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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diagnosis of tuberculosis (TB) in children is usually based on presumptions from several elements: clinical picture and course, x-rays, tuberculin test, and culture of pathology later on. TB is usually found in a child because of symptoms of primary disease, or through case-finding of a contact. TB is children is often a primary infection and may be gradual or acute in onset. Some of the symptoms of primary TB are low-grade fever, pallor, fatigue, and anorexia. The child may have erythema nodosum, a yellow module on the conjunctiva, hilar or mediastinal lymphadenopathy, a primary TB complex on the lung (3-10 mm), segmental density, or a positive PPD test. Children with pulmonary disease do not have adult-type cavity lesions, but may have a primary cavity that drains into the bronchi, mechanical complications, fistulas, or atelectasis. Acute TB often appears as meningitis. The pathognomonic signs are cerebrospinal fluid high in lymphocytes with very high albumin (0.6-2 g) and low glucose (0.4-0.2 g/l). TB organisms are rarely seen, but may be cultured. TB meningitis is also notable for choroidal tubercles, which are yellow nodules visible in the fundus. These presumptive signs, as well as increasing neurological findings, prompt immediate treatment. Children also may have acute miliary TB, marked by high fever, gastrointestinal symptoms, hepatosplenomegaly, dyspnea, cyanosis, and respiratory distress, with characteristic diffuse grainy spots on the chest x-ray. A child may have both conditions and may also have localized TB infection elsewhere. Thus, clinical findings may point to possible cultures of urine, gastric lavage, pleural fluid or biopsy, pericardial fluid, bone marrow, or ascitic fluid, any of which should be cultured to rule out other causes. The most common sites for extra-pulmonary TB are cervical nodes, spine, knee. shoulder, hip and peritoneum. Pelvic and urinary tract infections are rare in children.
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PMID:Diagnosis of tuberculosis in children. 1234 39

We describe an unusual case of pulmonary stenosis caused by calcific constrictive pericarditis associated with a congenital ventricular septal defect in a 16-year-old boy who had a 2-week history of progressive dyspnea, cyanosis, fatigue, and bilateral leg edema. Echocardiographic findings led to an initial diagnosis of tetralogy of Fallot; however, findings on chest radiography and CT were suggestive of calcific constrictive pericarditis with pulmonary stenosis, which was then confirmed on cardiac catheterization. Total pericardiectomy and repair of the ventricular septal defect resulted in a satisfactory outcome. Follow-up examinations at 6 and 20 months showed that the patient was asymptomatic and considered to have class I New York Heart Association functional status. To our knowledge, this is the first reported case of calcific constrictive pericarditis with pulmonary stenosis associated with a ventricular septal defect.
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PMID:Idiopathic calcific constrictive pericarditis causing pulmonary stenosis associated with a ventricular septal defect mimicking tetralogy of Fallot. 1269 33

Liver disease affects the lungs. The majority of patients exhibit mild to moderate arterial hypoxaemia essentially attributable to an alteration in ventilation/perfusion matching and limited by an increase in ventilation. A minority (some 10%) of patients exhibit a "hepatopulmonary syndrome" defined by severe hypoxaemia with arterial PO2 below 60 mm Hg, dyspnoea, cyanosis, digital clubbing, orthodeoxia, platypnoea and demonstrable pulmonary vascular dilatations causing a true pulmonary shunt and a diffusion/perfusion imbalance. The hepatopulmonary syndrome is incurable but resolves over time after liver transplantation. An even lower proportion of patients, approximately 1%, develop pulmonary hypertension. Clinically this "portopulmonary hypertension" resembles primary pulmonary hypertension, with dyspnoea and fatigue as the main symptoms, histopathology and response to prostacyclin therapy. Portopulmonary hypertension is irreversible. Liver transplantation mortality in patients with portopulmonary hypertension ranges from 50 to 100%. The common cause of the hepatopulmonary syndrome and portopulmonary hypertension is portal hypertension and portosystemic shunting, indicating that vasoactive and angiogenetic factors originating from the liver normally control the pulmonary circulation.
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PMID:Hepatopulmonary syndrome and portopulmonary hypertension. 1271 85

