Suramin-induced weakness from hypophosphatemia and mitochondrial myopathy. Association of suramin with mitochondrial toxicity in humans

Rago, Randall; Miles, Janet M.; Sufit, Robert; Spriggs, David R.; Wilding, George

doi:10.1002/1097-0142(19940401)73:7<1954::aid-cncr2820730729>3.0.co;2-h

Cited by 34 publications

(7 citation statements)

References 11 publications

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“…Both types of neuropathy were also seen in animal models ( Russell et al, 2001 ) . Because of toxicity, it has not entered widespread clinical use ( Rago et al, 1994 ) .…”

Section: Individual Classes Of Chemotherapy Drugs Associated With Cinmentioning

confidence: 99%

Chemotherapy‐induced neuropathy

Windebank

Grisold

2008

J Peripheral Nervous Sys

563

401

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Neurotoxic side effects of cancer therapy are second in frequency to hematological toxicity. Unlike hematological side effects that can be treated with hematopoietic growth factors, neuropathies cannot be treated and protective treatment strategies have not been effective. For the neurologist, the diagnosis of a toxic neuropathy is primarily based on the case history, the clinical and electrophysiological findings, and knowledge of the pattern of neuropathy associated with specific agents. In most cases, toxic neuropathies are length-dependent, sensory, or sensorimotor neuropathies often associated with pain. The platinum compounds are unique in producing a sensory ganglionopathy. Neurotoxicity is usually dependent on cumulative dose. Severity of neuropathy increases with duration of treatment and progression stops once drug treatment is completed. The platinum compounds are an exception where sensory loss may progress for several months after cessation of treatment ("coasting"). As more effective multiple drug combinations are used, patients will be treated with several neurotoxic drugs. Synergistic neurotoxicity has not been extensively investigated. Pre-existent neuropathy may influence the development of a toxic neuropathy. Underlying inherited or inflammatory neuropathies may predispose patients to developing very severe toxic neuropathies. Other factors such as focal radiotherapy or intrathecal administration may enhance neurotoxicity. The neurologist managing the cancer patient who develops neuropathy must answer a series of important questions as follows: (1) Are the symptoms due to peripheral neuropathy? (2) Is the neuropathy due to the underlying disease or the treatment? (3) Should treatment be modified or stopped because of the neuropathy? (4) What is the best supportive care in terms of pain management or physical therapy for each patient? Prevention of toxic neuropathies is most important. In patients with neuropathy, restorative approaches have not been well established. Symptomatic and other management are necessary to maintain and improve quality of life.

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“…Both types of neuropathy were also seen in animal models ( Russell et al, 2001 ) . Because of toxicity, it has not entered widespread clinical use ( Rago et al, 1994 ) .…”

Section: Individual Classes Of Chemotherapy Drugs Associated With Cinmentioning

confidence: 99%

Chemotherapy‐induced neuropathy

Windebank

Grisold

2008

J Peripheral Nervous Sys

563

401

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“…Many other agents such as fumaric acid 144 , suramin 145 , and imatinib 146 have also been associated with Fanconi syndrome in case reports. This field remained to be further explored as proximal tubule toxicity is common due to the existence of multiple drug transporters at the surface membrane, leading to very high uptake of drugs by this segment 147 .…”

Section: Drugs Causing Decreased Renal Acid Excretionmentioning

confidence: 99%

Drug-Induced Metabolic Acidosis

Pham

Moe

2015

F1000Res

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Metabolic acidosis could emerge from diseases disrupting acid-base equilibrium or from drugs that induce similar derangements. Occurrences are usually accompanied by comorbid conditions of drug-induced metabolic acidosis, and clinical outcomes may range from mild to fatal. It is imperative that clinicians not only are fully aware of the list of drugs that may lead to metabolic acidosis but also understand the underlying pathogenic mechanisms. In this review, we categorized drug-induced metabolic acidosis in terms of pathophysiological mechanisms, as well as individual drugs’ characteristics.

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“…It can prevent or inhibit the binding of several growth factors to the associated receptors and suramin thus antagonizes the ability of these factors to stimulate tumor growth. Muscle weakness during suramin treatment may also be associated with hypophosphatemia and mitochondrial myopathy (Rago et al, 1994). A case of acute, reversible, demyelinating polyneuropathy was observed by Stein et al (1989).…”

Section: Suraminmentioning

confidence: 99%