Platelet Abnormalities in Diabetic Peripheral Neuropathy

O'Malley, B C; Ward, J. D.; Timperley, W R; Porter, Neil; Preston, F. E.

doi:10.1016/s0140-6736(75)90610-8

Cited by 118 publications

(36 citation statements)

References 14 publications

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“…In Group A, no significant difference (P ¼ 0.78) in MPV was observed between patients with severe (15.7 AE 1. Increased MPV in the neuropathic group suggests platelet activation [1][2][3], in keeping with prior studies that have provided evidence for increased platelet aggregation and hyperproduction of prothrombotic factors in diabetic patients with neuropathy [8,9]. Experimental studies in the streptozotocin-induced diabetic rat have also revealed increased platelet aggregation in association with neuropathy [10,11].…”

supporting

confidence: 71%

“…Indeed, diabetes mellitus is thought to cause major disruption of several metabolic and vascular mechanisms, which contribute to the development of neuropathy [5]. For this reason, despite some evidence of a small role for platelet activation in the pathophysiology of neuropathy [5,[8][9][10][11], there is much more that remains to be determined [5]. Our finding, if confirmed upon replication, would suggest that there is increased platelet activation in neuropathic patients, irrespective of the severity of neuropathy.…”

mentioning

confidence: 55%

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Peripheral neuropathy is associated with increased mean platelet volume in type 2 diabetic patients

et al. 2005

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supporting

confidence: 71%

mentioning

confidence: 55%

Peripheral neuropathy is associated with increased mean platelet volume in type 2 diabetic patients

et al. 2005

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“…Increased sensitivity of diabetic platelets to aggregating agents as well as increased diabetic platelet production of thrombox-ane A 2 , a strong inducer of platelet aggregation, has been hypothesized to underlie such alterations. 1 This hypothesis is supported by the observation that vascular production of prostaglandin I 2 (prostacyclin), a potent inhibitor of platelet aggregation, has been reported to be lower in animals with experimentally induced diabetes compared with that in nondiabetic controls. 2 The kidney is one of the major producers of prostaglandin Ej (PGE 2 ) and prostaglandin F 2 , 3 as well as a minor producer of prostaglandin D 2 , thromboxane A 2 , and prostacyclin, 4 although relatively little attention has been paid to the role of the renal prostaglandins in experimental DM.…”

Section: Iabetes Mellitus (Dm) Is Associated Withmentioning

confidence: 90%

Hypertension in experimental diabetes mellitus. Renin-prostaglandin interaction.

Katayama¹,

Lee²

1985

Hypertension

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SUMMARY To investigate mechanisms involved in the high incidence of hypertension in diabetes mellitus, the relationship between renin-angiotensin production and renal prostaglandin E 2 synthesis was studied in rats 1 week after diabetes mellitus had been induced by streptozotocin injection. The diabetic rats became hypertensive, although plasma renin activity did not increase despite the plasma volume contraction resulting from polyurla and natriuresis. Subcutaneous insulin injection resulted in a marked increase in plasma renin activity, while more rigid control of diabetes mellitus achieved by constant insulin infusion decreased blood pressure. Cortical renin content and renin release as well as papillary prostaglandin E 2 synthesis in vitro were significantly lower in diabetic rats than in nondiabetic controls. Isoproterenol and prostaglandin E 2 stimulated renin release in controls, while diabetic rats responded only to isoproterenol. Insulin infusion by pump reversed these abnormalities. An additive effect of a maximum dose of isoproterenol (10"' M) and prostaglandin E 2 (10~4 M) on renin release was observed in nondiabetic controls and in diabetic rats treated with insulin pump, but not in untreated diabetic rats. The results suggest that 1) renal renin release and prostaglandin E 2 synthesis in diabetes mellitus are insulin dependent, 2) inappropriately lower plasma renin activity in diabetes mellitus may be attributed to a diminished renal renin pool and a lack of renin release in response to renal prostaglandin E 2 , the synthesis of which is also impaired in diabetes, 3) prostaglandin E 2 -induced renin release may operate independently from isoproterenol-induced renin release, and 4) impaired renal prostaglandin E 2 synthesis may contribute to the development of hypertension in the face of an unchanged prohypertensive renin-angiotensin II system. characteristic morphological and functional changes in the kidney. In addition, cardiovascular complications, including hypertension, atherosclerosis, and thrombotic disease, are more prevalent among diabetics than nondiabetics. Increased sensitivity of diabetic platelets to aggregating agents as well as increased diabetic platelet production of thrombox-

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“…Several studies have suggested that haemorheological abnormalities may contribute to impaired blood flow brought about by microvascu-lar disease [68]. Fibrin deposition [30] and platelet clumping [69] have been observed in endoneurial vessels in diabetic neuropathy. Diabetic erythrocytes have been found to be less deformable than normal [70] and would therefore be expected to travel at a slower velocity in capillaries.…”

Section: Haemorheological Abnormalitiesmentioning

confidence: 99%