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Query: UMLS:C0392680 (shortness of breath)
 5,217 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Iron deficiency, the most common cause of anemia, is prevalent in 10 percent to 30 percent of the world's population. Inadequate intake of iron may be an important causative factor, particularly when the body requires more iron than usual (e.g., during infancy, early childhood, adolescence, pregnancy and periods of blood loss). The popular increase of fiber in diets may increase the incidence of iron-deficiency anemia because too much fiber in the diet renders available iron unabsorbable. Symptoms in children include skin or conjunctival pallor, excessive sleepiness, learning disabilities, diminished attention span, tiredness, irritability or inappropriate behavior, and pica. Adults may have shortness of breath, decrease in exercise tolerance, palpitations, tachycardia, angina, congestive heart failure, orthopnea and edema. Iron deficiency occurs in sequential states and is measured by many laboratory tests. The levels of hemoglobin and hematocrit are both decreased, while the red blood cell count may be normal initially, but will decrease as the iron-deficiency state continues. The steps of treatment include correction of the underlying disorder, administration of the amount of iron needed and observation of the response to treatment.
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PMID:A guide to primary care of iron-deficiency anemia. 143 77

A prospective phase II trial was conducted to assess the feasibility, tolerance, and efficacy of a device designed for selective removal of rheumatoid factor from the plasma of rheumatoid arthritis patients. The device contained terpolymer hydrogel-coated plates with chemically attached, aggregated human immunoglobulin G, and it operated as an immunoaffinity column. Sixty-one patients aged 25 to 73 underwent weekly plasmapheresis treatments (the primary therapy phase). During the trial, patients continued current rheumatoid arthritis medications without dose adjustments. All patients received two to six treatments (primary therapy). Responding patients were eligible to continue apheresis treatment every 2 to 6 weeks (maintenance therapy). No serious, untoward side effects were noted in the course of this study; of 640 treatments, only 2 (in different patients) were aborted, one because of complaints of dizziness and angioedema and the other because of chest tightness and shortness of breath. Except for a significant (p less than 0.05) decrease in serum iron, no significant changes in complete blood count, serum electrolytes, renal and hepatic function tests, or serum C3 and C4 were noted. Although the trial was not designed to determine clinical efficacy, patients noted less morning stiffness, longer time to onset of fatigue, and improved global pain assessment (p less than 0.004); significant objective improvements were noted in joint pain, tenderness, swelling, and the number of affected joints (p less than 0.001). One-half of the treated patients had at least a 50 percent improvement in objective measures of antirheumatic activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Selective in vivo removal of rheumatoid factor by an extracorporeal treatment device in rheumatoid arthritis patients. 199 91

This report describes a rare case of bronchial mucosal injury caused by aspiration of a delayed-iron tablet. A 44-year-old woman had been taking delayed-iron tablets (Feto-Gradumet) regularly because of iron deficiency anemia, and accidentally aspirated a tablet into her bronchus. After this accident, she had complained of wheezing and shortness of breath. On bronchoscopy, the bronchial mucosa of left lower lobe initially showed remarkable swelling and redness, and became corroded and narrowed gradually by iron toxicity over several months, although we tried to remove some fragments of tablet as completely as possible. While we had examined her bronchi repeatedly by bronchoscopy, the bronchial mucosa gradually normalized during 15 months, but moderate stenosis of the left basal bronchus remained. The pathological findings showed infiltration of inflammatory cells, edema and granuloma formation in the submucosal region. This report suggests that the bronchial injury was due to the toxicity of persistent ferrous sulfate eluted from the iron tablet which had adhered firmly to the wet bronchial wall for a long time.
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PMID:[A case of remarkable bronchial stenosis due to aspiration of delayed-release iron tablet]. 274 79

