Indicator changes in jaundice syndrome
During the development of jaundice, the biochemical profile exhibits marked and predictable dynamics. At the peak of the disease, the activity of aminotransferases in the blood rises sharply, primarily alanine aminotransferase (ALT). Concurrently, a decrease in the prothrombin index (PTI) is recorded, indicating impaired synthetic function.
Positive dynamics begin to emerge in the second week after the onset of jaundice: bilirubin concentration and enzyme activity decrease significantly. A complete return of these indicators to reference values typically occurs by the 20th–25th day of the disease.
Biochemical markers of iron metabolism
To confirm iron deficiency anemia (IDA) in children, a complete blood count alone is insufficient; biochemical tests reflecting the depletion of micronutrient stores in tissues are necessary. Biochemistry changes first, allowing clinicians to distinguish latent deficiency from manifest disease.
Key indicators of iron metabolism:
- Serum iron: concentration drops (normal range is 14.3–28 µmol/L).
- TIBC (total iron-binding capacity of serum): compensatorily increases (normal range 55–65 µmol/L). Free transferrin content directly reflects this indicator.
- Ferritin: the protein responsible for intracellular storage. Its level decreases (below 12 µg/L according to WHO/UNICEF criteria).
- Transferrin: the transport protein for free iron. In deficiency, its saturation drops to 15% or less.
- Soluble transferrin receptor: its concentration rises above 7 mg/L, serving as a clear signal of tissue starvation.
Impact of inflammation on anemia diagnosis
Classic biochemical markers have vulnerabilities. For instance, ferritin is an acute-phase reactant. This means that inflammatory processes, uremia, or pregnancy can affect its concentration, artificially inflating the result and masking a real iron deficiency.
In such cases, modern indicators of iron-deficient erythropoiesis that are unaffected by inflammation come to the rescue:
- Ret-He (reticulocyte hemoglobin content): an iron shortage is indicated by a drop below 30.6 pg. Furthermore, its increase during treatment serves as the earliest marker of therapy efficacy, preceding the rise in hemoglobin.
- HYPO-He (percentage of hypochromic erythrocytes): increases above 5% in deficiency.
Evaluation of plasma factors in hemophilia
Within the biochemical and coagulological assessment of hemostasis, the diagnosis of hemophilia is based on identifying specific abnormalities. Prolongation of activated partial thromboplastin time (aPTT) and whole blood clotting time is typical for the disease.
Plasma clotting factor concentrations decrease, leading to impaired thromboplastin formation. A critical differential feature: the vascular-platelet link remains unaffected. Platelet count, bleeding time, and endothelial capillary fragility tests remain within normal limits.
Biochemical monitoring in COVID-19
In patients with suspected coronavirus infection, a general therapeutic biochemistry panel helps comprehensively assess disease severity and timely identify complications.
The mandatory list of tests includes:
- Pigment metabolism and proteins: total bilirubin, albumin.
- Renal markers: urea, creatinine.
- Energy and water-electrolyte balance: glucose, sodium, potassium, chlorides.
- Enzymes and inflammatory markers: AST, ALT, ferritin.
WHO/UNICEF triad for diagnosing IDA: drop in hemoglobin (below age-related norm), depletion of stores (ferritin <12 µg/L), and tissue starvation (soluble transferrin receptor >7 mg/L).
Class and exam questions
How does latent iron deficiency differ from manifest IDA in laboratory tests?
In latent deficiency, blood hemoglobin levels remain normal, but biochemical markers (serum iron and ferritin) are already reduced. In manifest IDA, hemoglobin drops below the age-related norm alongside depot depletion.
Why might ferritin be normal in the presence of true iron deficiency?
Ferritin is an acute-phase protein. In the presence of a concomitant inflammatory process, uremia, or during pregnancy, its level increases compensatorily, which can mask the depletion of tissue iron stores.
How rapidly do iron store indicators rise when treatment is initiated?
Ferritin levels, reflecting micronutrient accumulation, begin to reliably increase with a significant delay—only 2–3 weeks after starting medication.
What else to study on this topic
- Pathological changes in coagulogram: aPTT and thromboplastin formation.
- Erythrocyte indices (MCV, MCH, MCHC) and hypochromic microcytic anemia.
- Differential leukocyte count in CBC during viral infections.
- Assessment of the vascular-platelet hemostatic link (endothelial tests).
- Dynamics of hematological shifts at the peak of the icteric period.
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