Pulmonary arteriovenous malformations (PAVMs) are rare anomalies. The degree of right-to-left shunting, which can lead to cyanosis and paradoxical embolism causing neurological complications, determines the prognosis. We report two cases of PAVM and review the literature. A 45-year-old woman with clinical signs and symptoms of PAVM was examined using several different scanning techniques, which showed a large PAVM in the lower lobe of her right lung. A lobectomy was performed, which revealed a 5 cm diameter PAVM with one feeding artery and multiple veins. Intravenous angiography of a 7-year-old girl with symptoms of fatigue and acro-cyanosis confirmed the presence of a large PAVM in her right lower lobe. The PAVM had two major arteries arising from the aorta, which were ligated during a lobectomy. Both patients recovered well following surgery. Although PAVMs are rare, their neurological and haemodynamic consequences may be fatal. Interventional treatment techniques, including surgery, are usually curative.
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PMID:Surgical treatment of pulmonary arteriovenous malformation: report of two cases and review of the literature. 1610 51

Rosiglitazone is a peroxisome proliferator active receptor. gamma agonist, which increases insulin sensitivity in adipose tissue, muscle, and liver. Rosiglitazone is a member of the thiazolidinedione group, and because of its significantly positive effect on glycemic control, it is especially preferred in type 2 diabetic patients with a high cardiovascular disease risk. This drug, because of its decreasing effect on insulin resistance, is used alone or combined with type 2 diabetic drugs. A 73-year-old female patient was admitted to the emergency department with dyspnea, pink frothing phlegm, cyanosis, and tiredness. She was lethargic, uncooperative, and had no orientation. In arterial blood gases, hypoxemia and hypercapnia were found. She was taken to the general intensive care unit, and oxygen was applied via mask. The patient had a history of 10 years of diabetes mellitus, hypertension, and atherosclerotic cardiac disease, and she was using rosiglitazone for the past 6 weeks. Her chest x-ray was taken, and acute pulmonary edema was diagnosed. In her last echocardiography, which was performed 1 year before, no signs indicating cardiac failure and pleural effusion could be found. Therefore, it was concluded that pulmonary edema occurred as a complication of rosiglitazone use. After stabilizing the patient's vital signs, blood glucose levels, and lactate levels, medical treatment of diabetes mellitus was rearranged, and she was discharged on the seventh day after her admittance. In a patient with diabetes mellitus who has been admitted to the intensive care unit because of acute pulmonary edema, for differential diagnosis, use of rosiglitazone should be kept in mind during the determination of treatment. Therefore, the authors aim to discuss the effect of rosiglitazone on creating acute pulmonary edema with a case report presentation.
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PMID:Acute pulmonary edema due to rosiglitazone use in a patient with diabetes mellitus. 1669 44

