Plasma cell myeloma is known to cause expansion of a single clone of munoglobulin (Ig) which results in the secretion of a unique homogeneous monoclonal protein (M component). However, there are cases which reported that it can also cause production of two different clones of these monoclonal proteins. Although it is relatively very rare as the prevalence is only 2% of all plasma cell myeloma cases, the clinical features are said to be similar to monoclonal gammopathy. It is suggested that these biclonal gammopathy results from either one monoclonal cell clone in monoclonal gammopathy or two different monoclonal cell clones. Whichever the mechanism of the disease be, the response to treatment seems to be similar as compared to the monoclonal cases although some reports shows chemoresistant. Here, we report a rare case of plasma cell myeloma with IgG (lambda) and IgA (lambda) type of biclonal gammopathy, the clinical presentation, the haematological and biochemical markers as well as the response to the treatment.
Keywords: biclonal gammopathy, M protein, plasma cell myeloma
Chronic myeloid leukemia (CML) patients who have BCR-ABL T315I mutation, usually present in the advance phase of the disease with overall survival (OS) shorter than those without the mutation. This study aimed to determine the prevalence of T315I mutation amongst imatinib mesylate (IM) resistant CML patients and to compare the OS between T315I-mutated and non-T315I-mutated patients. Sixty consecutive CML patients who were treated with IM for at least 18 months and their treatment responses, were recorded. The mutation analysis was done using allele-specific oligonucleotide reverse transcriptase-polymerase chain reaction (RT-PCR) assay followed by direct sequencing technique. Forty-two patients (70%) were found to have IM-resistance. Five out of 42 patients had detectable T315I mutation. Median OS of IM-resistant T315I-mutated patients was 96 months (95% CI:54-138) compared to 84 months (95% CI:48-120) in non T315I-mutated patients, although this was found to be statistically insignificant (p = 0.43). The present study showed a higher prevalence of T315I mutation as compared to a few local studies. Median OS of T315I-mutated patients were observed to be longer than non-T315-mutated patients. Further studies encompassing larger cohort of patients are required to confirm this finding.