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Psychogenic nonepileptic seizure (PNES) is a sudden change in a person's behavior, perception, thinking, or feeling that is usually time limited and resembles, or is mistaken for, epilepsy but does not have the characteristic electroencephalographic (EEG) changes that accompanies a true epileptic seizure [1]. It is considered that PNES is a somatic manifestation of mental distress, in response to a psychological conflict or other stressors [2]. A wide spectrum of clinical presentation includes syncope, generalized tonic-clonic seizure, simple and complex partial seizure, myoclonic seizure, frontal lobe seizures and status epilepticus [3]. Coexistence of epilepsy and PNES is seen in approximately 9% of cases [5]. Between 25-30% of patients referred to tertiary centers and initially diagnosed as refractory epilepsy were on further examination diagnosed as PNES [6, 7]. In DSM-IV [12] PNES are usually categorized under conversion disorder with seizures or convulsions. However, psychiatric basis of PNES may be anxiousness (panic attack), somatization or factitious disorder, simulation, dissociative disorders and psychosis [1]. ⋯ PNES is often replaced with epilepsy and in number of cases clinical differentiation is not easy. One should be acquainted with clinical presentation of PNES as well as its psychiatric origin in order to adequately recognize and treat the disorder.
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Endogenous Cushing's syndrome is a clinical state resulting from prolonged, inappropriate exposure to excessive endogenous secretion of cortisol and hence excess circulating free cortisol, characterized by loss of the normal feedback mechanisms of the hypothalamo-pituitary-adrenal axis and the normal circadian rhythm of cortisol secretion [2]. The etiology of Cushing's syndrome may be excessive ACTH secretion from the pituitary gland, ectopic ACTH secretion by nonpituitary tumor, or excessive autonomous secretion of cortisol from a hyperfunctioning adrenal adenoma or carcinoma. Other than this broad ACTH-dependent and ACTH-independent categories, the syndrome may be caused by ectopic CRH secretion, PPNAD, MAH, ectopic action of GIP or catecholamines, and other adrenel-dependent processes associated with adrenocortical hyperfunction. ⋯ A multitude of normal nonpituitary cells from different organs and tissues have been shown to express the POMC gene from which ACTH is derived. The tumors most commonly associated the ectopic ACTH syndrome arise from neuroendocrine tissues, APUD cells. POMC gene expression in non-pituitary cells differs from that in pituitary cells both qualitatively and quantitatively [8]. Aggressive tumors, like small cell cancer of the lung (SCCL) preferentially release intact POMC, whereas carcinoids rather overprocess the precursor, releasing ACTH and smaller peptides like CLIP. Some tumors associated with ectopic ACTH syndrome express other markers of neuroendocrine differentiation like two specific prohormone convertases (PCs). Assessment of vasopressin (V3) receptor gene expression in ACTH-producing nonpitultary tumors revealed bronchial carcinoid as a particular subset of tumors where both V3 receptor and POMC gene may be expressed in pattern indistinguishable from that in corticotroph adenoma [9]. In most, but not all, patients with ectopic ACTH syndrome, cortisol is unresponsive to high-dose dexamethason suppression test, what is used as diagnostic tool. It is not clear if the primary resistance resulted from structural abnormality of the native glucocorticoid receptor (GR), a low level of expression, or some intrinsic property of the cell line [9]. It appears that ectopic ACTH syndrome is made of two different entities. When it is because of highly differentiated tumors, with highest level of pituitary-like POMC mRNA, expressing PCs, high level of V3 receptors and GR, like bronchial carcinoids, it might be called ectopic corticotroph syndrome. In contrast, when it is caused by aggressive, poorly differentiated tumors, with much lower expression of V3 receptor, like SCCL, it might be called aberrant ACTH secretion syndrome. Carcinoid tumors have been reported in a wide range of organs but most commonly involve the lungs, bronchi, and gastrointestinal tract. They arise from neuroendocrine cells and are characterized by positive reactions to markers of neuroendocrine tissue, including neuron specific enolase, synaptophysin, and chromogranina [11]. Carcinoid tumors are typically found to contain numerous membrane-bound neurosecretory granules composed of variety of hormones and biogenic amines. One of the best characterized is serotonin, subsequently metabolized to 5-hydrohy-indolacetic acid (5-HIAA), which is excreted in the urine. In addition to serotonin, carcinoid tumors have been found to secrete ACTH, histamine, dopamine, substance P, neurotensin, prostaglandins and kallikrein. The release of serotonin and other vasoactive substances is thought to cause carcinoid syndrome, which manifestations are episodic flushing, weezing, diarrhea, and eventual right-sided valvular heart disease. These tumors have been classified as either well-differentiated or poorly differentiated neuroendocrine carcinomas. The term "pulmonary tumorlets" describes multiple microscopic nests of neuroendocrine cells in the lungs [12]. Pulmonary carcinoids make up approximately 2 percents of primary lung tumors. The majority of these tumors are perihilar in location, and patients often presents with recurrent pneumonia, cough, hemoptisis, or chest pain. The carcinoid syndrome occurs in less than 5 percent of cases. Ectopic secretion of ACTH from pulmonary carcinoid accounts for 1 percent of all cases of Cushing's syndrome. They are distinct clinical and pathologic entity, generally peripheral in location. Although they are usually typical by standard histologic criteria, they have mush greater metastatic potential than hormonally quiescent typical carcinoids [13]. Surgical treatment therefore should be one proposed for more aggressive malignant tumors. In all cases of ACTH-dependent Cushing's syndrome with regular pituitary MRI and bilateral inferior petrosal sinus sampling, thin-section and spiral CT scanning of the chest should be routine diagnostic procedure [14]. We present thirty-one year old patient with typical pulmonary carcinod with ACTH ectopic secretion consequently confirmed by histology.
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Ruptured abdominal aortic aneurysm is one of the most urgent surgical conditions with high mortality that has not been changed in decades. Between 1991-2001 total number of 1058 patients was operated at the Institute for Cardiovascular Diseases of Clinical Centre of Serbia due to abdominal aortic aneurysm. Of this number, 288 patients underwent urgent surgical repair because of ruptured abdominal aortic aneurysm. ⋯ Important intraoperative factors that influence the outcome of surgical treatment can be defined. Therapeutic efforts should be concentrated on those factors that are possible to correct, which would hopefully lead to better survival of patients. Nevertheless, screening for abdominal aortic aneurysm and elective surgical intervention before rupture occurs should be the best solution for this complex problem.