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Mohsen S Eledrisi

Publications and source records attributed to Mohsen S Eledrisi.

10 recordsLinked to original sources
PubMed2006

Overview of the diagnosis and management of diabetic ketoacidosis.

Diabetic ketoacidosis is an acute complication of diabetes mellitus that can be life-threatening if not treated properly. Once thought to occur only in patients with type 1 diabetes, diabetic ketoacidosis has been also observed in patients with type 2 diabetes under certain conditions. The basic underlying mechanism for diabetic ketoacidosis is insulin deficiency coupled with elevated levels of counter-regulatory hormones, such as glucagon, cortisol, catecholamines, and growth hormone. Diabetic ketoacidosis can be the initial presentation of diabetes mellitus or precipitated in known diabetic patients by many factors, most commonly infection. The management of diabetic ketoacidosis involves careful clinical evaluation, correction of metabolic abnormalities, identification and treatment of precipitating and comorbid conditions, appropriate long-term treatment of diabetes, and plans to prevent recurrence. Certain areas need further research, such as indications for the use of bicarbonate and phosphates and the use of intravenous rapid-acting insulin.

Acid-Base Equilibrium↗
PubMed2002

Vascular inflammation and the renin-angiotensin system.

It is now well established that vascular inflammation is an independent risk factor for the development of atherosclerosis. In otherwise healthy patients, chronic elevations of circulating interleukin-6 or its biomarkers are predictors for increased risk in the development and progression of ischemic heart disease. Although multifactorial in etiology, vascular inflammation produces atherosclerosis by the continuous recruitment of circulating monocytes into the vessel wall and by contributing to an oxidant-rich inflammatory milieu that induces phenotypic changes in resident (noninflammatory) cells. In addition, the renin-angiotensin system (RAS) has important modulatory activities in the atherogenic process. Recent work has shown that angiotensin II (Ang II) has significant proinflammatory actions in the vascular wall, inducing the production of reactive oxygen species, inflammatory cytokines, and adhesion molecules. These latter effects on gene expression are mediated, at least in part, through the cytoplasmic nuclear factor-kappaB transcription factor. Through these actions, Ang II augments vascular inflammation, induces endothelial dysfunction, and, in so doing, enhances the atherogenic process. Our recent studies have defined a molecular mechanism for a biological positive-feedback loop that explains how vascular inflammation can be self-sustaining through upregulation of the vessel wall Ang II tone. Ang II produced locally by the inflamed vessel induces the synthesis and secretion of interleukin-6, a cytokine that induces synthesis of angiotensinogen in the liver through a janus kinase (JAK)/signal transducer and activator of transcription (STAT)-3 pathway. Enhanced angiotensinogen production, in turn, supplies more substrate to the activated vascular RAS, where locally produced Ang II synergizes with oxidized lipid to perpetuate atherosclerotic vascular inflammation. These observations suggest that one mechanism by which RAS antagonists prevent atherosclerosis is by reducing vascular inflammation. Moreover, antagonizing the vascular nuclear factor-kappaB and/or hepatic JAK/STAT pathways may modulate the atherosclerotic process.

Acute-Phase Proteins↗
PubMed2002

Noninvasive blood glucose monitoring with optical coherence tomography: a pilot study in human subjects.

OBJECTIVE: To study the feasibility of noninvasive blood glucose monitoring using optical coherence tomography (OCT) technique in healthy volunteers. RESEARCH DESIGN AND METHODS: An OCT system with the wavelength of 1,300 nm was used in 15 healthy subjects in 18 clinical experiments. Standard oral glucose tolerance tests were performed to induce changes in blood glucose concentration. Blood samples were taken from the right arm vein every 5 or 15 min. OCT images were taken every 10-20 s from the left forearm over a total period of 3 h. The slope of the signals was calculated at the depth of 200-600 micro m from the skin surface. RESULTS: A total of 426 blood samples and 8,437 OCT images and signals were collected and analyzed in these experiments. There was a good correlation between changes in the slope of noninvasively measured OCT signals and blood glucose concentrations throughout the duration of the experiments. The slope of OCT signals changed significantly (up to 2.8% per 10 mg/dl) with variation of plasma glucose values. The good correlation obtained between the OCT signal slope and blood glucose concentration is due to the coherent detection of backscattered photons, which allows measurements of OCT signal from a specific tissue layer without unwanted signal from other tissue layers. CONCLUSIONS: This pilot study demonstrated the capability of the OCT technique to monitor blood glucose concentration noninvasively in human subjects. Further studies with a larger number of subjects including diabetic subjects are planned to validate these preliminary results.

Adult↗
PubMedDate not supplied

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3-Iodobenzylguanidine↗
PubMedDate not supplied

Insulinoma in a patient with tuberous sclerosis: is there an association?

OBJECTIVE: To describe a patient with tuberous sclerosis who, on initial assessment, had neurologic symptoms, which were ultimately found to be caused by an insulinoma. METHODS: We present a case report with clinical, laboratory, and radiologic data. The literature is reviewed relative to tuberous sclerosis and islet cell tumors, and a possible association is discussed. RESULTS: A 43-year-old man with a history of tuberous sclerosis required medical attention because of mental confusion and slurred speech and was found to have hypoglycemia. Neuroradiologic imaging showed no new lesions to account for his symptoms. His physical examination was striking for a large abdominal mass, which showed increased uptake on octreotide scanning. After surgical resection, the mass measured 21 cm and was found to be an insulinoma. Blood glucose values were normal postoperatively and on follow-up, and the patient had no recurrence of the symptoms. CONCLUSION: From this report, we emphasize two findings. First, we draw clinicians' attention to the possibility of an association between islet cell tumors and tuberous sclerosis and suggest consideration of this diagnosis in patients with tuberous sclerosis who have new or worsening neurologic symptoms. Second, the insulinoma we describe is, to our knowledge, the largest to be reported thus far in the literature.

Adult↗
PubMedDate not supplied

Diabetes insipidus as a consequence of neurologic involvement in Behcet's syndrome.

OBJECTIVE: To describe a case of central diabetes insipidus that was associated with Behçet's syndrome. METHODS: We present a case report, including clinical, laboratory, and radiologic data. The pertinent literature is reviewed relative to diabetes insipidus and Behçet's syndrome, and a discussion about a possible association is presented. RESULTS: A 32-year-old man presented with diplopia and severe headaches and was found to have transverse sinus thrombosis. He reported having recurrent mouth and genital ulcers for 3 months before the current consultation. On the basis of the clinical picture, Behçet's syndrome was diagnosed. During hospitalization of the patient, polyuria and polydipsia developed, along with hypernatremia and hypotonic urine, indicative of diabetes insipidus. After desmopressin treatment was initiated, considerable improvement in clinical status and laboratory data was evident and persisted during follow-up. CONCLUSION: Behçet's syndrome, probably through vasculitic mechanisms, may result in central diabetes insipidus. This case report emphasizes that Behçet's syndrome should be considered in the differential diagnosis of diabetes insipidus.

Adult↗