The chronic myeloproliferative diseases (CMDs) are a group of conditions characterized by unregulated blood cell production, that due either to excessive numbers of erythrocytes, leukocytes or platelets, or their defective function cause symptoms and signs of fatigue, headache, ruddy cyanosis, hemorrhage, abdominal distension, and the complications of vascular thrombosis. In the late 19th century Vaquez provided the first description of polycythemia vera (PV) and Hueck defined idiopathic myelofibrosis (IMF). In 1920, di Guglielmo established criteria for patients with essential thrombocythemia (ET). In 1951, Dameshek argued that these disorders, along with chronic myelogenous leukemia (CML) display many similar clinical and laboratory features [Dameshek W. Some speculations on the myeloproliferative syndromes. Blood 1951;6:372-5], and grouped them. In 2002, the World Health Organization expanded the definition of CMDs to also include chronic neutrophilic leukemia (CNL), chronic eosinophilic leukemia/hypereosinophilic syndrome (CEL/HES) and systemic mast cell disorder (SMCD) [Vardiman JW, Harris NL, Brunning RD. The World Health Organization (WHO) classification of the myeloid neoplasms. Blood 2002;100:2292-302]. While the molecular pathogenesis of CML is well known [Melo JV, Deininger MW. Biology of chronic myelogenous leukemia-signaling pathways of initiation and transformation. Hematol Oncol Clin North Am 2004;18:545-68], and the causes of CEL/HES and SMCD have been identified in about half of all cases [Gotlib J, Cools J, Malone III JM, Schrier SL, Gilliland DG, Coutre SE. The FIP1L1-PDGFRalpha fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and management. Blood 2004; 103:2879-91; Valent P, Akin C, Sperr WR, Horny HP, Metcalfe DD. Mast cell proliferative disorders: current view on variants recognized by the World Health Organization. Hematol Oncol Clin North Am 2003; 17:1227-41], until very recently the etiologies of the three classically defined CMDs, PV, IMF and ET, were poorly understood. Each of these disorders is characterized by excessive hematopoiesis, a process usually dependent on one or more hematopoietic growth factors (HGFs). This review will focus on how our knowledge of the molecular mechanisms by which HGFs are produced, bind cell surface receptors and transduce survival and proliferative signals have provided the platform on which the multiple origins of CMDs can be understood and novel therapeutic interventions designed.
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PMID:Hematopoietic growth factors, signaling and the chronic myeloproliferative disorders. 1705 68

We present a 39-year-old male patient with Down syndrome who was evaluated for fatigue, palpitations and bouts of cyanosis. Physical examination showed features of trisomy-21(Down syndrome), with a slow pulse rate, distant cardiac sounds and absent apex beat. He had normal jugular venous pressure without pulsus paradoxus. The ECG showed QRS microvoltage and flattened P and T segments. The 48-hour ambulatory ECG depicted normal sinus rhythm with intermittent short PR interval without tachyarrhythmias. The chest Xray revealed cardiomegaly without pulmonary venous congestion. Although serial transthoracic echocardiographic examination demonstrated pericardial effusion with features of tamponade, there were no overt signs of clinical cardiac tamponade. Biochemically, the serum thyroxine of 3 pmol/l (normal 10 to 25) and thyroid-stimulating hormone of 160 mU/l (normal 0.20 to 4.20)) were compatible with hypothyroidism. The patient was treated with L-thyroxine sodium daily, which was gradually increased to 0.125 mg daily. Within a few months he lost weight and became more alert; furthermore, the symptoms of hypothyroidism and the pericardial effusion resolved. It can be concluded that Down syndrome may be associated with hypothyroidism and pericardial effusion. These were alleviated following hormone replacement. Regular evaluation of thyroid function tests is important in Down syndrome. (Neth Heart J 2007;15:67-70.).
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PMID:Down syndrome associated with hypothyroidism and chronic pericardial effusion: echocardiographic follow-up. 1761 63

Two women with Eisenmenger syndrome, aged 63 and 45 years, presented with different symptoms: the first patient had peripheral oedema, proteinuria, progressive fatigue and cyanosis and the other had increasing dyspnoea and blue lips. The first patient was successfully treated with diuretics but experienced a collum fracture that occurred after hypovolemic collapse caused by diuretic use. She was given sildenafil and underwent hip surgery with spinal anaesthesia 10 days later. In the following weeks, the patient was haemodynamically stable but then died suddenly; no autopsy was performed. The second patient was given oxygen therapy at home and bosentan. After 6 months the symptoms of dyspnoea resolved and her 6-minute walking distance increased from 453 to 512 m. The life expectancy of patients with congenital heart disorders such as Eisenmenger syndrome has improved dramatically, due in part to the efficacy of novel agents that inhibit endothelial-cell proliferation. With these advances, treatment of these patients is no longer restricted to tertiary-care centres. Therefore, community cardiologists, pulmonologists and internists should be aware of these congenital heart disorders and the available treatment options.
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PMID:[Two patients with Eisenmenger syndrome treated with novel agents that target vasodilation of the pulmonary capillary bed]. 1823 58

