Henoch–Schönlein purpura triggered by Mycoplasma pneumoniae in a female infant

To the Editor,

Henoch–Schönlein purpura (HSP) is an immunoglobulin A‐mediated, autoimmune, hypersensitivity vasculitis of childhood that results in a series of symptoms, including a purpuric rash occurring on the lower extremities, abdominal pain, arthritis, and renal involvement. The occurrence of HSP peaks between 5 and 6 years of age, and male infants are more often affected than female infants [1]. Although the etiology of this disease remains unclear, many antigens, such as infective agents, foods, drugs, vaccinations, and insect bites, are reported to be involved in the onset of HSP. A survey on the clinical characteristics of childhood HSP in Jinan, China, demonstrated that 57.5% of cases suffered from respiratory infection; and among them, 82.6% of cases had a streptococcal infection with elevated antistreptolysin O titers [2]. However, Mycoplasma pneumoniae (MP)‐related HSP is an unusual condition and most reports do not mention it.

A 19‐month‐old female infant was admitted to our department with a 3‐day history of fever, cough, hematochezia, and a purpuric rash on her lower limbs. The birth and medical history were nonsignificant. On admission, her blood pressure was 80/35 mmHg, heart rate was 133/min, axillary temperature was 39.80°C, respiratory rate was 46/min, and oxygen saturation was 96%. A few fine, moist rales were heard over the lower lobes of both lungs. The cardiac physical examination result was unremarkable. The abdomen showed no clinical signs of peritoneal irritation, masses, or enlarged organs. Specific serum immunoglobulin M antibodies for MP and fecal occult blood test were both positive. Her initial blood counts were as follows: white blood cells, 8.55 × 10⁹/L with 67.34% neutrophils, 28.04% lymphocytes, and 4.24% monocytes; hemoglobin, 94 g/L; and platelets, 298 × 10⁹/L. Other blood chemistries included: thrombin time, 12.90 seconds; activated partial thromboplastin time, 43.30 seconds; d dimers, 7.24 mg/mL; procalcitonin, 74.72 mg/mL; and C‐reactive protein, 12 mg/L. Chest X‐ray showed patches of pneumonia at both hilar regions radiating outward along the course of the bronchovascular markings. Antinuclear antibody and antineutrophil cytoplasmic antibody were both negative. Urinary analysis and an abdominal ultrasound scan demonstrated no abnormal findings. The electrocardiogram result was normal and echocardiography confirmed normal ejection fraction with no evidence of infective endocarditis. The patient was diagnosed as having HSP in combination with MP infection, and was treated with intravenous erythromycin (30 mg/kg/d) and methylprednisolone (10 mg/kg/d for 3 days). After 7 days of hospitalization, the fever, cough, hematochezia, and skin lesions gradually resolved.

Because there is no definitive test for the diagnosis of HSP, the 1990 American College of Rheumatology criteria for HSP are still the most commonly used criteria for diagnosis [1]. In this report, our patient fulfilled three criteria (nonthrombocytopenic purpura, young age, and gastrointestinal involvement), and thus, the diagnosis of HSP was made undoubtedly. However, her age of presentation is unusual. According to our recent study, HSP is a childhood disease with most patients in the age group between 3 and 15 years, and only 3.11% of the cases were reported to be under the age of 3 years [3].

HSP is an extremely rare extrapulmonary manifestation of MP infection. Timitilli et al [4] investigated extrapulmonary manifestations among 92 children with MP infection, and found that only one 5‐year‐old girl had HSP. In our patient, MP is prone to trigger the onset of HSP. The etiology of MP‐associated HSP is mainly attributed to the host response to antigens on MP, such as immune‐complex‐mediated injury, cytotoxic T‐cell‐mediated immune responses, and autoimmune reactions. In addition, a recent study by Kurata et al [5] indicated that interleukin‐10 and interleukin‐17A may also be involved in the extrapulmonary complications of MP infection. A combination of macrolides and methylprednisolone is effective in alleviating extrapulmonary manifestations and radiological findings. In this report, our patient recovered gradually after treatment with erythromycin and methylprednisolone. However, it is worthwhile to note that although gastrointestinal hemorrhage in our patient was not exacerbated, the potential gastrointestinal adverse reactions induced by erythromycin should also be monitored.