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Biomedical subjects

Rayaz A Malik

Publications and source records attributed to Rayaz A Malik.

13 recordsLinked to original sources
PubMed2005

Effects of angiotensin type-1 receptor antagonism on small artery function in patients with type 2 diabetes mellitus.

Endothelial dysfunction has been demonstrated to occur in small arteries from patients with type 2 diabetes and hypertension. The effects of angiotensin II receptor blockade on vessel function were examined using pressure myography in a randomized 12-week double-blind placebo-controlled parallel group study using candesartan cilexitil. The maximal vascular response to acetylcholine (Ach) was impaired at baseline and improved with candesartan. This improvement was primarily caused by an effect in the nitric oxide component of Ach-mediated dilatation. The degree of endothelial dysfunction directly correlated with serum low-density lipoprotein cholesterol levels. Sodium nitroprusside-induced endothelium-independent dilatation was reduced in diabetic patients and intervention with candesartan lead to an improvement in EC50 with no change in maximal response. Vasoconstriction to norepinephrine was normal and did not change with intervention, but responses to angiotensin II were reduced after candesartan in diabetic patients. These results demonstrate that even brief treatment with angiotensin II receptor blockade is associated with a significant improvement in resistance vessel endothelial function.

Acetylcholine↗
PubMed2005

Recent developments in the assessment of efficacy in clinical trials of diabetic neuropathy.

A large number of measures may be employed in clinical practice and for epidemiologic studies to quantify and risk stratify diabetic patients with neuropathy. However, not all measures are suitable for assessing the benefits of therapeutic intervention. Therefore, for the purpose of this review we focus on measures that may be employed to define the efficacy of interventions in clinical trials of human diabetic neuropathy. Two major types of end points are used: 1) those that assess symptoms for defining efficacy in painful diabetic neuropathy, and 2) those that assess neurologic deficits that assess the effects of treatments that may prevent further degeneration or promote repair.

Clinical Trials as Topic↗
PubMed2004

Diabetic cardiomyopathy: mechanisms, diagnosis and treatment.

Independent of the severity of coronary artery disease, diabetic patients have an increased risk of developing heart failure. This clinical entity has been considered to be a distinct disease process referred to as 'diabetic cardiomyopathy'. Experimental studies suggest that extensive metabolic perturbations may underlie both functional and structural alterations of the diabetic myocardium. Translational studies are, however, limited and only partly explain why diabetic patients are at increased risk of cardiomyopathy and heart failure. Although a range of diagnostic methods may help to characterize alterations in cardiac function in general, none are specific for the alterations in diabetes. Treatment paradigms are very much limited to interpretation and translation from the results of interventions in non-diabetic patients with heart failure. This suggests that there is an urgent need to conduct pathogenetic, diagnostic and therapeutic studies specifically in diabetic patients with cardiomyopathy to better understand the factors which initiate and progress diabetic cardiomyopathy and to develop more effective treatments.

Adrenergic beta-Antagonists↗
PubMed2004

Corneal nerve tortuosity in diabetic patients with neuropathy.

PURPOSE: Corneal confocal microscopy is a reiterative, rapid, noninvasive in vivo clinical examination technique capable of imaging corneal nerve fibers. Nerve fiber tortuosity may indicate a degenerative and attempted regenerative response of nerve fibers to diabetes. The purpose of this study was to define alterations in the tortuosity of corneal nerve fibers in relation to age, duration of diabetes, glycemic control, and neuropathic severity. METHODS: The cornea and collected images of the subbasal nerve plexus of 18 diabetic patients (stratified into mild, moderate, and severe neuropathic groups using conventional clinical measures of neuropathy) and 18 age-matched nondiabetic control subjects were scanned, and a novel mathematical paradigm was applied to quantify the extent of nerve tortuosity, which was termed the tortuosity coefficient (TC). RESULTS: TC was significantly different between the four clinical groups (F(3) = 12.2, P < 0.001). It was significantly greater in the severe neuropathic group than in control subjects (P < 0.003) and in the mild (P < 0.004) and moderate (P < 0.01) neuropathic groups. TC did not correlate significantly with the age (r = -0.003, P > 0.05), duration of diabetes (r = -0.219, P > 0.05), or hemoglobin A1c (HbA1c; r = 0.155, P > 0.05) of diabetic patients. CONCLUSIONS: Corneal confocal microscopy allows rapid, noninvasive in vivo evaluation of corneal nerve tortuosity. This morphologic abnormality relates to the severity of somatic neuropathy and may reflect an alteration in the degree of degeneration and regeneration in diabetes.

