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Clinical Toxicology of Copper
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Sonal Sekhar Miraj, Mahadev Rao
Symptomatic methemoglobinemia patients should receive methylene blue. This normally happens at the levels of methemoglobin >20%–30%. Administer oxygen while preparing for methylene blue therapy. Methylene blue promotes the transformation of methemoglobin to hemoglobin by enhancing the enzymatic action of the methemoglobin reductase. The initial dose is 1–2 mg/kg/dose intravenously over 5 min. The dose may be repeated if cyanosis does not disappear within 60 min. Failure of methylene blue treatment indicates an inadequate dose of methylene blue, G-6-PD deficiency, or NADPH-dependent methemoglobin reductase deficiency. Hyperbaric oxygen may be beneficial if methylene blue is ineffective. Hyperbaric oxygen increases the dissolved oxygen that can protect the patient while the body reduces methemoglobin. Another alternative to methylene blue is ascorbic acid, a reducing agent, which can be given 100–500 mg twice daily either orally or intravenously. The hypotensive episodes can be treated with fluids, dopamine, and noradrenaline. For rhabdomyolysis, initial replacement of 4–6 L/day with close monitoring for fluid overload, mannitol (100 mg/day), and urine alkalinization are considerable in the early course of the disease, however, there is no clear evidence for these strategies.
Pesticides and Chronic Diseases
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
January 2010 EDTA/DMPS challenge test was performed and it found to have elevated levels. The lead levels were 12 times the reference range. The patient began weekly chelation using 2000 mg IV EDTA immediately following intravenous glutathione. After several months, he experiences extreme fatigue and muscle soreness following the infusions. Chelation treatment was discontinued until January 2011. He experienced rhabdomyolysis with CPK at 1600, elevated myoglobin, cola-colored urine, and acute pain in both thigh and biceps muscle. Treatment was discontinued. He described that it was activated by EDTA, glutathione, and vitamins as well as hyperthermic conditions. The patient visited a neurologist who ruled out carnitine deficiency and suspected a glycogen storage disorder, biopsy suggested. A calcium deficiency was identified but it is still questionable as to whether or not the calcium deficiency may be contributing to the rhabdomyolysis, but hyperthermic conditions were still precipitating the symptoms.
Histopathological and inflammatory response in multiple organs of rats exposed to crack
Published in International Journal of Environmental Health Research, 2022
Daniel Souza, Barbara Rosarioa, Breno Casagrandea, Milena Viana, Debora Estadella, Rogerio Peres, Camilo Dias Seabra Pereira, Rogerio Peres
In humans, there are few studies investigating crack cocaine toxicity in hepatic and renal tissue so far. Some case reports can be found in the scientific literature, which describe degeneration and necrotic processes in hepatic and renal tissues, emphasizing the correlation between renal injury and rhabdomyolysis, due to the massive destruction of muscle fibers (Dinis-Oliveira et al. 2012; Goel et al. 2014). Anyway, our results are fully in line with these findings (Alvarez et al. 1999; Vidyasankar et al. 2015). Our experimental group that remained 72 hours without crack cocaine administration (withdrawn), after 5 days of treatment with 18 mg/kg (G2), showed liver regeneration. These results are similar to the findings of Shuster et al. (1977). However, no signs of tissue regeneration were detected to kidney exposed crack cocaine.
Exertional rhabdomyolysis and acute kidney injury in endurance sports: A systematic review
Published in European Journal of Sport Science, 2021
Daniel Rojas-Valverde, Braulio Sánchez-Ureña, Jennifer Crowe, Rafael Timón, Guillermo J. Olcina
Rhabdomyolysis is a condition caused by the release of proteins into the bloodstream with various etiologies (Chlíbková et al., 2015). There are multiple categories of rhabdomyolysis according to their etiology; trauma, muscle hypoxia, genetic defects, infections, changes in body temperature, metabolic or electrolytic disorders, idiopathic or physical effort (Bosch, Poch, & Grau, 2009). When the rhabdomyolysis is caused by strenuous physical exercise, it is known as exertional rhabdomyolysis (ER) (Parmar, Chauhan, DuBose, & Blake, 2012). Exertional rhabdomyolysis (ER) is a relatively uncommon condition with an incidence of approximately 29.9 per 100.000 patient years (Tietze & Borchers, 2014). This condition is caused by damage of the striated muscle due to strenuous physical exertion leading to muscle disintegration, commonly triggering the release of myoglobin (MB), and other cellular contents to the extracellular space and circulatory system (Kupchak, Kraemer, Hoffman, Phinney, & Volek, 2014), such as electrolytes and sarcoplasmic proteins, including serum creatine kinase (S-CK), aspartate transaminase (AST), aldolase, alanine transaminase (ALT) and serum lactate dehydrogenase (S-LDH) (Abbas, Brown, Rietveld, & Hoek, 2019; McVane, Andreae, Fernando, & Strayer, 2019).