Risk factors for K-RAS proto-oncogene mutation in colorectal cancer

K-rats is an important onco-gene on chromosome 12 and encodes p21 Ras-protein, which is a growth promoting protein. Specific point mutations in codons 12 and 13 are prevalent in colorectal cancer [CRC] patients. Recognition of K-ras mutations may be helpful in screening and early diagnosis of CRC. This study aimed at investigating the association between potential variables known or suspected to be related to risk of CRC and occurrence of K-ras mutations, explaining how such variables play a role in CRC tumorigenesis. Eighty CRC patients were examined for RBC folic acid by enzyme chemi-luminescence and K-ras proto-oncogene genotyping for codon 12 mutations by enriched PCR-RELP technique. RBC folic acid level was significantly deficient in CRC patients with K-ras mutation [23 patients, mean RBC folate= 100.96+51.3 ng/ml] than those without the mutation [57 patients, mean RBC folate = 216.6+116.4 ng/ml][P<0.01], suggesting that decreased folic acid may be a risk factor for K-ras mutation development. Gender also was found to be another predicting risk factor, in spite of being masked by the accentuated folic acid deficiency in females. Folic acid supplementation should be mandatory, and those at high-risk of CRC should be screened for the risk of K-ras mutation using the prediction equation method depending on sex and RBC folate followed by close monitoring for those a high risk for the mutation

Cystatin C as marker of glomerular filtration rate in children with nepthrotic syndrome

Nephrotic syndrome [NS] is the most common chronic renal disease of childhood. The rapid and accurate evaluation of renal function is important to detect the extent and progress of renal affection. Glomerular filtration rate [GFR] is the best marker for renal function. Serum cystatin C; a cysteine proteinase inhibitor; has been proposed as a sensitive marker for GFR. Our study was conducted on 50 patients with NS [23 with minimal change disease 'MCD', 12 with focal segmental glomerulosclerosis 'FSGS' and 15 with mesangioproliferative glomerulonephritis 'MP'], as well as 20 age and sex matched normal controls. In addition to routine assessment, creatinine clearance and serum cystatin C were measured in a trial to evaluate the importance of serum cystatin C versus serum creatinine in the detection of early impairment of renal function. Our results showed a significant 'positive' correlation between the creatinine clearance and the 'reciprocals' of both serum cystatin C and serum creatinine in all the 70 studied cases [P<0.0005]. The correlation was significantly better for serum cystatin C [r = 0.879] than the serum creatinine [r = 0.776]. Also serum cystatin C was significantly higher in nephrotic patients than in controls [P < 0.0005] while the serum creatinine was less significantly elevated [P < 0.05]. Mean while, serum cystatin C showed higher negative and positive predictive values [95% and 92% respectively] as compared to serum creatinine [88% and 76% respectively] in the detection of impairment of GFR, denoting the ability of serum cystatin C to detect the early changes in renal function. The reference interval of serum cystatin C as measured in our controls was independent on age or sex, and ranged between 0.6-1.32 mg/L. The highest diagnostic accuracy [95.7%] was obtained when the upper limit of 1.43 mg/L was used. So we could conclude that serum cystatin C is more sensitive and specific than serum creatinine in the detection of early impairment of GFR