Pulmonary clinical manifestations

The spectrum of Systemic Lupus Erythematosus (SLE) includes latent lupus, discoid lupus, drug-induced lupus, neonatal lupus, lupus profundus, neuropsychiatric lupus, lupus vasculitis, pulmonary lupus, etc. The disease course is characterized by unpredictable exacerbations, drug-induced remissions and spontaneous remissions. SLE is characterized by a wide range of variable individual clinical manifestations which are controllable at early stages. 

Lymphadenopathy is most often not clinically manifested however, bright yellow plaques and a cholesterol ester content 100-fold higher than normal have been documented for both normal-size and enlarged lymph nodes in Tangier patients. Biopsies of bone marrow and the affected tissues have revealed many foam cells that are smaller than those observed in lipid storage diseases. In addition, these cells contain sudanophilic deposits which are not membrane-bound, as is the case for lysosomal storage diseases. Foam cells have also been found in otherwise normal skin, ureters, renal pelvises, tunica albuginea (white fibrous capsule) of testicles, mitral and tricuspid valves, and aorta, coronary, and pulmonary arteries. 

Eike SEE, PAN has a wide range of clinical manifestations. These include fever, weight loss, severe abdominal and musculoskeletal pain, tachycardia, acute glomerulonephritis, polyneuritis, myocardial inferction, and such pulmonary manifestations as bronchial asthma. The frequency of this disease is approximately 8 per 1,000 population, but the clinical diagnosis rate is considerably lower than postmortem studies suggest. In the United States incidence is reported to range from 3 to 4.5 cases per 100,000 population per year. Renal involvement is one of the most common and devastating aspects of... 

Clinical signs of overhydration are rare in horses with normal cardiac and renal function. The most important clinical sign of overhydration is pulmonary edema, manifested by dyspnea and a pink-white foamy nasal discharge. Treatment for overhydration should include i.v. furosemide (frusemide) (0.5-1 mg/kg) and a reduction in the rate of fluid administration. Intranasal oxygen... 

Burns JL, Ramsey BW, Smith AL. Clinical manifestation and treatment of pulmonary infections in cystic fibrosis. Adv Pediatr Infect Dis 8 53-66, 1993. 

Aberrant thrombus formation and deposition on blood vessel walls imderlies the pathogenesis of acute cardiovascular disease states which remain the principal cause of morbidity and mortality in the industrialized world [1,2,3]. Plasma proteins, proteases and specific cellular receptors that participate in hemostasis have emerged as important risk considerations in thrombosis and thromboembolic disorders. The clinical manifestations of the above disease states include acute coronary artery and cerebrovascular syndromes, peripheral arterial occlusion, deep vein thrombosis and pulmonary/renal embolism [3]. The most dilabilitating acute events precipitated by these disorders are myocardial infarction and stroke. In addition, the interplay between hemostatic factors and hypertension (4) or atherosclerosis (5) dramatically enhances the manifestation of these pathologic states. 

Heart disease is the most well-identified form of target-organ damage. A thorough cardiac and pulmonary examination can identify cardiopulmonary abnormalities. Clinical manifestations include left ventricular hypertrophy, coronary heart disease (e.g., angina, prior myocardial infarction, and prior coronary revascularization), and heart failure. These complications may lead to cardiac arrhythmias, angina, myocardial infarction, and sudden death. Coronary heart disease and associated cardiac events are the most common causes of death in hypertensive patients. 

The most serious clinical manifestation of CMV disease and the leading cause of infectious death in HSCT recipients is interstitial pneumonia (IP), which is associated with an 85% mortality rate if untreated. This clinical syndrome manifests as fever, dyspnea, hypoxia, nonproductive cough, and diffuse pulmonary infiltrates. As many as 40% of allogeneic HSCT patients will develop IP of these patients with IP, up to 40% of cases are the result of CMV. IP also may result from other infectious (P. jiroveci, varicella-zoster virus) and noninfectious causes (pulmonary damage by radiation and chemotherapy). ... 

