Areekul S, Churdchu K, Cheeramakara C, Wilairatana P, Charoenlarp P
Department of Tropical Radioisotopes, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand.
Southeast Asian J Trop Med Public Health. 1995 Mar;26(1):46-50.
Serum transcobalamin II (TCII) levels were determined in 56 patients with P. falciparum malaria infection. They were divided into 3 groups: severe (malarial parasite > 5% or patients with cerebral malaria or renal insufficiency), moderate (1-5% infection without complications) and mild (1% infection). Elevated serum TCII values were found only in patients with severe malaria infection. These values correlated directly with parasitemia, blood urea nitrogen and creatinine, but were not correlated with alkaline phosphatase. As 17 patients with azotemia had elevated serum TCII levels while other 3 patients with normal BUN and creatinine concentrations had serum TCII levels within the normal limits. These findings indicated that malarial patients with renal insufficiency had increased serum TCII. A possible mechanism is the reduced TCII-B12 that filtered through the glomeruli due to the reduced renal blood flow with the decreased its uptake by proximal tubular cells resulting in the decreased degradation of TCII by the tubular lysosomal enzymes. Determination of serum TCII level may be used as an indicator of renal function in malarial patients with renal insufficiency.
对56例恶性疟原虫感染患者测定了血清转钴胺素II(TCII)水平。他们被分为3组:重症组(疟原虫>5%或患有脑型疟疾或肾功能不全的患者)、中度组(感染率为1%-5%且无并发症)和轻度组(感染率为1%)。仅在重症疟疾感染患者中发现血清TCII值升高。这些值与疟原虫血症、血尿素氮和肌酐直接相关,但与碱性磷酸酶无关。因为17例氮质血症患者血清TCII水平升高,而其他3例血尿素氮和肌酐浓度正常的患者血清TCII水平在正常范围内。这些发现表明,肾功能不全的疟疾患者血清TCII升高。一种可能的机制是,由于肾血流量减少,通过肾小球滤过的TCII-B12减少,近端肾小管细胞对其摄取减少,导致肾小管溶酶体酶对TCII的降解减少。测定血清TCII水平可作为肾功能不全疟疾患者肾功能的指标。