Superior vena cava syndrome is a rare complication of pacemaker implantation. Narrowing and occlusion of the superior vena cava is often asymptomatic due to the formation of decompressive collateral pathways to the right atrium. We present a case in which an anomalous venous pathway allowed decompression of the systemic venous return into the left atrium, resulting in arterial desaturation, cyanosis, and fatigue.
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PMID:Cyanosis produced by superior vena caval stenosis. 1829 Dec 6

A large proportion of patients with congenital heart disease (CHD), in particular those with relevant systemic-to-pulmonary shunts, will develop pulmonary arterial hypertension (PAH) if left untreated. Persistent exposure of the pulmonary vasculature to increased blood flow, as well as increased pressure, may result in pulmonary obstructive arteriopathy, which leads to increased pulmonary vascular resistance that, if it approaches or exceeds systemic resistance, will result in shunt reversal. Eisenmenger's syndrome, the most advanced form of PAH associated with CHD, is defined as CHD with an initial large systemic-to-pulmonary shunt that induces severe pulmonary vascular disease and PAH, with resultant reversal of the shunt and central cyanosis. The histopathological and pathobiological changes seen in patients with PAH associated with congenital systemic-to-pulmonary shunts, such as endothelial dysfunction of the pulmonary vasculature, are considered similar to those observed in idiopathic or other associated forms of PAH. A pathological and pathophysiological classification of CHD with systemic-to-pulmonary shunt leading to PAH has been developed that includes specific characteristics, such as the type, dimensions and direction of the shunt, extracardiac abnormalities and repair status. A clinically oriented classification has also been proposed. The prevalence of PAH associated with congenital systemic-to-pulmonary shunts in Western countries has been estimated to range between 1.6 and 12.5 cases per million adults, with 25-50% of this population affected by Eisenmenger's syndrome. Clinically, Eisenmenger's syndrome presents with multiple organ involvement, with progressive deterioration of function over time. The signs and symptoms of Eisenmenger's syndrome in the advanced stages include central cyanosis, dyspnoea, fatigue, haemoptysis, syncope and right-sided heart failure. Survival of patients with Eisenmenger's syndrome is clearly less than that of the general population, but appears to be better than that of patients with idiopathic PAH in a comparable functional class. The treatment strategy for patients with PAH associated with congenital systemic-to-pulmonary shunts and, in particular, those with Eisenmenger's syndrome is based mainly on clinical experience rather than being evidence based. General measures include recommendations for physical activity, pregnancy, infections, air travel, exposure to high altitudes and elective surgery, and that psychological assistance be provided as necessary. Phlebotomies are required only when hyperviscosity of the blood is evident, usually when the haematocrit is >65%. The use of supplemental oxygen therapy is controversial and it should be used only in patients in whom it produces a consistent increase in arterial oxygen saturation. Oral anticoagulant treatment with warfarin can be initiated in patients with pulmonary artery thrombosis and absent, or only mild, haemoptysis. The following three classes of drugs targeting the correction of abnormalities in endothelial dysfunction have been approved recently for the treatment of PAH: (i) prostanoids; (ii) endothelin receptor antagonists; and (iii) phosphodiesterase-5 inhibitors. The efficacy and safety of these compounds have been confirmed in uncontrolled studies in patients with PAH associated with corrected and uncorrected congenital systemic-to-pulmonary shunts, as well as in patients with Eisenmenger's syndrome. One randomized controlled trial reported favourable short- and long-term outcomes of treatment with the orally active dual endothelin receptor antagonist bosentan in patients with Eisenmenger's syndrome. Lung transplantation with repair of the cardiac defect or combined heart-lung transplantation are options for Eisenmenger's syndrome patients with a poor prognosis. A treatment algorithm based on the one used in the treatment of PAH patients is proposed for patients with PAH associated with corrected and uncorrected congenital systemic-to-pulmonary shunts and Eisenmenger's syndrome.
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PMID:Management of pulmonary arterial hypertension associated with congenital systemic-to-pulmonary shunts and Eisenmenger's syndrome. 1848 98


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