User:Shirwan

Shirwan Mirza, MD, FACP, FACE

Endocrinology, Diabetes, and Metabolism

Chairman: Department of Medicine Auburn Memorial Hospital Auburn, NY

Clinical Assistant Professor of Medicine Upstate Medical University, Syracuse, NY

Publications:

1. Conn's Current Therapy, 2006 Diabetes Mellitus in Adults

2. Conn's Current Therapy, 2007 Diabetes Mellitus in Adults

3. Secondary forms and genetic syndromes of diabetes mellitus A chapter in: Medical Management of Diabetes Mellitus Edited by Jack L. Leahy et al 761 pp. New York, Marcel Dekker, 2000. $99.75. ISBN 0-8247-8857-5.

More than 150 million people in the world have diabetes, the prevalence of which is increasing so rapidly that the management of diabetes is a priority in all branches of medicine. The new therapies and rapidly evolving evidence are making us all reevaluate our practice. We can no longer be one-dimensional "sugar doctors" but, instead, must address the three dimensions of cardiovascular risk prevention: glycemia, lipid levels, and blood pressure.

In addition to knowing the evidence, we all need practical advice. The detached reviewer can point to the inadequate number of randomized controlled studies of the treatment of diabetic ketoacidosis, but this is of little help to the clinician in the emergency room. When facing difficult clinical situations, we turn to wiser, more experienced colleagues. These experts use both personal experience and the evidence base to provide the best care for patients.

Leahy and his colleagues go a long way toward achieving their aim of writing a how-to manual for the care of patients with diabetes. They have commissioned experts to write chapters on clinical topics. The result is a book that is not intended to be encyclopedic but that focuses on practical advice. It is good to see that the chapter authors commit themselves to particular regimens and use such phrases as "we have found this approach useful." Many of the chapters have been written with the clarity of thought that typifies the wise clinician. There are some jewels; for example, reading Maryniuk's chapter on medical nutritional therapy was like being at an inspired educational session that leaves you knowing that you need to change your practice.

Inevitably, there is a considerable delay in publishing a multiauthored textbook, and changes in management during the past 18 months are not included in this book. In 2000 it seems surprising that the book does not cover in detail the use of insulin–glucose infusions in acute myocardial infarction or islet-cell transplantation.

At times the editor's pen has been too lenient; one suspects series editor, Burton Sobel, was proposing optimal treatment for diabetes, not "optical" treatment. The style used to cite references differs from one chapter to another. In addition, there is little cross-referencing of information between chapters. In some cases, different opinions are offered about a topic discussed in two different chapters (e.g., the best therapy for diabetic gastroparesis). This, however, reflects the reality of clinical practice.

There is an inevitable North American bias to this book. European readers will therefore have to remember their 18-times table to convert the glucose values in this book into millimoles per liter. Other transatlantic differences include the fact that metformin has been available in Europe for decades. In the United Kingdom Prospective Diabetes Study, it was effective in both controlling glycemia and preventing complications in obese patients. In the United Kingdom, we would consider metformin, with its anorectic properties, the clear treatment of choice in overweight patients.

Many of my minor quibbles result from the style of the book, which emphasizes opinions. It is always easier to disagree with opinions than with matters of fact. There will never be a randomized, controlled trial that addresses every clinical situation, so we will always need the wisdom of experienced clinicians, extrapolating from what evidence there is. This book goes a long way toward providing the distilled wisdom of the North American diabetes community, and we can all learn from it.

Andrew T. Hattersley, D.M. Royal Devon and Exeter Hospital Exeter EX2 5AX, United Kingdom

4. New Year Sherko Bekas

15 May 1997 | Volume 126 Issue 10 | Pages 825-826

The meadow that remained arid despite last year's kisses of rain I will make green this year, said the cloud. With that beautiful flower that I did not thread in my hair last year I will adorn myself this year, said the garden. That beautiful tall tree with whom I did not dance last year I will ask to dance this year, said the breeze. The New Year's crown that I wore last year will look much smaller than this year's crown, said the mountain top. The brooks with whom I dallied last year I will ask for their hands this year, said the lake. The horizon in which I did not fly last year will be this year's destination of my journey, said the bird. The dark-eyed letters that I did not know last year I will slip over my hand as a bracelet this year, said the little girl. The whirlwind by which I was thrown back last year I will break through this year, said the horse. The candles on my twelve fingers radiate more hope this year than last year's did, said the candlestick on the table. The grain of wheat that I did not manage to store in my ant-hill I will take there this year, said the ant. The poem that is shy like a deer and that last year I could not tame or acquaint with my eyes I will tame this year and take into the bright attic of my poetry-book and let it sleep in my arms, said finally I.

