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Published on: November 29, 2024
[The sequelae of Hansen's disease. (Pathologic viewpoint of etiologies, morphologies and countermeasures)]
1Leprosy Research Center, National Institute of Infectious Diseases, 4-2-1, Aoba, Higashimurayama, Tokyo-189-0002, JPN. e-mats@nih.go.jp
Insights
Chemotherapy for Hansen's disease in Japan led to increased glomerulonephritis, while peripheral nerve damage, caused by arteriolitis and infarction, not Mycobacterium leprae, is a significant aftermath requiring new treatments.
Area of Science:
- Pathology
- Neurology
- Infectious Diseases
Context:
- Hansen's disease (leprosy) management has evolved with chemotherapy.
- Post-chemotherapy sequelae in Japan show a shift from tuberculosis to glomerulonephritis.
- Peripheral nerve injuries remain a significant, poorly managed consequence of Hansen's disease globally.
Purpose:
- To investigate the pathological causes of peripheral nerve damage in Hansen's disease autopsy cases from the 1960s to 1990s.
- To differentiate the roles of Mycobacterium leprae and associated arteriolitis in axonal damage.
- To highlight the need for improved therapeutic strategies for nerve and blood vessel regeneration.
Summary:
- Autopsy cases revealed arteriolitis and subsequent infarction as primary causes of peripheral nerve axonal damage in Hansen's disease.
- Accumulation of Mycobacterium leprae without vascular changes did not invariably lead to axonal damage.
- These findings suggest arteriolitis-induced nerve damage is common during the chemotherapy era.
Impact:
- Identifies arteriolitis and infarction as key pathological mechanisms in Hansen's disease neuropathy.
- Suggests current chemotherapy regimens may inadvertently increase risk of vascular complications affecting nerves.
- Underscores the urgent need for regenerative therapies for peripheral nerves and blood vessels in Hansen's disease patients.
Abstract:
The proportion of glomerulonephritis, often a sequence of arteriolitis, among the sequelae of Hansen's disease after the introduction of chemotherapy increased markedly in Japan and nullified that of once prevalent tuberculosis after 1960s. However, most significant aftermath of the disease for numbers of years in the past have been peripheral nerve injuries worldwide for which effective countermeasures are yet to be developed. In this brief autopsy cases study from 1960s to 1990s, we confirmed the presence of cases in which arteriolitis and resulted infarction of peripheral nerves and not M. leprae itself were shown to be the major cause of axonal damages. There were also cases in which the accumulation of the bacilli without vascular changes did not damage the axons. The cases as these could not be solitary but should be rather common in this time of chemotherapy. If so, the methods to reconstruct nerves and blood vessels by promoting those regeneration should be developed to cope with the situation for surgeon, assisted by pathologists.
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