42 research outputs found
Henri Temianka Correspondence; (spivakovsky)
https://digitalcommons.chapman.edu/temianka_correspondence/2868/thumbnail.jp
A New Prognostic-Predictor Marker Of Cardiovascular Disease For Obstructive Sleep Apnea: Pentraxin 3
Acute Respiratory Distress due to Antipsychotic Drugs
We report a 36-year-old male schizophrenic patient who was treated with risperidone for a long time. Because of an acute psychotic reaction, haloperidol, chlorpromazine and olanzapine were administered additionally. After administration of these drugs, he developed acute respiratory distress that caused his death. We discuss the cause of this respiratory distress and conclude that it might be due to acute laryngeal dystonia caused by these antipsychotic drugs. Antipsychotic drug-induced laryngeal dystonia is rarely reported but it is a life threatening side effect. All physicians dealing with antipsychotic drug therapy must be aware of acute laryngeal dystonia, and an antiparkinsonian agent should be administered immediately
Myocardial performance index for detection of subclinical abnormalities in patients with sarcoidosis
Aim: The aim of this study was to evaluate ventricular functions in patients with sarcoidosis without an obvious heart disease by using tissue Doppler-derived left and right ventricular myocardial performance index (MPI)
A New Prognostic-Predictor Marker Of Cardiovascular Disease For Obstructive Sleep Apnea: Pentraxin 3
Obstructive sleep apnea syndrome (OSAS) is characterized by
intermittent complete or partial upper airway obstruction during sleep
causing hypoxia, sleep disruption, daytime sleepiness, mental and
physical effects is the second most common respiratory condition;
affecting 0.3- 4% of the middle- aged population (1). OSAS is strongly
associated with cardiovascular morbidity and mortality, including an
increased risk of endothelial dysfunction and atherosclerosis (2). The
increased prevalence of hypertension and atherogenesis among OSAS
patients has been attributed to sympathetic activation and endothelial
dysfunction, likely resulting from initiation and propagation of
inflammatory responses within the microvasculature (3). There is
increasing evidence that OSAS associated with inflammatory cytokines
and markers such as C-reactive protein (CRP), interleukin-6,
fibrinogen, tumor necrosis factor alpha which are closely-involved in
atherosclerosis, plaque formation and rupture (4). OSAS, a potent
activator of inflammation, inreases CRP which has been used as an
inflammatory biomarker for prediction of cardiovascular events;CRP is
named as classical short pentraxins and is a acute phase protein
produced from the liver in response to inflammatory mediators (5).
Pentraxin 3 (PTX3), a new defined member of the pentraxin family, is
produced from the major cell types involved in atherosclerotic lesions,
including vascular endothelial-smooth muscle cells, macrophages, and
neutrophils in response to inflammatory stimuli, however CRP is
produced only from liver (6,7). Furthermore, CRP represents a systemic
response to local inflammation, whereas PTX3 is rapidly produced
directly from damaged tissues and directly reflects only the
inflammatory state of the vasculature. The last but not the least PTX3
levels have been reported to be significantly elevated in acute
myocardial infarction (7). In the light of these knowledge, PTX3 is
able to reflect ACS condition better than CRP, it is highly possible
that PTX3 is a superior biomarker to predict future cardiovascular
events. Therefore, we speculate that OSAS, directly or indirectly,
induces a persisting systemic and vascular inflammation and may cause
PTX3 secretion. Since high PTX3 level is a sign of vascular
inflammation which is the trigger point for many diseases that may
occur secondary to OSAS, might also be a good marker of cardiovascular
disease in OSAS. Screening of PTX3 level in OSAS patients may be a
useful marker for evaluating the prognosis of OSAS. To address this
hypothesis, further prospective studies are warranted to evaluate the
role of PTX3 in patients with OSAS
Gemcitabine induced pulmonary toxicity with late onset
Gemcitabine is a nucleoside analog that has been increasingly used in the chemotherapy of solide tumors, including breast, pancreas ovary and non small cell lung cancer. It is generally well tolerated and has few side effects. Gemcitabine induced pulmonary complications range from mild dyspnea to death from ARDS. A 57- year- old man was treated with six cycles of gemcitabine because of pancreatic carcinoma in July, 2004.The patient had self limiting weakness, lack of appetite, nausea and no dyspnea in treatment period. One year later, he was admitted to a local hospital with exercises induced dyspnea. He had been given levofloxacin for 14 days. On admission to our hospital, his complaint kept on. A few inspiratory crackles were present at right base. CXR demonstrated interstitial infiltrations in the right lung lower zone. HRCT showed grand glass opacity and mild reticular patterns in right lung middle and lower lobes. Bronchoscopy was performed. Transbronchial biopsy revealed nonspecific interstitial pneumonia. Following the administration of oral corticosteroid, he had complete resolution of all signs and symptoms of gemcitabine toxicity
Biphasic anaphylaxis to gemifloxacin
Anaphylaxis have been documented as adverse effects of ciprofloxacin, ofloxacin, norfloxacin, levofloxacin, and moxifloxacin. However resistant and biphasic anaphlylactic reactions to gemifloxacin have not been reported to date. Management of severe anaphylaxis in the elderly can be complicated by concurrent medications such as beta (β) adrenergic, alpha (α) adrenergic blockers and angiotensin-converting enzyme (ACE) inhibitors. We report here in the case of a 60-year-old male who was taking on ACE inhibitor, α and β blockers and experienced a severe, resistant and biphasic anaphlylactic reaction to gemifloxacin mesylate
Evaluation of malignant mesothelioma in central Anatolia: A study of 67 cases
Background: Malignant mesothelioma (MM) is a fatal neoplasm which frequently results from exposure to asbestos or erionite. Method: Sixty-seven patients with MM were seen between 1990 and 2001. Their clinical and radiological features, as well as the therapy, were retrospectively evaluated. Results: In 51 patients (76.1%), the MM was confined to the pleura, in 14 patients it was exclusively peritoneal and in two patients, it involved both areas. Of the 67 cases, 35 (52.2%) were women. The mean (± SD) age for all cases was 57.6 ± 11.5 years. Dyspnea (67.2%), cough (55.2%) and chest pain (50.7%) were the most frequent symptoms of onset. Pleural effusion (92.4%) was the most common chest x-ray finding, whereas pleural effusion (60.8%), pleural nodules (34.7%) and pleural thickening (34.7%) were the most common computed tomography findings in pleural MM patients. The histological subtypes of MM were determined as epithelial in 60 patients (89.5%), sarcomatous in four patients (5.9%) and mixed in three patients (4.4%). Although 50.7% and 25.4% of the cases were exposed to erionite and asbestos, respectively, 23.9% of the cases recalled no exposure to asbestos or erionite. Exposures were environmental as opposed to occupational. Thirty-five patients (52.2%) were administered chemotherapy, and follow-up data were available for 22 patients. For these patients, the two-year survival rate was 22% and the two-year progression-free interval was 15.7%. There were no differences between patients with asbestos and erionite exposure. Conclusion: MM should be considered when exudative pleural effusion is detected in a patient who has been exposed to asbestos or erionite. MM is a major public health problem in parts of Turkey and compulsory environmental control of fibrous mineral should be considered. © 2004 Pulsus Group Inc. All rights reserved
Evaluation of Malignant Mesothelioma in Central Anatolia: A Study of 67 Cases
BACKROUND: Malignant mesothelioma (MM) is a fatal neoplasm which frequently results from exposure to asbestos or erionite