The Secret Diary of A Rose: A Kurdish Anthology of Poems; Translated by Shirwan Mirza, MD; University of Vermont; Burlington, VT 05405

5.  Calles-Escandon J, Mirza SA, Sobel BE, Schneider DJ.

Diabetes. 1998 Feb;47(2):290-3. Links Induction of hyperinsulinemia combined with hyperglycemia and hypertriglyceridemia increases plasminogen activator inhibitor 1 in blood in normal human subjects. Department of Medicine, The University of Vermont College of Medicine, Burlington 05405, USA. jcallese@zoo.uvm.edu Hypofibrinolysis caused by increased plasminogen activator inhibitor 1 (PAI-1) has been implicated in the vasculopathy of type 2 diabetes, typified by increased insulin, glucose, and triglycerides. However, short-term infusions of insulin have not increased PAI-1 in normal subjects. We hypothesized that induction of increased insulin accompanied by increased glucose and triglycerides would increase PAI-1. Accordingly, 30% glucose and 10% Intralipid were infused for 6 h in ten normal lean individuals (54 +/- 3 years) resulting in increased insulin (42 +/- 5 microU/dl), glucose (200 +/- 24 mg/dl), and triglycerides (425 +/- 45 mg/dl), simulating changes in type 2 diabetes. In contrast to results with infusion of saline alone (n = 16) and euglycemic-hyperinsulinemic clamps (n = 10, serum insulin = 89 +/- 7 microU/dl), PAI-1 in blood increased significantly 6 h after the onset of infusion (15 +/- 5 ng/ml, P < 0.05 vs. baseline = 7.4 +/- 1.1, saline 6 h = 3.4 +/- 1.1, and insulin alone 6 h = 3.7 +/- 0.8) and remained elevated for an additional 6 h (combined infusion = 13.8 +/- 3.8 ng/ml, saline = 6.7 +/- 2 ng/ml, insulin alone = 7.8 +/- 1.7 ng/ml, P = 0.06). Our data suggest that combined hyperinsulinemia, hypertriglyceridemia, and hyperglycemia are likely to contribute to hypofibrinolysis of type 2 diabetes by increasing the blood levels of PAI-1. Moreover, these results underscore the potential importance of modifying insulin resistance as well as achieving glycemic and lipidemic control in individuals with type 2 diabetes.

6. Calles-Escandon J, Garcia-Rubi E, Mirza S, Mortensen A. Type 2 diabetes: one disease, multiple cardiovascular risk factors. Department of Internal Medicine, University of Vermont, Burlington 05401, USA. jcallese@zoo.uvm.edu Coron Artery Dis. 1999;10(1):23-30.

Type 2 diabetes mellitus is a major independent risk factor for coronary artery disease. Atherosclerosis accounts for about 80% of all deaths from type 2 diabetes, of which roughly 75% are attributable to coronary artery disease and the remainder to cerebrovascular or peripheral vascular events [1]. The earlier onset and accelerated course of atherosclerosis in individuals with type 2 diabetes mellitus is multifactorial. Type 2 diabetes is associated with abnormalities in lipoprotein metabolism and increased propensity for oxidative damage. The hyperglycemia of patients with type 2 diabetes, in itself, may accelerate vascular damage. Type 2 diabetes is a hypercoagulable state attributable to enhanced coagulation and decreased fibrinolysis, as well as platelet hyperaggregability and endothelial dysfunction. Hypertension is common in individuals with type 2 diabetes and has a major impact in the accelerated atherosclerosis of this disease. This review provides an overview of selected aspects of these alterations.