Cornea↗
PubMed2003

Current and future strategies for the management of diabetic neuropathy.

Diabetic neuropathy is common, related to increased morbidity and mortality, and has no effective treatment at present. Interventions based on putative pathways thought to contribute to damage and repair of nerve fibres have yielded little success to date. Pain is a potentially debilitating manifestation of diabetic neuropathy and has many potential sites of origin and, hence, modulation. Its cause is unclear and it does not respond well to traditional pain therapies, proposed to mediate their benefits via multiple peripheral and central mechanisms. A better understanding of the mechanisms leading to nerve fibre degeneration and regeneration as well as pain has recently resulted in the development of a more targeted approach to the treatment of diabetic neuropathy. Thus, specific NMDA receptor antagonists and more specific neuronal serotonin and norepinephrine (noradrenaline) uptake inhibitors offer promise in the treatment of painful diabetic neuropathy. A number of treatments which include the aldose reductase inhibitors and neurotrophins have failed to reach the clinical arena. However, the antioxidant alpha-lipoic acid, as well as compounds which correct vascular dysfunction and hence neuropathy, such as ACE inhibitors and protein kinase C-beta inhibitors, have demonstrated more success.

Diabetic Neuropathies↗
PubMed2002

Focal and multifocal neuropathies.

The focal and multifocal neuropathies affect only a minority of patients with diabetes; however, they form a major clinical problem in terms of diagnosis, development of significant symptoms and signs, and often inadequate therapy. Diagnosis requires accurate and detailed clinical history and neurologic examination combined with targeted neurophysiologic tests, which differ considerably from those carried out in day-to-day practice. Because of their relatively infrequent occurrence, treatment is not evidence based.

Diabetic Neuropathies↗
PubMed2002

Offloading diabetic foot wounds using the scotchcast boot: a retrospective study.

A retrospective study was conducted to evaluate treatment outcomes associated with the treatment of diabetic foot ulcers using the Scotchcast boot. Data were extracted from the records of 180 patients with diabetes, 150 (83.3%) male, with a mean age of 55.3 +/- 10.9 years undergoing treatment for noninfected, non-ischemic neuropathic diabetic foot wounds at a university teaching hospital's tertiary care outpatient clinic. All patients who met the criteria were treated with the Scotchcast boot as the sole form of pressure relief. The average follow-up for each patient was 85.9 +/- 30.6 months (range 34.2 to 147.7 months). The mean time to healing for all patients was 130.5 +/- 106.7 days. Superficial (Grade 1) wounds healed significantly faster than deep (Grade 3) wounds (111.5 +/- 98.2 versus 180.8 +/- 138.8 days, P = 0.01) and 144 (80%) wounds healed during the follow-up period. Of the 36 (20%) that did not heal with Scotchcast boot therapy, 10 went on to more proximal amputation (5.6% of total population), two required surgical intervention to heal their wounds (0.6% of total population), one patient died with an unhealed wound (0.6% of total population), 23 patients (12.8% of total population) were lost to follow-up, and 47 (26%) died. Experience and the results of this and other studies suggest that this removable modality may be useful in outpatient care of deeper or complex wounds that require frequent inspection, but a device that ensures compliance may be the preferred treatment of superficial wounds.

Analysis of Variance↗