Survival After Severe Rhabdomyolysis Following Monensin Ingestion

Blain, Michela; Garrard, Alexander; Poppenga, Robert H.; Chen, Betty; Valento, Matthew; Gittinger, Melissa H.

doi:10.1007/s13181-017-0616-6

Cited by 18 publications

(13 citation statements)

References 8 publications

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“…However, these mechanisms are not only efficient against coccidians, but also can act against mammalian cells, primarily on cardiac and peripheral muscle tissues. Clinical signs of acute rhabdomyolysis, such as muscle weakness and myocardial insufficiency, have been observed in a small number of cases of acute intoxications with monensin and other ionophoric compounds, both in animals and humans, due to accidental ingestion of the pure compounds [9,10,11,12]. The authorization of coccidiostats as feed additives is based on studies that demonstrate the safety of their use in relation to the target species at the highest proposed levels of incorporation in feed or water, and at multiples of that level to establish a margin of safety [13].…”

Section: Introductionmentioning

confidence: 99%

“…Although some acute toxicity cases in humans, due to the ingestion of pure molecules, have been registered [9,10,11,12], major concerns are addressed toward chronic toxicity due to long-term exposure to low coccidiostat levels [7]. The European Food Safety Authority (EFSA) and the Joint FAO/WHO Expert Committee on Food Additives (JECFA) established, on the basis of toxicological data, acceptable daily intakes (ADIs) for all regulatory anticoccidials, ranging from the lowest values for HFG (0.00003 mg/kg body weight/day) to the highest values for NIC (0.2 mg/kg body weight/day) [25].…”

Section: Introductionmentioning

confidence: 99%

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Occurrence and Residue Concentration of Coccidiostats in Feed and Food of Animal Origin; Human Exposure Assessment

Roila

Branciari

Pecorelli

et al. 2019

Foods

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Occurring central Italy, 262 unmedicated feed samples and 353 samples of animal tissues and eggs are tested for coccidiostats between 2012 and 2017. A validated multi-residue HPLC-MS/MS method is applied for the simultaneous determination of the 11 coccidiostats licensed in the EU. The dietary exposure to coccidiostats through poultry meat and eggs is calculated for high consumers, and the contribution to acceptable daily intake of coccidiostats is evaluated. The occurrence of positive feed samples ranges from 17.2% in 2012 to 28.3% in 2017, with an average percentage of positive samples of 25%, while 3.8% of feed samples are non-compliant with a concentration ranging from 0.015 mg/kg for diclazuril to 56 mg/kg for narasin. Positive samples of animal tissues, on average, are 34.7%, fully compliant, while 16% of eggs are positive and violative residues are found in 2%. These noncompliant samples show a concentration varying from 2.4 µg/kg to 1002 µg/kg. The contribution of poultry meat and egg consumption to the acceptable daily intake of each coccidiostat is below 1%, highlighting a low direct risk to public health.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Occurrence and Residue Concentration of Coccidiostats in Feed and Food of Animal Origin; Human Exposure Assessment

Roila

Branciari

Pecorelli

et al. 2019

Foods

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“…In India, there were seven human cases of poisoning with maduramicin in porridge by mistake, and four patients unfortunately died after 48 h, with a varying degree of rhabdomyolysis [18]. Other drugs of the same ionophore class, such as monensin and salinomycin, have been reported to cause human intoxication with different levels of rhabdomyolysis in China and other countries [24][25][26]. In addition, extensive use of maduramicin and other ionophores in the livestock production industry increased the environmental release and posed potential risk to ecology safety and public human health in recent years [20,33].…”

Section: Discussionmentioning

confidence: 99%

Ionophore Toxin Maduramicin Produces Haff Disease-Like Rhabdomyolysis in a Mouse Model

