7 mmHg, and HCO3 -21.2 mmol/L. Infection work-ups were initiated thoroughly and finally sputum PCR for Mycoplasma pneumoniae (M. pneumoniae) was strong positive and serum IgM antibody for M. pneumoniae was also positive. Upon coming into our hospital, only moxifloxacin (0.4 g once daily intravenously) and oxygen therapy were administrated. Three days later on day 10 after onset, patient symptoms were significantly improved. However, at night on day 10, the patient presented passing dark urine and jaundice next early morning. Lab analysis showed WBC count was 28.87×109 with 67% neutrophils, platelet count 127×109/mm3 and hemoglobin 82 g/dl, high LDH level (1388 U/L) and hyperbilirubinemia (TBIL 73.9 μmol/L, IBIL 47.40 μmol/L, and DBIL 26.50 μmol/L). The blood smear showed red cell agglutination (Figure 1C). So hemolytic anemia was concerned and was treated by intravenous methylprednisolone (80 mg, Q12h) and immunoglobulin (35 g/d). Unfortunately, the hemoglobin quickly dropped to 3.2 g/dl in the following 36 hours and IBIL elevated to 9.56 μmol/L even received 240 mg methylprednisolone. A Coombs test was positive only for complement. The patient was transferred into ICU for plasmapheresis. After three-time plasmapheresis and steroids decrement to 40 mg/d, the patient's hemoglobin did not drop again and gradually went up to 4.3 g/L and bilirubin came down to normal level and went back general ward. He was discharged with hemoglobin 8.2 g/dl on day 23. Before he was discharged, a cold agglutinin test was found to be positive with antibody titre 1: 512. The patient was followed on day 30 after onset. He recovered very well and hemoglobin reached 12.3 g/dl. Lung field was also clear (Figure 1D).Figure 1.: Chest X-ray of the patient. A: Small opacity in right upper lung and large dense opacity in left lung on day 4 after onset. B: Bilateral opacities progressed with left lung consolidation on day 7. C: Blood smear show red cell agglutination. D: Clear lung field on day 30.During the course of M. pneumoniae infection old agglutinin antibody IgM is produced and associated with hemolysi.1 Besides cold agglutinin titer test, direct Coomb’ test is the major method for autoimmune hemolytic anemia diagnose. Post M. pneumoniae pneumonia cold agglutinin disease is usually self-limiting and most patients recover with supportive care. Antibiotics are likely to be of limited value in M. pneumoniae associated hemolytic anemia. Corticosteroids and plasmapheresis have not shown much promise. However, in two cases reported by Nasu2 and Tsurata et al,3 it is stated that corticosteroid therapy is sometimes necessary for the treatment of severe anemia. Unfortunately, our patient did not response by high-dose methylprednisolone. So this situation, plasmapheresis could rescue life in the lethal hemolytic anemia secondary to severe mycoplasma pneumonia. (Received May 3, 2014) Edited by Ji Yuanyuan
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