A case report is presented of a 78-year-old patient with recurrent gastrointestinal bleeding who required frequent hospitalizations and several blood transfusions, both of which ceased after the institution of estrogen-progesterone therapy. The patient was hospitalized in April 1985 with weakness and shortness of breath. Her hemoglobin was 9.8. Indices were suggestive of a microcytic hypochromic anemia. Bone marrow revealed absent iron stores. The patient denied a prior history of melena, hematochezia, or hematemesis. There was no history of peptic ulcer disease. The patient was taking no medications, and she denied alcohol abuse and a family history of bleeding. The physical examination revealed a pale and weak appearing women in no acute distress. An aortic stenosis and mitral insufficiency murmur was her only positive physical finding. Hemoccult positive stool was detected on rectal examination. The patient was transfused with 2 units of packed cells and underwent an evaluation. Subsequently, the patient required 4 more hospitalizations requiring blood transfusions. In October 1985, the patient underwent an exploratory laparotomy and an intraoperative endoscopy of the entire gastrointestinal tract. There was evidence of bleeding in the cecum near the ileocecal valve. The patient underwent an ascending colectomy. The histopathology of the specimen revealed angiodysplasia of the cecum. Postoperatively, during a 5-month period, the patient required 16 units of blood. In March 1985, Enovid E was started, and the patient has not required further hospitalizations or a blood transfusion since. The only side effects of the estrogen-progesterone combination which this patient experienced were vaginal bleeding and mild systolic hypertension. In patients with gastrointestinal angiodysplasia who have cryptogenic gastrointestinal bleeding, despite the use of therapeutic endoscopy and surgery, possibly a trial of estrogen-progesterone therapy should be considered.
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PMID:Estrogen-progesterone therapy for recurrent gastrointestinal bleeding secondary to gastrointestinal angiodysplasia. 325 72

Two solderers exposed to fumes of galvanized metal reported a history of shortness of breath and fever which occurred during the evening and night of days spent at work. Specific inhalation challenges performed by asking subjects to do soldering on galvanized iron revealed a late bronchospastic reaction. One subject also demonstrated a significant increase in oral temperature and peripheral neutrophils. Environmental measurements revealed the presence of zinc after soldering on galvanized metal. This contaminant was not present after a control exposure while soldering on iron. Although metal fume fever has been described in workers exposed to fumes of galvanized metal, this is the first account of occupational asthma due to this agent.
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PMID:Occupational asthma due to fumes of galvanized metal. 360 11

Dietary cells and the vitamins B12 and folate are necessary for the production of the red blood cells (erythrocytes), which carry oxygen from the lungs to the tissues and carbon dioxide from tissues to lungs. Deficiency of either one results in anaemia, which is characterised by low haemoglobin concentration. Symptoms result from reduced tissue oxygenation and include weakness, lethargy, palpitation, headache and shortness of breath. The first-time laboratory test of all patients suspected of being anaemic is the full blood count. Results of a full blood count may suggest the anaemia is caused by a nutritional deficiency of B12 folate or iron. Laboratory measurement of the concentration in blood of iron and vitamin B12 and folate, along with several other tests described here, are useful in the differential diagnosis of the anaemic patients.
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PMID:Deficiency testing for iron, vitamin B12 and folate. 760 52

A 43-year-old man began having malaise, chills, and fever 12 hours after cutting a galvanized steel grating with an acetylene torch at work. Over the next 72 hours, his symptoms persisted and became worse with progressive shortness of breath. He was admitted to the hospital and begun on antibiotics and steroids. The next day his condition had deteriorated to the point that he had to be intubated. Chest x-ray film and computed tomography showed patchy and interstitial infiltration bilaterally, consistent with acute respiratory distress syndrome. Open lung biopsy showed focal mild interstitial pneumonia. Multiple laboratory studies were negative for an infectious or an immune process. The patient remained on mechanical ventilation for 10 days and was discharged from the hospital 2 days after extubation. He continued to improve, with minimal symptoms and a return to normal activity levels several months after the incident with no continued treatment. Re-creation of his exposure was done under controlled circumstances, with air sampling revealing elevated air levels for cadmium and zinc and borderline levels of arsenic, manganese, lead, and iron.
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PMID:Acute respiratory distress syndrome in a welder exposed to metal fumes. 1034 99

