Germanium intoxication with sensory ataxia

Asaka, Tomoya; Nitta, Eishun; Makifuchi, Takao; Shibazaki, Yoichi; Kitamura, Yoshihisa; Ohara, Hiroyasu; Matsushita, Kazunobu; Takamori, Masaharu; Takahashi, Yoshihiro; Genda, Akira

doi:10.1016/0022-510x(95)00032-w

Cited by 28 publications

(4 citation statements)

References 14 publications

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“…Chronic neuropathies consist of CIAN [1]and neuropathy associated with paraproteinemia [16, 17, 18], and hereditary neuropathies include hereditary posterior column ataxia of Biemond [19]. Besides preceding diseases, several diseases with sensory ataxic neuropathy such as Sjögren’s syndrome [5], mitochondrial disease [20], neuropathy associated with human immunodeficiency virus infection [21, 22]and germanium intoxication [23]have been reported. CIDP, however, was not included in the classification of ataxic neuropathies [1].…”

Section: Discussionmentioning

confidence: 99%

Ataxic Form of Chronic Inflammatory Demyelinating Polyradiculoneuropathy: Clinical Features and Pathological Study of the Sural Nerves

et al. 2001

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We investigated clinical and pathological features of the sural nerves of 5 patients with the ataxic form of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and compared these features with those of chronic ataxic neuropathies due to other causes. The CIDP patients presented with slowly progressive ataxia with deep sensory impairment. The durations of the symptoms from onset were relatively short in CIDP (4–8 months) and cancer (3 and 10 months), but long in chronic idiopathic ataxic neuropathy (24–260 months). Corticosteroid therapy elicited a good response in all the patients with CIDP, but a poor response in the patients with other ataxic neuropathies. Sural nerve biopsy of CIDP patients showed a slight or moderate loss of myelinated fiber. This report suggests that ataxic form of CIDP is a steroid-responsive ataxic neuropathy, and large myelinated fibers of the sural nerves in ataxic form of CIDP were better preserved than those in nerves with other chronic ataxic neuropathies.

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Section: Discussionmentioning

confidence: 99%

Ataxic Form of Chronic Inflammatory Demyelinating Polyradiculoneuropathy: Clinical Features and Pathological Study of the Sural Nerves

et al. 2001

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“…Первинними симптомами інтоксикації є втрата ваги, втома, розлади шлунково-кишкового тракту (нудота, блювання, відсутність апетиту та діарея), анемія, м'язова слабкість. Тривала інтоксикація викликає гостру ниркову недостатність (Nagata et al, 1985;Asaka et al, 1995;Chen & Lin, 2011). У деяких пацієнтів ниркова функція залишалася порушеною навіть після відміни германієвих препаратів (Van der Spoel et al, 1990).…”

Section: рівні споживання германію з продуктами харчування та потреба...unclassified

Germanium: distribution, migration and accumulation in the natural environment

Sobolev,

Gutyj,

Melnychenko

et al. 2023

SMLNUVMBA

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In this paper we attempt to generalize information published in the scientific literature about the distribution, migration and accumulation of chemical forms of germanium in the natural environment, with the main attention paid to the content of this trace element in various components of the environment. Despite the fact that germanium is found in the lithosphere, hydrosphere and atmosphere it is one of the least studied elements in mineral and geochemical terms. It belongs to rare scattered elements with a relatively high migration capacity in the earth's crust and on its surface. Depending on the physical and chemical conditions, the mineral and lithogenesis of germanium can exhibit different properties, which determines the variety of ways of its migration. The nature and form of migration of germanium in the natural environment is not determined only by its chemical properties but also by a complex set of reactions of interaction with various underground water addendums, the granulometric and chemical-mineralogical composition of soil-forming rocks and soils, biogenic and technogenic processes. Studies have shown that the content of germanium in natural waters, soils and plants can vary widely and depends on many factors. In particular, its concentration in groundwater and surface water depends on the natural geological environment, pressure, temperature, meteorological and anthropogenic factors; soil by their type, region, features of soil-forming processes, chemical composition of the parent rocks, climatic conditions and amounts of organic substances; in plants by their species and varietal facilities, the growth stage of the plants, the availability of soils by this element, the forms of germanium compounds in the soil (inorganic or organic), the ability of soil to retain labile form of germanium and climatic conditions. Analysis of the actual content of germanium in diets indicates an insufficient level of provision of the human body with this trace element, due to its low concentrations in food and water. However, it has been suggested that any products with a high content of germanium may pose a risk to human health through its toxic effects.

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“…However, prolonged intake can lead to internal accumulation, like in patients taking germanium as dietary supplements. Chronic germanium poisoning causes peripheral neuropathy presenting with sensory ataxia and muscle weakness due to myopathy (Asaka et al 1995;Fujimoto et al 1992). Cerebellar ataxia is extremely rare.…”

Section: Germaniummentioning

confidence: 99%

Cerebellotoxic Agents

Manto

2021

Handbook of the Cerebellum and Cerebellar Disorders

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The cerebellum is particularly vulnerable to neurotoxic agents and poisoning. People of all ages can be affected by cerebellar damage due to neurotoxicity, ranging from fetuses to the elderly. Elderly patients are more vulnerable to injury, as well as patients with silent cerebellar lesions, such as preexisting structural lesions. Purkinje neurons are a main target of cerebellotoxic substances. The main causes of TOICS (toxic-induced cerebellar syndrome) are acute and chronic ethanol ingestion, drugs, and environmental exposure. Cerebellar structures are among the most sensitive targets of the central nervous system (CNS) to ethanol intake. In addition to ethanol, drugs such as phenytoin, antineoplastics, lithium salts, and heroin can cause an irreversible cerebellar syndrome. Environmental causes of TOICS include chronic exposure to metals, benzene derivatives, and hyperthermia. Recently, deposits of Gadolinium, a heavy metal of the lanthanide group, have been reported in the cerebellum (dentate nuclei) and globus pallidus following repeated administration of linear Gd-based contrast agents (GBCAs). Both the mechanism of these deposits and their fate are unknown. As a general rule, cerebellar syndromes associated with toxic insults should not be underestimated. In particular, since patients may develop life-threatening edema of the posterior fossa in several circumstances, urgent management may be required. Preventative measures should be considered. The clinical significance of deposits of Gadolinium in the cerebellum is currently undetermined.

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Germanium intoxication with sensory ataxia

Cited by 28 publications

References 14 publications

Ataxic Form of Chronic Inflammatory Demyelinating Polyradiculoneuropathy: Clinical Features and Pathological Study of the Sural Nerves

Ataxic Form of Chronic Inflammatory Demyelinating Polyradiculoneuropathy: Clinical Features and Pathological Study of the Sural Nerves

Germanium: distribution, migration and accumulation in the natural environment

Cerebellotoxic Agents

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