Stanislas, a 58 -year -old nurse, consults following the creation of a biological assessment highlighting an anomaly of protein electrophoresis (albumin anomaly), the other biological parameters being completely normal (NFS, ionic assessment, creatinine, hepatic assessment, CRP).
He is very worried because he feels a little tired following a bronchitis that a colleague had treated by 3rd generation Cephalosporine. In order to obtain a faster result, the patient had decided to inject the ceftriaxone at the rate of 3 g/day for 5 days. He strongly thinks that the biological anomalies observed are related to his act.
After a completely reassuring assessment, we were able to confirm that this bisalbuminemia was actually linked to these high doses of cephalosporin. A biological control carried out a month later showed normalization of electrophoresis.
INTRODUCTION
Bisalbuminemia is an anomaly observed after the electrophoresis which was described for the first time in 1955 by Scheurlen.
It is rare dysproteinemia. Its prevalence is between 0.003 and 0.1 %. Regarding the impact, it varies according to the populations observed. Thus the Caucasians and Asians have an impact between 1/1,000 and 1/10,000, while the Amerindians have an incidence which is around 1 %.
Note that this biological anomaly is detected more frequently currently due to a technique change to carry out this dosage. Previously, electrophoresis was indeed carried out with agarose gel, while currently we use a capillary electrophoresis having a greater sensitivity.
Albumin helps maintain intravascular oncotic pressure, and promotes the transport of endogenous and exogenous substances.
In the bisalbuminemia two migrations are observed: a rapid migration (anodic migration), and a slow -type migration (cathodic migration).
The different etiologies
Bisalbuminemia can be of genetic origin, linked to:
– Fabry’s disease: Lysosomal pathology combining renal failure, transient ischemic accidents, arrhythmias, diffuse pain and desangikeratomas.
-– Alport syndrome: illness due to a mutation of the gene coding for the synthesis of collagen, in which there is renal damage (nephritic syndrome), ENT anomalies (deafness) and ophthalmological anomalies (cataract).
More frequently, it is an anomaly acquired linked to:
– a digestive pathology: pancreatic pseudo-cyst (rupture promotes, through pancreatic enzymes, partial proteolysis of albumin);
– renal pathology such as glomerulonephritis, diabetic or hypertensive nephropathies, nephrotic syndromes;
– an use of beta -lactams with high doses which promotes a fixation of this antibiotic on part of albumin;
– a myeloma with a complex between albumin and IGA (most often) or IgM (more rarely);
– Other less frequent causes: liver adenocarcinoma, Alzheimer’s disease, sarcoidosis, hypothyroidism.
Support
The treatment of a bisalbuminemia is above all that of responsible etiology.
The genetic bisalbuminemia persists throughout the patient’s life, while the bisalbuminemia acquired is most often transient.
Bibliography:
1. Lefrère B, Dedôme E, Garcia- Hejl C, et al. Bisalbuminies: About a case. The 2018 internal medicine review; 39 (12): 950-954.
2. Zoulati G, El Boukhrissi F, Yéya Maïga R, et al. A case of bisalbuminemia associated with nephrotic syndrome induced by non-steroidal anti-inflammatory drugs. Health Notebooks therapeutic medicine 2021; 30 (2): 131-135.
3. El Boukhrissi F, Balouch L, Moudden K, et al. Bisalbuminemia occurring outside the usual situations. The 2016 internal medicine review; 37 (7): 505-506.
