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Nerve grafting in leprosy
the exact location of nerve damage. However, examination of nerve trunk segments removed histological muscle reconstruction in lepromatous and during graft borderline tuberculoid leprosy (mean duration of sensory loss > 33 years),’ and that of nerves dissected from amputated legs of leprosy patients (mean sensory loss > 18-7 years) (Aug 28, p 521), showed virtually the same pattern. In both groups the predilective damage sites showed, instead of the presumed fibrotic block, the presence of numerous regenerating axons (our report, Aug 28, p 521, and ref 4). This finding indicates that in both groups the block takes place somewhere more distally than the predilective damage site, whose excision is recommended by Pereira et a1.l Thus, the difference between the duration of sensory loss in the two groups does not seem as important as suggested by Pereira and colleagues in their Oct 23 report. Successful nerve regeneration and sensory recovery are dependent on the presence of Schwann cells, which are plentiful throughout the nerve distal to traumatic injury. By contrast, we showed that there are no Schwann cells in the distal-most segments of the nerves supplying glabrous skin in advanced leprosy. Similarly, damage to dermal nerves in hairy skin across the leprosy spectrum is documented in both earlys and advanced disease.6 Unfortunately, the muscle graft reconstruction project in leprosy1 was launched without assessing the presence or absence of nerves and Schwann cells in the glabrous skin to be reinnervated. I therefore suggest that skin samples from the instep should be histologically investigated for Schwann cells before muscle graft reconstruction. The sensory recovery is a complex issue (Nov 20, p 1300) and it is generally agreed that the methods for sensory testing are difficult to standardise. Since preoperative and postoperative sensory examination in the pilot study was done by a member of the surgical team,1 I also suggest that the sensory assessment should be done by a group of independent neurologists. evidence
Figure: Atherosclerotic true lumen (X 249)
changes In false but not In
The development of the lesion in both cases was probably related to the presence of clotted blood. Pathologists have recognised microscopic findings similar to those seen in atherosclerosis in organising thromboses in non-vascular tissue. The 80% homology of apoprotein(a) with plasminogen5 also suggests that thrombosis may be a factor. The usefulness of aspirin in reducing myocardial infarction and death adds to the evidence supporting the role of thrombosis, and these two case-reports also support this view. Both patients had normal serum cholesterols. In one no endothelium was identified in the false channel with atherosclerosis so endothelial factors are unlikely to have been involved. Charles M Grossman,
Anthony N D’Agostino
Departments of Medicine and Pathology, Good Samaritan Hospital and Medical Centre, Portland, Oregon 97210, USA
1 Editorial. Atherosclerosis goes to the wall. Lancet 1992; 339: 647-48. Duguid JB. Thrombosis as a factor in the pathogenesis of aortic atherosclerosis. J Pathol Bacterial 1948: 60: 57-61. 3 Fuster V, Badimon L, Badimon JJ, Chesebro JH. Pathogenesis of coronary artery disease and the acute coronary syndromes. N Engl J Med 1992; 326: 242-50, 310-18. 4 Robbins SL, Cotram RS, Kumar V. Pathologic basis of disease. Philadelphia: Saunders, 1979: 624. 5 McLean JW, Tomlinson JE, Kuang W-J, et al. cDNA sequence of human apoliprotein(a) is homologous to plasminogen. Nature 1987; 330: 132-37.
2
on
T L Miko Department of Pathology, University of Sheffield Medical School, Sheffield S10 2UL, UK
Pereira JH, Palande DD, Subramanian A, Narayanakumar TS, Curtis J, Turk JL. Denatured autologous muscle graft in leprosy. Lancet 1991; 338: 1239-40. 2 Pereira JH, Cowley SA, Gschmeissner SE, Bowden REM, Turk JL. Denatured muscle grafts for nerve repair: an experimental model of nerve damage in leprosy. J Bone Joint Surg [Br] 1990; 72-B: 874-80. 3 Sabin TD, Swift TR. Leprosy: In: Dyck PJ, Thomas PK, Lambert EH, Bunge R, eds. Peripheral neuropathy, 2nd ed. Philadelphia: Saunders, 1984. 4 Miko TL, Gschmeissner SE, Le Maitre C, Kinfu Y, Kazen R, Pereira JH. Regeneration at the predilective damage sites of nerve trunks in treated leprosy. Lepr Rev (in press). 5 Karanth SS, Springall DR, Lucas S, et al. Changes in nerves and neuropeptides in skin from 100 leprosy patients investigated by immunocytochemistry. J Pathol 1989; 157: 15-26. 6 Dastur DK. Cutaneous nerves in leprosy: relationship between histopathology and cutaneous sensibility. Brain 1955; 78: 615-33. 1
Nerve
grafting in leprosy
