Neuropathology of the oesophagus in diabetes mellitus

Smith, Barbara

doi:10.1136/jnnp.37.10.1151

Cited by 72 publications

(32 citation statements)

References 11 publications

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“…In patients with multifocal neuropathies, they have been reported by Said et al [35], Raff et al [32], in the present study and in one of three cases briefly communicated by Costigan et al [15]. They have also been observed in autonomic nerves and ganglia in patients with diabetic autonomic neuropathy [ 17] and in relation to oesophageal nerve plexuses [38]. It therefore seems likely that a vasculitic or other inflammatory process can be superimposed on diabetic neuropathy, possibly on an autoimmune basis or, as suggested by Said et al [35], diabetes may render the nerves more susceptible to an intercurrent inflammatory process.…”

Section: Discussionsupporting

confidence: 79%

Epineurial microvasculitis in proximal diabetic neuropathy

1998

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Amongst the focal and multifocal neuropathies that are associated with diabetes mellitus one of the most common is a proximal predominantly motor lower limb neuropathy. Recent evidence has indicated that, at least in a proportion of cases, this may have an inflammatory basis. We have examined a consecutive series of 15 cases of proximal diabetic neuropathy (diabetic amyotrophy). These were characterized by proximal pain and asymmetric proximal or generalized lower limb muscle weakness, associated in some cases with radicular sensory involvement. Two-thirds of the patients had an accompanying distal symmetric sensory polyneuropathy. Biopsy of the intermediate cutaneous nerve of the thigh, a sensory branch of the femoral nerve, showed epineurial microvasculitis in 3 patients and nonvasculitic epineurial inflammatory infiltrates in another case. In a further case, microvasculitis was found in both in the sural nerve and a quadriceps muscle biopsy specimen. The detection of inflammatory changes appeared to be correlated with the occurrence of sensory radicular involvement. Whether similar changes are present in muscle nerves in this predominantly motor syndrome requires further study. Nevertheless, the present observations confirm the view that secondary vasculitic or other inflammatory reactions may contribute to some forms of diabetic neuropathy.

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Section: Discussionsupporting

confidence: 79%

Epineurial microvasculitis in proximal diabetic neuropathy

1998

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“…Estudos morfológicos do nervo vago foram conduzidos, na maioria, em seu segmento abdominal, sendo demonstrado redução severa da densidade das fibras amielínicas, sendo os axônios "sobreviventes", de pequeno diâmetro 43 . Smith 44 demonstrou anormalidade na inervação do esôfago em 18 dos 20 pacientes dia- 46 , que demonstraram, em 5 casos necropsiados, perda severa das fibras mielíni-cas vagais. Guo et al 47 estudaram segmentos vagais cervicais, torácicos e abdominais, de 4 pacientes diabéticos necropsiados.…”

Section: -Neuropatia Diabética Autonômicaunclassified

Diabete Como Modelo De Neuropatia Autonômica

Sato

Migliaccio

Carmo³

et al. 2006

Medicina (Ribeirão Preto)

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RESUMO: Modelo do Estudo:O presente estudo é uma revisão de literatura sobre a neuropatia diabética, especialmente a neuropatia autonômica diabética, enfatizando as recentes descobertas sobre o assunto, com modelos experimentais da doença.Importância do problema: Comprometimento do sistema nervoso autônomo ocorre em uma variedade de doenças sistêmicas, das quais o diabetes mellitus é a mais comum. Alterações no sistema nervoso periférico em animais geneticamente diabéticos ou com diabete induzida experimentalmente têm sido amplamente investigadas, na esperança de que as alterações encontradas em modelos animais possam reproduzir algumas das alterações da neuropatia diabéti-ca humana precoce, levando ao melhor entendimento sobre o mecanismo da doença. Vários agentes químicos são citotóxicos para as células beta do pâncreas porém, apenas o aloxane e a estreptozotocina (STZ) tem sido sistematicamente investigados e são amplamente empregados para induzir diabete nos animais. Em geral, STZ é mais eficaz e mais específica para as células beta do pâncreas que o aloxane. Embora estudos morfológicos tenham sido realizados em vários nervos periféricos de ratos diabéticos induzidos com STZ, tais como sural, fibular e tibial, informações sobre alterações patológicas em nervos autonômicos são limitadas.Comentários: Recentemente, estudamos as alterações do nervo depressor aórtico (NDA) em ratos diabéticos agudos (15 dias após injeção de STZ). Nossos resultados mostraram características de atrofia axonal em 5 dos 10 nervos estudados. Um estudo de microscopia de luz, conduzido em nosso laboratório, o nervo vago cervical de ratos diabéticos crônicos (12 semanas após injeção de STZ), mostrou resultados discretos, a favor da perda de fibras mielíni-cas finas. Outro estudo recente do nosso laboratório mostrou uma redução do número de fibras mielínicas pequenas dos nervos renais, nos ratos diabéticos crônicos, resultado mais evidente que o observado no nervo vago. Por outro lado, as alterações do NDA (atrofia axonal) se assemelham mais aos resultados obtidos com outros nervos somáticos, confirmando o caráter altamente variável do diabete, no acometimento dos nervos periféricos.

