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Sickle cell disease (SCD) is linked to zinc deficiency, evidenced by low zinc levels and increased urinary excretion. This deficiency may explain growth issues and hypogonadism in affected men.
Area of Science:
- Biochemistry
- Hematology
- Human Physiology
Background:
- Sickle cell disease (SCD) is a genetic blood disorder affecting red blood cells.
- Clinical manifestations of SCD include growth retardation and hypogonadism, particularly in men.
- Trace element imbalances are suspected contributors to SCD pathology.
Purpose of the Study:
- To investigate trace element status, specifically zinc, in adult patients with sickle cell disease.
- To correlate clinical findings with biochemical data related to zinc metabolism in SCD patients.
- To explore potential mechanisms underlying zinc deficiency in sickle cell disease.
Main Methods:
- Analysis of trace elements in plasma, red blood cells, and hair from 84 adult SCD patients.
- Measurement of urinary zinc excretion in SCD patients and controls.
- Assessment of clinical parameters including height, weight, and secondary sexual characteristics.
Main Results:
- Eighty percent of SCD patients were below the 50th percentile for weight.
- Growth retardation was observed in 11 patients (6 men, 5 women).
- Zinc levels were decreased in plasma, red blood cells, and hair, while urinary zinc excretion was elevated in SCD patients compared to controls.
Conclusions:
- Hyperzincuria (increased urinary zinc excretion) is a potential mechanism for zinc deficiency in sickle cell disease.
- Zinc deficiency may be implicated in the growth retardation and hypogonadism observed in men with SCD.
- Further research into trace element supplementation for SCD management is warranted.
Abstract:
Trace elements in 84 adult patients (38 men and 46 women) with sickle cell disease (SCD) were reflected in clinical and biochemical data. Height was retarded in six men and five women. Eighty percent of the SCD patients in this sample were below the 50th percentile from the normal mean for weight. Twenty-eight men showed a lack of facial and body hair, and five additional subjects showed only scanty facial hair. Whereas zinc in plasma, red blood cells, and hair was decreased, the excretion of zinc in urine was increased in SCD patients as compared to the controls. We believe that one of the mechanisms accounting for zinc deficiency in SCD may be hyperzincuria and that growth retardation and hypogonadism in men so commonly seen in SCD may be related to zinc deficiency.