Clinical manifestation. It includes several syndromes a) pulmotoxic and irritative syndrome - expressed by catarrhal changes on the contact mucosa and respiratory tract, toxic pulmonary oedema b) hemotoxic syndrome - expressed by severe hemolysis of different degrees, in the severe forms - hemolytic shock and anaemia c) hepatal syndrome - characterised by subicterus or icterus, increased liver and bilirubinaemia d) renal syndrome - by oliguria or anuria, pathological deviations in the urine and acute kidney insufficiency. In the extremely severe forms consciousness is disordered. Laboratory blood and urine chemical tests show evidence of phenol metabolites, data for blood damage (increased values of free hemoglobin, reduced number of erythrocytes), positive liver tests etc. 

Nitrofurantoin may cause pulmonary reactions manifested by sudden onset of dyspnea, chest pain, cough, fever, and chills. These reactions may occur rapidly (few hours) or slowly (few weeks). Chest X-rays show alveolar infiltrates or effusions an elevated sedimentation rate and eosinophilia are also present. Resolution of clinical and radiological abnormalities occurs within 24 to 48 hours after discontinuation. 

Clinical manifestations of overdose include unsteady gait, slurred speech, sustained nystagmus, somnolence, confusion, respiratory depression, pulmonary edema, and coma. 

Clinical manifestations of overdose with secobarbital include unsteady gait, slurred speech, sustained nystagmus, somnolence, confusion, respiratory depression, pulmonary edema, areflexia, and coma. Typical shock syndrome with tachycardia and hypotension, jaundice, hypothermia, followed by fever, and oliguria may occur. 

Abdominal tuberculosis (TB) is rare in childhood and usually a diagnostic challenge, particularly in the absence of active pulmonary infection, and because clinical manifestations and results of laboratory studies are nonspecific. Intestinal TB can involve any segment of the gastrointestinal tract, but has a predilection for the ileocecal valve and the adjacent ileum and cecum (Parker 2003 Engin and Balk 2005). 

Tune to event curves, based on detailed information on 629 patients, were calculated by Mudd et al. for the main clinical manifestations of homocystinuria [24], The data demonstrated that the risk for a vascular event was 25 % by age 16 years and 50 % by age 30 years for both B -responsive and B -unresponsive forms of homocystinuria (Fig. 14.2). Of the patients in whom events occurred, 51 % had peripheral vein thrombosis (with 25 % having pulmonary embolism), 32 % had cerebral vascular accidents, 11 % had peripheral arterial occlusion, 4 % had myocardial infarction, and 2 % had other ischemic events [24]. 

In acute toxicity, the main clinical manifestations are pulmonary edema, allergy, nausea, vomiting, and hemorrhage. 

In chronic toxicity, the clinical manifestations are pulmonary syndrome, skin syndrome, allergy, gastrointestinal irritations, nausea, cardiomyopathy, hematological disorders, and thyroid lesion. 

In the lung, ischaemia-reperfusion does not necessarily imply hypoxia-reoxygenation, if ventilation is maintained during the period when blood flow is impaired. Pulmonary ischaemia-reperfusion injury is clinically manifest as pulmonary oedema... 

The pulmonary toxic changes produced by anti-neoplastic agents show a structure of morphological and clinical manifestations, including noncar-diogenic pulmonary oedema and pneumonitis/fib-rosis. Hypersensitivity reactions may be associated with eosinophilic infiltration and usually lead to little residual damage. 

The authors reported that the clinical manifestations of coma, status epilepticus, cardiogenic shock, metabolic acidosis, and pulmonary edema were compatible with previously reported fatal cases of acute diphenhydramine poisoning. 

The prevalence of ILD in SjS depends on the methods used for detection. In historical series primary and secondary SjS were pooled (193-199). Lung involvement is usually subclinical. In the largest prospective study, containing 100 patients with primary SjS, about 5% had abnormal radiography, and a reduction in FVC and DLco was found at presentation in 12% and 10%, respectively (197). BAL yields an alveolitis in about half of cases without clinical manifestations (147,200). HRCT reveals abnormalities in a third of unselected patients with primary SjS (201) and in up to 89% of patients with respiratory symptoms (202), but significant pulmonary fibrosis in only approximately 20% (201,202). Over two-thirds of dyspneic patients with primary SjS have interstitial abnormalities on transbronchial biopsy (203). 

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