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“…Diabetic autonomic neuropathy (DAN), a wellknown complication of type 1 diabetes, impairs several classes of nerves (3,11,43), including peripheral sympathetic nerves (31,45). However, clinically significant DAN takes months to develop in rodents (28,30) and years to decades in humans (24).…”

mentioning

confidence: 99%

Impaired glucagon response to sympathetic nerve stimulation in the BB diabetic rat: effect of early sympathetic islet neuropathy

Mundinger¹,

Mei²,

Figlewicz³

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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Impaired glucagon response to sympathetic nerve stimulation in the BB diabetic rat: effect of early sympathetic islet neuropathy. Am J Physiol Endocrinol Metab 285: E1047-E1054, 2003. First published July 22, 2003 10.1152/ajpendo.00136. 2003.-We investigated the functional impact of a recently described islet-specific loss of sympathetic nerves that occurs soon after the autoimmune destruction of ␤-cells in the BB diabetic rat (35). We found that the portal venous (PV) glucagon response to sympathetic nerve stimulation (SNS) was markedly impaired in newly diabetic BB rats (BB D). We next found a normal glucagon response to intravenous epinephrine in BB D, eliminating the possibility of a generalized secretory defect of the BB D ␣-cell as the mediator of the impaired glucagon response to SNS. We then sought to determine whether the glucagon impairment to SNS in BB D was due solely to their loss of islet sympathetic nerve terminals or whether other effects of autoimmune diabetes contributed. We therefore reproduced, in nondiabetic Wistar rats, an islet nerve terminal loss similar to that in BB D with systemic administration of the sympathetic neurotoxin 6-hydroxydopamine. The impairment of the glucagon response to SNS in these chemically denervated, nondiabetic rats was similar to that in the spontaneously denervated BB D. We conclude that the early sympathetic islet neuropathy of BB D causes a functional defect of the sympathetic pathway to the ␣-cell that can, by itself, account for the impaired glucagon response to postganglionic SNS. norepinephrine; 6-hydroxydopamine; neuropathy HUMAN AUTOIMMUNE TYPE 1 DIABETES is characterized by a major impairment of the glucagon response to insulininduced hypoglycemia (15) that is evident early in the course of the disease (6). BioBreeder diabetic rats (BB D), one of the best animal models of human autoimmune diabetes, exhibit this specific glucagon impairment after only 1 wk of diabetes (25). Defects in several mechanisms have been proposed to mediate the impairment (15,40,44). We have favored the hypothesis of autonomic defects, because an important role of autonomic inputs to the islet in mediating the glucagon response to hypoglycemia has been demonstrated in both nondiabetic animals (5,19,20,22) and humans (17). We have focused specifically on damage to sympathetic nerves of the islet because central glucopenia results in activation of pancreatic sympathetic nerves (10, 21), and this activation can, by itself, mediate most of the glucagon response to insulin-induced hypoglycemia (18). We hypothesized that, early in autoimmune type 1 diabetes, there is damage to the sympathetic pathway to the islet that contributes to the early impairment of the glucagon response to hypoglycemia seen in this disease.Diabetic autonomic neuropathy (DAN), a wellknown complication of type 1 diabetes, impairs several classes of nerves (3, 11, 43), including peripheral sympathetic nerves (31, 45). However, clinically significant DAN takes months to develop in rodents (28, 30) and years to d...

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Neuropathology of the oesophagus in diabetes mellitus

Cited by 72 publications

References 11 publications

Epineurial microvasculitis in proximal diabetic neuropathy

Epineurial microvasculitis in proximal diabetic neuropathy

Diabete Como Modelo De Neuropatia Autonômica

Impaired glucagon response to sympathetic nerve stimulation in the BB diabetic rat: effect of early sympathetic islet neuropathy

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