These data indicate that medial calcification in MS lesions is an active process potentially orchestrated by phenotypically modified VSMCs.

showed no response to naloxone. Three months later he was admitted in respiratory failure refractory to all treatment. Necropsy showed chronic bronchitis, bullous emphysema, and right ventricular hypertrophy. The intercostal muscles were thin and fibrous, and histology of these and the diaphragm and psoas showed changes of chronic denervation. Histology of the spinal cord was not obtained. DiscussionNaloxone reverses the apnoeic response to hypoxia in neonatal rabbits2 but, even in large doses, has no effect on respiration in hypoxic man.' Respiratory failure in this patient was thought to be caused by a combination of chronic airflow obstruction and weakness of the respiratory muscles (possibly due to chronic spinal muscular atrophy).4 Intravenous naloxone produced an increase in minute ventilation and general agitation when he was acutely ill. The increase in oxygen saturation was greater than expected for the increase in ventilation, suggesting improved ventilation-perfusion matching, but the response occurred only in the acute illness.These findings suggest that there may be overproduction of, or increased sensitivity to, endorphins in acute respiratory failure. Naloxone is beneficial in shock,5 the postulated mechanism being that endorphins inhibit the interaction of catecholamines with their receptors. Such an action might account for the changes in ventilation-perfusion balance in our patient. Medial arterial calcification and diabetic neuropathy M E EDMONDS, N MORRISON, J W LAWS, P J WATKINS Abstract X-ray examinations of the feet, knees, and hands were performed on 20 diabetics with severe neuropathy and 20 diabetics with no evidence of neuropathy but with a similar mean age and duration of diabetes. All were under 53 years old with no clinical evidence of peripheral vascular disease. Medial arterial calcification was much more common and extensive in the patients with neuropathy, occurring in the feet in 15 and in the hands in eight compared with in four (p <0 001) and none (p <0 001) of the controls respectively. Although there was some correlation between calcification and both proteinuria (p <0 05) and proliferative retinopathy (p <0 02), the association between calcification and neuropathy (p <0 001) was much stronger.Neuropathy, with sympathetic denervation of the smooth muscle of the tunica media, may be important in the aetiology of medial arterial calcification.

No abstract

Altered platelet morphology and function have been reported in patients with diabetes. They are likely to be associated with the pathological processes and increased risk of vascular disease seen in these patients. Mean platelet volume (MPV), platelet count, and megakaryocyte (MK) ploidy (DNA content) were measured in (1) nondiabetics with normal coronary arteries, (2) nondiabetics with coronary artery atherosclerosis, (3) diabetics without evidence of vascular complications, and (4) diabetics with vascular disease. The platelet count (+/- SD) was increased in all groups but only significantly in the diabetics with vascular disease (236 +/- 65 versus 250 +/- 54 versus 257 +/- 64 versus 295 +/- 90 [P < or = .05] x 10(9)/L, for groups, I, II, II, and IV, respectively). The MPV was significantly increased in patients with atherosclerosis (7.0 +/- 0.4 versus 8.0 +/- 1.2 [P < or = .05] versus 7.2 +/- 0.9 versus 8.1 +/- 0.9 [P < or = .05] IL). Geometric mean MK ploidy was significantly increased in all groups compared with controls (16 +/- 1.5 versus 18.7 +/- 1.8 [P < or = .05] versus 19.8 +/- 1.6 [P < or = .05] versus 20.1 +/- 2.7 [P < or = .05]). Furthermore, some patients with vascular disease and/or diabetes had a modal ploidy shift from 16 (the normal mammalian modal ploidy) to 32, with a concomitant reduction of MKs in the 8 and 16 ploidy classes. This shift was seen particularly in the diabetics with vascular disease (P = .007). Interleukin-6 (IL-6) levels were measured and were elevated in patients with atherosclerosis; the highest levels were found in the diabetic patients (0.7 +/- 0.9 versus 5.3 +/- 5.5 [P < or = .05] versus 2.5 +/- 2.8 versus 6.7 +/- 5.5 [P < or = .05] ng/L). In the diabetic patients with atherosclerosis, fibrinogen levels were also increased (2.85 +/- 0.76 versus 3.34 +/- 1.32 versus 2.43 +/- 1.50 versus 5.59 +/- 1.72 [P< or = .05] g/L). Furthermore, IL-6 levels correlated with MK ploidy (r = .45, P = .009) and fibrinogen levels (r = .5, P = .0001). This study demonstrates that patients with vascular disease, particularly diabetics, have an altered MK ploidy distribution, showing a shift toward higher ploidy in association with an increased platelet mass (count x volume). Changes in platelets in diabetes probably reflect MK changes, which themselves are a response to systemic change.

Depression is associated with a persistent twofold increased risk of mortality in people with their first DFU at 5 years.

Satisfactory relief of intractable vomiting from diabetic gastroparesis was achieved by a novel radical surgical procedure. Histopathological findings suggest that gastromyopathy may contribute to the production of this syndrome.

Patients who develop recurrent foot ulceration delay in reporting symptoms, when compared with diabetic patients whose foot ulceration does not recur. The relapsers also have evidence of poorer glycaemic control, more neuropathy and increased alcohol intake.

These studies imply that both medial and intimal vascular calcification are regulated processes; however the aetiology of each pathology differs.