What is Lathyrism?

This topic contains 2 replies, has 3 voices, and was last updated by  Abdul Rahman 2 months, 1 week ago.

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  • #1390

    Soprano Tinga
    Participant

    I read in Harper’s Illustrated Biochemistry that there is a disease called Lathyrism (Page 15 of 30th edition of this book).

     

    I searched on the internet for more information on this disease but there are very few mentions of this disease in authenticate medical websites. Two websites that caught my attention are –

    1. Wikipedia

    2. NCBI website

     

    Informations on Wikipedia is good but Wikipedia is not an authentic website. The NCBI website is authentic but there is very few information on that page, you can check it.

     

    Can someone give me a bit more information and detailed mechanism of this medical condition.

    • This topic was modified 5 months, 1 week ago by  Soprano Tinga. Reason: Links to the mentioned websites
    • This topic was modified 5 months, 1 week ago by  Soprano Tinga. Reason: Links to the mentioned websites
  • #1667

    Sherlock Holmes
    Participant

    Lathyrism or neurolathyrism is a neurological disease of humans and domestic animals, caused by eating certain legumes of the genus Lathyrus. This problem is mainly associated with Lathyrus sativus (also known as Grass pea, Kesari Dal, Khesari Dal or Almorta) and to a lesser degree with Lathyrus cicera, Lathyrus ochrus and Lathyrus clymenum[1] containing the toxin ODAP.

  • #1739

    Abdul Rahman
    Participant

    Okay, so I just tried to collect and present some info about lathyrism.

     

    1. Lathyrism, one of the oldest neurotoxic diseases known to Man, results from excessive consumption of the chickling pea, Lathyrus sativus, and certain related species. Once prevalent throughout Europe, N. Africa, Middle East and parts of the Far East, the disease is presently restricted to India, Bangladesh and Ethiopia. Lathyrism is a form of irreversible, non-progressive spastic paraparesis associated with poorly understood degenerative changes in spinal cord. Domestic animals, notably the horse, also develop hindlimb paralysis after prolonged feeding on lathyrus fodder. Experimental animal models of lathyrism have been reported but none has been satisfactorily investigated, and concurrence between these experimental diseases and the human condition is unproven. The culpable agent in lathyrus species that precipitates paralysis also is unknown. Current attention is focused on the glutamate analog, beta-(N)-oxalyl-amino-L-alanine acid (BOAA). While this compound is present in those lathyrus species that induce spastic paraparesis and, in large doses, reportedly causes neuropathological changes similar to glutamate neurotoxicity, there is little to compare these neuropathological changes with those found in human lathyrism. Chronic primate feeding studies utilizing BOAA need to be carried out to determine whether this agent is responsible for human lathyrism. Some species of lathyrus, notably Lathyrus odoratus, are unable to induce human lathyrism but contain a compound, beta-aminopropionitrile (BAPN), that induces pathological changes in bone (“osteolathyrism”) and blood vessels (“angiolathyrism”) of experimental animals without damaging the nervous system. However, related compounds, dimethylaminopropionitrile (DMAPN) and beta, beta’-iminodipropionitrile (IDPN), are chronic neurotoxins in humans and animals, respectively.

    – From NCBI

    Kheshri Dal

     

    2.

    Risk factors[6]
    Cooking with clay implements
    Eating green unripe and boiled pea forms
    Blood group O[7]
    Protective factors[6]
    Soaking the green peas prior to cooking with fresh water
    Eating with antioxidants or mixed with cereals rich in sulphur-based amino acids

    Presentation
    The onset of neurolathyrism is usually sudden and coincident with the monsoon season. Early symptoms include:Walking difficulties
    Unbearable cramps
    Leg weakness
    Spastic paralysis develops which becomes irreversible.
    Pyramidal tract involvement causes:Motor weakness
    Increased tone
    A lurching scissoring gait caused by involvement of the thigh extensors and adductors and gastrocnemius
    Extensor plantar responses
    Very brisk knee and ankle tendon reflexes, often clonic
    Hoffmann’s sign and exaggerated biceps and/or triceps tendon jerks in the most severely affected
    There are no objective sensory signs but perverse sensations in the legs are frequently reported at the onset. Walking difficulties often begin suddenly but may also appear subacutely or insidiously. Some people experience partly reversible symptoms suggestive of a diffuse CNS excitation of somatic, motor and autonomic function.[8] Spasticity can be more marked than the motor weakness.[9]
    Lathyrism is not simply a paralytic syndrome, as angiolathyrism causes sudden death: the toxin changes the elasticity of the aorta causing aortic aneurysm that may rupture.
    Osteolathyrism affects skeletal development: cartilages and bones grow abnormally leaving the body deformed.[3] Children suffer skeletal deformity and poor cerebral development.
    Differential diagnosis
    Other causes of hypertonic paraparesis – for example:

    Pott’s paralysis
    Konzo
    HTLV-1 infection

    Management
    The disease is usually nonprogressive but irreversible. Tolperisone, a centrally acting muscle relaxant, has been shown to produce significant reduction in the spasticity in neurolathyrism patients.[10] Other than that there is remarkably little in the literature about the drug treatment of the condition.

    Prevention
    Public health education about the dangers of lathyrism is obviously important but the harsh reality is that people may face a choice between lathyrism or starvation. Food preparation measures can help:

    Boiling in water or repeated steeping in hot water and discarding the extracts can detoxify the seeds.
    Roasting the seeds at 140║C for 15 to 20 minutes results in 80-90% destruction of the neurotoxins.
    Soaking the seeds or dhal overnight and decanting the water before cooking eliminates about 90% of the toxin.
    The dangers of lathyrism are often known along with knowledge of how to detoxify Lathyrus but drought conditions can lead to fuel and water shortages preventing the necessary steps from being taken.

    One goal for prevention is to develop a plant with the resilience of chickpea to extreme climatic conditions, with its nutritional content and taste but without toxin (‘zero BOAA’ strains). Genetic modification could offer safer food and the utilisation of marginal farming land. Some varieties of chickpea that contain a much lower amount of toxin have been developed and may become more widely cultivated.[11]

    – From Patient.info

     

    3. beta-N-Oxalyl amino-L-alanine (L-BOAA); synonym beta-N-oxalyl-alpha,beta-diaminopropionic acid (beta-ODAP) is a naturally occurring non-protein amino acid present in the chickling pea from the plant Lathyrus sativus grown in drought prone areas. Ingestion of L-BOAA as a staple diet results in a progressive neurodegenerative condition, neurolathyrism, a form of motor neuron disease which affects the upper motor neurons and anterior horn cells of the lumbar spinal cord. L-BOAA is an excitatory acid and acts as an agonist at the AMPA receptor. One of the primary effects of L-BOAA toxicity is the inhibition of mitochondrial complex I selectively in the motor cortex and lumbar spinal cord. Recent evidence has suggested that the mitochondrial dysfunction is a consequence of oxidation protein thiol groups as a result of generation of reactive oxygen species. Mitochondrial complex I is highly to vulnerable to inactivation through oxidation of vital sulfhydryl groups. Thiol antioxidants such as alpha-liopic acid offer a method of protecting mitochondrial function. A common mechanism involving oxidation of protein thiol groups may underlie neurodegeneration occurring through mitochondrial dysfunction induced by excitatory amino acid.

    – From NCBI

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