SiR-Pereira and colleagues report promising preliminary results on nerve grafting in all types of leprosy (Oct 23, p 1060 and ref 1). They remove the superficially located segments of the posterior tibial, median, and ulnar nerves (predilective damage sites) and replace them with muscle grafts, aiming to regain protective sensation. The muscle grafting of large mixed peripheral nerves at the predilective damage site attracted much interest during the 14th International Leprosy Congress (Orlando, USA, Aug 29 to Sept 4, 1993). The attitude of the leprosy surgeons was polarised. On the one hand, in the USA this surgery is out of the question, whereas several surgeons working in countries where the ethical regulations are looser indicated that they would try muscle grafting in leprosy. It seems that this measure is going to be put into operation before its value has been proved or disproved. Pereira and colleagues’ experimental model2 is based on the hypothesis that the nerve damage in leprosy, caused by intraneural granulomas, may be segmental at the level of the predilective damage sites-ie, the leprotic nerve damage may be analogous to traumatic nerve injury. This is not so in lepromatous leprosy in which the haematogeneously spreading leprosy bacilli colonise the cooler, superficial parts of the body, and thus the sensory loss is mainly intracutaneous. In borderline tuberculoid leprosy there is no unequivocal
Prevalence of mitochondrial gene mutations in families with diabetes mellitus SIR-As diabetes mellitus seems to be, in some cases, maternally transmitted, a mitochondrial origin has been suspected. Indeed, a single A—G transition at nucleotide pair 3243 of mitochondrial DNA in the tRNA
Figure: Atherosclerotic true lumen (X 249)
changes In false but not In
The development of the lesion in both cases was probably related to the presence of clotted blood. Pathologists have recognised microscopic findings similar to those seen in atherosclerosis in organising thromboses in non-vascular tissue. The 80% homology of apoprotein(a) with plasminogen5 also suggests that thrombosis may be a factor. The usefulness of aspirin in reducing myocardial infarction and death adds to the evidence supporting the role of thrombosis, and these two case-reports also support this view. Both patients had normal serum cholesterols. In one no endothelium was identified in the false channel with atherosclerosis so endothelial factors are unlikely to have been involved. Charles M Grossman,
Anthony N D’Agostino
Departments of Medicine and Pathology, Good Samaritan Hospital and Medical Centre, Portland, Oregon 97210, USA
1 Editorial. Atherosclerosis goes to the wall. Lancet 1992; 339: 647-48. Duguid JB. Thrombosis as a factor in the pathogenesis of aortic atherosclerosis. J Pathol Bacterial 1948: 60: 57-61. 3 Fuster V, Badimon L, Badimon JJ, Chesebro JH. Pathogenesis of coronary artery disease and the acute coronary syndromes. N Engl J Med 1992; 326: 242-50, 310-18. 4 Robbins SL, Cotram RS, Kumar V. Pathologic basis of disease. Philadelphia: Saunders, 1979: 624. 5 McLean JW, Tomlinson JE, Kuang W-J, et al. cDNA sequence of human apoliprotein(a) is homologous to plasminogen. Nature 1987; 330: 132-37.
2
on
T L Miko Department of Pathology, University of Sheffield Medical School, Sheffield S10 2UL, UK
Pereira JH, Palande DD, Subramanian A, Narayanakumar TS, Curtis J, Turk JL. Denatured autologous muscle graft in leprosy. Lancet 1991; 338: 1239-40. 2 Pereira JH, Cowley SA, Gschmeissner SE, Bowden REM, Turk JL. Denatured muscle grafts for nerve repair: an experimental model of nerve damage in leprosy. J Bone Joint Surg [Br] 1990; 72-B: 874-80. 3 Sabin TD, Swift TR. Leprosy: In: Dyck PJ, Thomas PK, Lambert EH, Bunge R, eds. Peripheral neuropathy, 2nd ed. Philadelphia: Saunders, 1984. 4 Miko TL, Gschmeissner SE, Le Maitre C, Kinfu Y, Kazen R, Pereira JH. Regeneration at the predilective damage sites of nerve trunks in treated leprosy. Lepr Rev (in press). 5 Karanth SS, Springall DR, Lucas S, et al. Changes in nerves and neuropeptides in skin from 100 leprosy patients investigated by immunocytochemistry. J Pathol 1989; 157: 15-26. 6 Dastur DK. Cutaneous nerves in leprosy: relationship between histopathology and cutaneous sensibility. Brain 1955; 78: 615-33. 1
Nerve
grafting in leprosy
SiR-Pereira and colleagues report promising preliminary results on nerve grafting in all types of leprosy (Oct 23, p 1060 and ref 1). They remove the superficially located segments of the posterior tibial, median, and ulnar nerves (predilective damage sites) and replace them with muscle grafts, aiming to regain protective sensation. The muscle grafting of large mixed peripheral nerves at the predilective damage site attracted much interest during the 14th International Leprosy Congress (Orlando, USA, Aug 29 to Sept 4, 1993). The attitude of the leprosy surgeons was polarised. On the one hand, in the USA this surgery is out of the question, whereas several surgeons working in countries where the ethical regulations are looser indicated that they would try muscle grafting in leprosy. It seems that this measure is going to be put into operation before its value has been proved or disproved. Pereira and colleagues’ experimental model2 is based on the hypothesis that the nerve damage in leprosy, caused by intraneural granulomas, may be segmental at the level of the predilective damage sites-ie, the leprotic nerve damage may be analogous to traumatic nerve injury. This is not so in lepromatous leprosy in which the haematogeneously spreading leprosy bacilli colonise the cooler, superficial parts of the body, and thus the sensory loss is mainly intracutaneous. In borderline tuberculoid leprosy there is no unequivocal
Prevalence of mitochondrial gene mutations in families with diabetes mellitus SIR-As diabetes mellitus seems to be, in some cases, maternally transmitted, a mitochondrial origin has been suspected. Indeed, a single A—G transition at nucleotide pair 3243 of mitochondrial DNA in the tRNA