A 28-year-old female presented for evaluation of left flank pain and polyuria after having been exposed to cadmium in the jewelry manufacturing industry for approximately 3 years. This patient possessed both elevated 24-hr urinary ss2-microglobulin and elevated blood cadmium levels. Approximately 6 months after initial presentation, the patient resigned from her job due to shortness of breath, chest pain, and anxiety. Exposure to cadmium in the jewelry industry is a significant source of occupational cadmium exposure. Other occupational sources include the manufacture of nickel-cadmium batteries, metal plating, zinc and lead refining, smelting of cadmium and lead, and production of plastics. Cadmium is also an environmental pollutant that accumulates in leafy vegetables and plants, including tobacco. Major toxicities anticipated from cadmium exposure involve the renal, pulmonary, and, to a lesser extent, gastrointestinal systems. These include the development of renal proximal tubular dysfunction, glomerular damage with progressive renal disease, and respiratory symptoms including pneumonitis and emphysema. Low-level cadmium exposure has also been associated with increased urinary calcium excretion and direct bone toxicity, effects that recent research suggests may result in the development of osteoporosis. The body burden of cadmium, over half of which may reside in the kidneys, is most often measured through the use of urinary cadmium levels. Blood cadmium measurements generally reflect current or recent exposure and are especially useful in cases with a short exposure period and only minimal accumulation of cadmium in the kidneys. Both ss2-microglobulin and alpha1-microglobulin serve as organ-specific, early-effect biomarkers of tubular proteinuria and thus play a role in identifying early signs of cadmium-induced renal damage in those with potential exposures. In addition to ensuring workplace compliance with Occupational Safety and Health Administration-mandated monitoring and screening measures, it is prudent for those with cadmium exposure to maintain adequate intake of both iron and calcium, appropriate measures even in the absence of exposure.
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PMID:Cadmium exposure and nephropathy in a 28-year-old female metals worker. 1246 Aug 7

Many patients in our nephrology department who have anaemia and chronic kidney insufficiency (CKI) show evidence of congestive heart failure (CHF). This triad of anaemia, CKI and CHF is known as the cardio-renal anaemia syndrome. The three conditions form a vicious circle, in which each condition is capable of causing or being caused by another. Anaemia can increase the severity of CHF and is associated with a rise in mortality, hospitalization and malnutrition. Anaemia can also further worsen renal function and cause a more rapid progression to dialysis than is found in patients without anaemia. Uncontrolled CHF can cause rapid deterioration of renal function and anaemia. CKI can also cause anaemia, as well as worsen the severity of CHF, and is associated with increased mortality and hospitalization in patients with CHF. Aggressive therapy against CHF with all the conventional medications at the accepted doses often fails to improve the CHF if anaemia is also present but is not treated. In studies in which the anaemia was corrected with s.c. erythropoietin and, in some cases, with i.v. iron, however, the cardiac function improved, as assessed by measurement of the left ventricular ejection fraction and oxygen utilization during maximal exercise. Symptomatic patient functioning improved, as monitored by shortness of breath and fatigue on exertion, and the need for hospitalization and oral and i.v. diuretics markedly decreased. The quality of life, as judged by different criteria, also improved. The glomerular filtration rate, which fell rapidly when the anaemia was untreated, stabilized in patients when their anaemia was treated. Nephrologists need to assess the cardiac status of all patients with CKI carefully, and this includes an echocardiogram along with possibly measuring the levels of B-type natriuretic peptide. Nephrologists also need to use the indicated agents for CHF at the recommended doses, while cardiologists and internists need to be more aware of the importance and lethal effects of even mild anaemia and the benefits of its treatment in CHF and CKI. Cooperation between these specialists will allow better and much earlier treatment of the anaemia, CHF and CKI, and prevent the deterioration of all three conditions.
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PMID:The cardio-renal anaemia syndrome: does it exist? 1460 93

This is a population-based study on the prevalence of respiratory symptoms assessed by a mail questionnaire. The objective was to examine if work in an iron mine increased the risk of airway symptoms or obstructive diseases. The exposed group consisted of 114 previous or current male miners. Referents, 2472 males from the province, had never been employed by the mining company or worked as miners. Age, smoking and a family history of asthma were considered as possible confounders. The miners had an increased risk for respiratory symptoms (OR=2.2, 95% CI=1.4-3.1) including recurrent wheeze (OR= 2.4, 95% CI= 1.5-3.9), longstanding cough (OR= 1.8, 95% CI = 1.0-3.2), and for physician-diagnosed chronic bronchitis (OR=2.2, 95% CI= 1.0-4.5). Attacks of shortness of breath and asthma manifestations were similar between miners and referents. Higher risks in miners were found particularly among the non-smokers for physician-diagnosed chronic bronchitis (OR=9.2, 95% CI= 3.0-28) and for symptoms as well. A family history of asthma was less common among miners (9.2% vs. 17%, p < 0.05). We conclude that miners in a modern underground iron mine had an increased risk of respiratory symptoms. In contrast to other studies, this increased risk was particularly found in nonsmokers. A family history of asthma may be an important confounder in occupational studies of respiratory diseases.
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PMID:Respiratory symptoms and obstructive lung diseases in iron ore miners: report from the obstructive lung disease in northern Sweden studies. 1557 54


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