Abstract
Cold Agglutinin Disease is a hemolytic anemia associated with cold reactive autoantibodies. Although the acute form of cold agglutinin disease can be attributed to autoimmune or infectious diseases and lymphoproliferative diseases, it has, to the best of our knowledge, so far，never been reported as secondary to mycoplasma pneumonia in a type 2 diabetic individual. In this paper, we report a case of cold agglutinin disease following mycoplasma pneumonia in a 47-year-old female patient with type 2 diabetes and schizophrenia. Cold agglutinin test and direct Coombs’ test was positive. Anti-mycoplasma anti-body titre by complement fixation was high (Anti-IgG was negative and Anti-C3d was positive) and was accompanied by hemolytic anemia. Her general condition, including Cold Agglutinin Disease improved after conservative therapy with antibiotics, hypoglycemic agents and short-term use of steroids. The patient recuperated and was discharged in good health after 7 days’ stay in the hospital. She remains clinically well with no recurrence of anemia. The simultaneous occurrence of cold agglutinin disease, mycoplasma infection and diabetes mellitus is rare and accumulation of case reports is required to gain better insight of this case scenario.
Highlights
More than a century has elapsed since cold agglutinins were discovered, a case of cold agglutinin disease complicated by mycoplasma infection in a type 2
Using intravenous immunoglobulin in patients with cold agglutinin disease superseded by Mycoplasma pneumonia infection has been proved beneficial in inhibiting hemolysis until spontaneous clearance of the IgM antibodies occurs [18, 19]
This was replicated in a case of cold agglutinin disease associated with Mycoplasma pneumonia, reported by Inoue F. et al stating that obvious clinical improvement was noted after treating with minocycline and prednisolone [20]
Summary
More than a century has elapsed since cold agglutinins were discovered, a case of cold agglutinin disease complicated by mycoplasma infection in a type 2. Cold Agglutinin Disease is characterized by an auto-antibody which has the capability to agglutinate red blood cells at temperatures lower than that of the body and subsequently to induce complement activation, as a consequence of which there is lysis of red blood cells, resulting in impaired blood flow to the digits, nose and ears. Typical clinical manifestation of cold agglutinin disease includes cold-induced circulatory symptoms as well as hemolytic anemia of varying degrees of severity and episodes of hemoglobinuria and acrocyanosis, which tend to exacerbate or alleviate upon exposure to low temperatures. Cold agglutinin antibodies are mainly specific for the I/i and H red blood cells membrane systems [5] and the possible triggering factors include various infectious agents (e.g. mycoplasma, Ebstein Barr virus) and lymphoproliferative disorders (Waldenstroms macrogammaglobulinemia)
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