Biomedical subjects

H Erhan Dincer

Publications and source records attributed to H Erhan Dincer.

6 recordsLinked to original sources

PubMed2005

Deleterious effects of sleep-disordered breathing on the heart and vascular system.

Obstructive sleep apnea (OSA) is the most common form of sleep-disordered breathing, affecting 5-15% of the population. It is characterized by intermittent episodes of partial or complete obstruction of the upper airway during sleep that disrupts normal ventilation and sleep architecture, and is typically associated with excessive daytime sleepiness, snoring, and witnessed apneas. Patients with obstructive sleep apnea present risk to the general public safety by causing 8-fold increase in vehicle accidents, and they may themselves also suffer from the physiologic consequences of OSA; these include hypertension, coronary artery disease, stroke, congestive heart failure, pulmonary hypertension, and cardiac arrhythmias. Of these possible cardiovascular consequences, the association between OSA and hypertension has been found to be the most convincing. Although the exact mechanism has not been understood, there is some evidence that OSA is associated with frequent apneas causing mechanical effects on intrathoracic pressure, cardiac function, and intermittent hypoxemia, which may in turn cause endothelial dysfunction and increase in sympathetic drive. Therapy with continuous positive airway pressure has been demonstrated to improve cardiopulmonary hemodynamics in patients with OSA and may reverse the endothelial cell dysfunction. Despite the availability of diagnostic measures and effective treatment, many patients with sleep-disordered breathing remain undiagnosed. Therefore, OSA continues to be a significant health risk both for affected individuals and for the general public. Awareness and timely initiation of an effective treatment may prevent potential deleterious cardiovascular effects of OSA.

Arrhythmias, Cardiac↗

PubMed2005

A case of tubulointerstitial nephritis and uveitis in an adult male.

We report a case of tubulointerstitial nephritis and uveitis (TINU) syndrome in an adult male. A 40-year-old man was found to have bilateral anterior uveitis and mild renal insufficiency with high urinary beta-2 microglobulin. Work up for connective tissue and infectious diseases were negative. His kidney function normalized spontaneously and remained normal at 1 year without intervention. Uveitis responded completely to local corticosteroid treatment and has not recurred.

Adult↗

PubMed2005

Compartment syndrome and fatal rhabdomyolysis in sickle cell trait.

Sickle cell trait is a relatively common condition in the African-American population. Individuals with this condition may have any of several complications under rare circumstances. We report a patient who presented with extensive compartment syndrome leading to death. A 31-year-old African-American male with known history of sickle cell trait developed extensive compartment syndrome followed by rhabdomyolysis, severe acidosis, acute renal failure, and coagulopathy. Although the patient underwent multiple fasciotomies for extensive compartment syndrome and received aggressive resuscitation with massive transfusions of blood, blood products and intravenous fluids, he died. Multiple compartment syndromes in patients with sickle cell trait represent a very unusual complication and can cause significant morbidity and mortality. Avoidance of strenuous exercise, especially in hot climates, early diagnosis, and aggressive therapy are very important to prevent this catastrophic complication.

Acidosis↗

PubMed2003

Pathophysiology of pulmonary hypertension due to lung disease.

Pulmonary hypertension (PH) often complicates the course of patients with advanced lung disease, and it is associated with a worse prognosis. Per the recent classification of pulmonary hypertensive disorders, PH due to lung disease is considered as a separate category within a group of disorders that was previously referred to as "secondary" PH. Among the lung diseases associated with PH, the incidence and clinical course of PH is best known for patients with COPD. Per studies in patients with COPD and other lung disorders, it is evident that the pathophysiology and treatment of these disorders is generally distinct from that of pulmonary arterial hypertensive disorders. Changes in the pulmonary vasculature that accompany elevations in pulmonary vascular pressure are generally referred to as pulmonary vascular remodeling. Chronic hypoxia is well known to cause pulmonary vascular remodeling and PH, and it is the major mechanism implicated for the development of PH in patients with lung disease. Other mediators have also been implicated in the pathogenesis of PH in animal models and patients with PH, including patients with pulmonary diseases. General features of pulmonary vascular remodeling are discussed with particular emphasis on those changes that have been described in patients with lung diseases. Recent discoveries in these areas are also reviewed, and findings in pulmonary arterial hypertensive diseases are contrasted with those found in patients with PH due to lung diseases. Some of these discoveries have already led to new treatment strategies for patients with the most severe forms of PH. PH due to lung diseases shares some common pathophysiologic features with pulmonary arterial hypertension. Therefore, it is likely that these discoveries and new treatments will also be extended to benefit patients with PH due to lung disease.

Animals↗

PubMed2003

Proteinuria: how to evaluate an important finding.

Proteinuria is a common laboratory finding in outpatients and should not be discounted. When it is due to a glomerular disease, early diagnosis is important to prevent further renal damage. Proteinuria may also be a marker for progressive atherosclerosis.

Algorithms↗

PubMed2002

Asymptomatic hyperuricemia: to treat or not to treat.

Treatment of asymptomatic hyperuricemia is not necessary in most patients, unless perhaps they have very high levels of uric acid or are otherwise at risk of complications, such as those with a personal or strong family history of gout, urolithiasis, or uric acid nephropathy.

Age Factors↗