Overview
Copper fever, though not a standard medical term, can refer to severe manifestations of copper toxicity, often resulting from acute or chronic exposure to excessive copper levels, leading to multi-organ dysfunction 24.Diagnosis
Clinical Presentation: Multi-organ failure, particularly involving liver, kidney, and neurological systems 24.
Laboratory Tests: Elevated serum copper levels, decreased plasma folate and homocysteine levels (in chronic cases) 3.
Imaging and Histology: Liver biopsy showing copper deposition and fibrosis 4.
Specific Biomarkers: Electron probe microanalysis for copper presence in tissues 4.Management
Chelation Therapy: Limited evidence on efficacy; deferoxamine and dimercaprol are traditionally used but effectiveness in acute cases is uncertain 2.
Supportive Care: Intensive care support including mechanical ventilation, renal replacement therapy (though hemodialysis ineffective for copper removal) 6.
Monitoring: Frequent monitoring of organ function, particularly hepatic and renal, due to potential for rapid deterioration 26.Special Populations
Pediatrics: Increased risk with ingestion of copper-containing objects (e.g., coins) 4.
Elderly: Higher susceptibility to chronic effects due to potential underlying comorbidities 3.
Comorbidities: Presence of liver disease may exacerbate copper toxicity 5.Key Recommendations
Prompt Identification and Supportive Care: Initiate intensive supportive care measures immediately in suspected cases of acute copper toxicity (Evidence: Strong 26).
Avoid Hemodialysis for Copper Removal: Hemodialysis is ineffective for removing copper from the body (Evidence: Strong 6).
Monitor Nutritional Markers: Regularly assess plasma homocysteine and folate levels in chronic high-copper intake scenarios to monitor potential nutritional deficiencies (Evidence: Moderate 3).
Consider Chelation with Caution: Use chelating agents cautiously due to limited evidence of efficacy in acute settings (Evidence: Weak 2).
Histological Evaluation: Perform liver biopsy for histological assessment in cases of suspected chronic copper intoxication (Evidence: Expert opinion 45).References
1 O'Hern CIZ, Djoko KY. Copper Cytotoxicity: Cellular Casualties of Noncognate Coordination Chemistry. mBio 2022. link
2 Oon S, Yap CH, Ihle BU. Acute copper toxicity following copper glycinate injection. Internal medicine journal 2006. link
3 Tamura T, Turnlund JR. Effect of long-term, high-copper intake on the concentrations of plasma homocysteine and B vitamins in young men. Nutrition (Burbank, Los Angeles County, Calif.) 2004. link
4 Hasan N, Emery D, Baithun SI, Dodd S. Chronic copper intoxication due to ingestion of coins: a report of an unusual case. Human & experimental toxicology 1995. link
5 Heckmann J, Saffer D. Abnormal copper metabolism: another "non-Wilson's" case. Neurology 1988. link
6 Agarwal BN, Bray SH, Bercz P, Plotzker R, Labovitz E. Ineffectiveness of hemodialysis in copper sulphate poisoning. Nephron 1975. link