Gao

Song

Zuo

et al. 2020

IJERPH

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Maduramicin is a toxic ionophore antibiotic that is isolated from Streptomyces, frequently occurring in an aquatic environment. To understand the potential role of maduramicin in crayfish consumption related Haff disease, a mouse model was established in this study. Two exposure routes of maduramicin in the abdominal muscle and the hepatopancreas tissue homogenates of crayfish were given intragastrically to mice in different doses for seven days. Action changes, clinical symptoms, feed consumption, body weight, blood biochemistry, and histopathology examination of mice were observed and analyzed. In the natural exposure group, relatively low concentration of maduramicin in crayfish muscle and hepatopancreas had no obvious effects on mental state, body weight, blood biochemical indexes, or histologic appearance. However, in the artificial exposure group, with increasing concentrations, maduramicin in crayfish muscle and hepatopancreas homogenates both induced mental sluggishness and weight loss of mice. Blood biochemical examination showed that 3.5 mg·kg−1 and 7 mg·kg−1 maduramicin in crayfish tissue homogenates significantly increased levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), lactate dehydrogenase (LDH), and creatine kinase (CK). Additionally, histopathological examination showed that multiple organs were damaged by maduramicin, including degeneration of liver cells, shedding of renal epithelial cells, and disturbance and partial lysis of myocardial and skeletal muscle filaments in the mice. In summary, maduramicin may not cause Haff disease through contamination of the aquatic environment under normal conditions. Maduramicin can be used as a potential toxin tool to establish a rhabdomyolysis disease animal model for drug development.

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“…The rhabdomyolysis induced by monensin poisoning is firstly due to increased intracellular sodium concentration, which causes a secondary increase in cytosolic calcium. The accumulation of intracellular calcium may be related to the elevation of calcium influx through the Na þ / Ca 2þ exchange pump, the reduction of calcium outflow to extracellular fluid, and the release of calcium from sarcoplasmic reticula and mitochondria (Blain et al, 2017). The significant increase in intracellular calcium is thought to exert vital roles in monensininduced damage of skeletal muscle and cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

“…It has been previously reported that acute monensin poisoning can cause significant rhabdomyolysis and fatal acute renal failure, eventually leading to multiple organ failure and even death (Caldeira et al, 2001; Kouyoumdjian et al, 2001). Another report showed that one case of monensin poisoning also had rhabdomyolysis as the main manifestation but unaccompanied by renal failure, and patients survived after clinical treatment (Blain et al, 2017). Herein, we report two human cases of monensin poisoning with severe rhabdomyolysis and hepatotoxicity caused by oral ingestion.…”

Section: Introductionmentioning

confidence: 99%

Rhabdomyolysis and hepatotoxicity following accidental monensin ingestion: A report of two cases

2020

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Background: Monensin is a commonly used veterinary antibiotic with a narrow safety range. Overdose of monensin can cause animal poisoning or even death. Monensin poisoning is rare in humans, and there is no effective detoxification protocol in clinical treatment. Objective: We report here two cases of monensin-induced rhabdomyolysis and hepatotoxicity by oral ingestion. The two patients were a couple and both were admitted to the hospital due to oral ingestion of monensin 5 days prior. Patient 1, with a past history of chronic bronchitis and hypertension, presented with severe rhabdomyolysis, hepatotoxicity, and hypoxemia. After treatment with fluid replacement and alkalinization of urine, his condition deteriorated the next day and irreversible cardiopulmonary arrest occurred. Patient 2 was diabetic and using oral hypoglycemic drugs and had obvious rhabdomyolysis from the fifth day of admission. After treatment with fluid replacement, urine alkalization, and continuous renal replacement therapy (CRRT), the patient recovered and was discharged 1 month later. Discussion: The ingestion of monensin can lead to life-threatening toxicity, with rhabdomyolysis and hepatotoxicity as the main manifestations. Comprehensive treatment including CRRT in the early stage of rhabdomyolysis may improve the condition and prognosis.

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Survival After Severe Rhabdomyolysis Following Monensin Ingestion

Abstract: Monensin is a veterinary medication not approved for human use by the US Food and Drug Administration. Though poorly studied in humans, this case demonstrates the severe harm that may occur following ingestion.

Cited by 18 publications

References 8 publications

Occurrence and Residue Concentration of Coccidiostats in Feed and Food of Animal Origin; Human Exposure Assessment

Occurrence and Residue Concentration of Coccidiostats in Feed and Food of Animal Origin; Human Exposure Assessment

Ionophore Toxin Maduramicin Produces Haff Disease-Like Rhabdomyolysis in a Mouse Model

Rhabdomyolysis and hepatotoxicity following accidental monensin ingestion: A report of two cases

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