MATERIALS AND METHODS: A total of 128 diabetic patients with foot ulcers were recruited and divided into two groups, consisting of 73 patients in the IDFU group and 55 in the non-infected diabetic foot ulcer (NIDFU). The severity of infection in IDFU patients was graded based on the Infectious Disease Society of America-International Working Group on the Diabetic Foot classification. Blood samples from all the patients were collected for measurement of PCT, high sensitivity C-reactive protein (hs-CRP) and white cell count (WBC). The area under the receiver operating curves (AUC) were then constructed and analysed.
RESULTS: PCT, hs-CRP and WBC levels were significantly higher in the IDFU group compared to NIDFU with hs-CRP demonstrated the highest AUC (0.91; p <0.001) followed by PCT (0.814; p < 0.001) and lastly WBC (0.775; p < 0.001). The best cut off value, sensitivity and specificity for the presence of infection in diabetic foot, were 3.47 mg/dL, 80% and 89% for hs-CRP, 0.11 ng/ml, 70% and 87% for PCT and 11.8x109/L, 60% and 90% for WBC. All the infection markers showed significant positive correlations with infection severity of DFU.
CONCLUSION: This study showed that hs-CRP is a more sensitive marker for diagnosing IDFU. Although PCT is useful in differentiating IDFU from NIDFU, the use of PCT is not necessary as it adds little value to the current practice.
CASE REPORT: A 69-year-old man presented with a three-day-history of worsening generalized body weakness, poor oral intake, nausea, significant loss of weight and lower back pain. He was diagnosed as primary PCL, based on hypercalcaemia, renal insufficiency, anaemia, thrombocytopenia, lytic bone lesions, 24% abnormal plasma cells in peripheral blood, immunophenotype of clonal plasma cells which were positive for CD38, CD138 and CD56 markers with kappa light chain restriction, 49% abnormal plasma cells in bone marrow, monoclonal paraprotein (IgG kappa) in serum and urine, and positive IGH rearrangement (Fluorescence in-situ hybridisation, FISH). He achieved complete remission after four cycles of Bortezomib-based therapy. There was a plan for high-dose therapy plus autologous haematopoietic cell transplantation. A month later, the disease relapsed, as evidenced by 94% abnormal plasma cells in his bone marrow aspirate, complex karyotype and abnormal FISH results. He passed away a few days later, from severe septicaemia. Time-to-progression of disease was 1 month and overall survival was 5 months.
DISCUSSION: This case report illustrates the clonal evolution and aggressive nature of primary PCL with older age at presentation, leading to a shorter duration of remission and overall survival.