Cases reported "Pneumonia"

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1/112. Long-term extracorporeal bilirubin elimination: A case report on cascade resin plasmaperfusion.

    Acute hepatic failure develops as a disease entity of rather diverse origin. With disease progression, toxic bilirubin levels may cause severe complications which include AV-nodal blockage, cardiac arrhythmia, impaired consciousness, generalized seizures, and status epilepticus. Treatment choices to prevent clinical deterioration comprise of costly and limited available orthotopic liver transplantation, utilization of extracorporeal bioartificial liver support devices and haemoperfusion/plasmaperfusion treatment with activated charcoal/anion exchange filters. Here, we present a patient with acute drug-induced cholestatic hepatitis. Excessively elevated bilirubin levels were accompanied by cardiac and cerebral complications. Extracorporeal resin perfusion treatment (Plasorba, BR-350) was successfully performed over a 50-day period without activation of the coagulation system or side effects. bilirubin levels were lowered to a minimum of 225 micromol/l, with concurrent clinical improvement. In conclusion, extracorporeal anion exchange plasmaperfusion may be a viable long-term treatment for hyperbilirubinaemic side effects in overt cholestatic hepatitis.
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2/112. methotrexate pneumonitis induced by intrathecal methotrexate therapy: a case report with pharmacokinetic data.

    A patient with adenocarcinoma of the breast metastatic to the leptomeninges was treated with 10 doses of intrathecal methotrexate (MTX) administered at intervals of 2 days. Following these treatments she developed fever, hypoxemia, and bilateral pulmonary infiltrates without documented pulmonary infection. autopsy findings were consistent with the pneumonitis that has been associated with intermittent oral, intramuscular, and intravenous MTX therapy. It is suggested that this patient's pulmonary process represented MTX pneumonitis following intrathecal MTX. cerebrospinal fluid and serum MTX concentrations determined retrospectively on frozen samples reflect an atypically rapid transport of MTX from this patient's cerebrospinal fluid to a slowly decaying systemic pool. Because of this, serum MTX levels probably exceeded 10-8M during the entire 20-day course of therapy, thus exposing the pulmonary parenchyma to significant drug concentrations for a prolonged interval. It is suggested that these unfavorable pharmacokinetics may have contributed to this patient's susceptibility to MTX pneumonitis.
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3/112. amoxicillin/clavulanate-associated hepatic failure with progression to stevens-johnson syndrome.

    OBJECTIVE: To describe a patient who developed hepatic failure, stevens-johnson syndrome (SJS), and died after receiving amoxicillin/clavulanate therapy. CASE SUMMARY: A 37-year-old white man without significant past medical history received a 10-day course of amoxicillin/clavulanate for treatment of pneumonia. Thirty-two days after starting amoxicillin/clavulanate, he developed jaundice, rash, pruritus, and increasing fatigue. On further evaluation, with the exclusion of toxicity from other drugs or diseases, the time course to development of cholestatic jaundice correlated with the use of amoxicillin/clavulanate. The patient consequently died with progressive hepatic failure, renal failure, and SJS. DISCUSSION: Hepatic injury has been reported with amoxicillin/clavulanate. signs and symptoms of jaundice and pruritus may appear up to to six weeks after stopping therapy. Most cases of liver injury have been benign and reversible on discontinuation of the amoxicillin/clavulanate. Reported hepatic reactions have been mainly cholestatic, with some mixed cholestatic/hepatocellular liver function test abnormalities. CONCLUSIONS: Clinicians should be aware of amoxicillin/clavulanate as a drug capable of causing hepatitis with eventual systemic dysfunction. While recovery is usually complete following withdrawal of the drug, in patients with rash associated with hepatic dysfunction, renal insufficiency, or other unusual symptoms, earlier consideration of initiating systemic steroids or liver transplantation referral, in hopes of avoiding progressive systemic response, might be worthwhile.
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4/112. fever and pneumonia in a steroid treated patient with systemic lupus erythematosus.

    Systemic lupus erythematosus is reported to affect the lungs in almost half of patients, but pleuritis is most commonly encountered. Acute pneumonitis is an uncommon but recognized manifestation of SLE. infection and drug reactions are more frequently diagnosed. The case discussed below permits consideration of the dilemmas typical of the SLE patient who presents with an acute pulmonary process.
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5/112. Recurrent flu-like illness with migrating pulmonary infiltrates of unknown aetiology.

    Migrating pulmonary infiltrates present a difficult diagnostic and therapeutic challenge. We report on eight patients (mean age 51 years, range 32-78 years, with a prolonged history of migrating pulmonary infiltrates of unknown aetiology despite a very elaborate search for infectious causes, hypersensitivity pneumonitis or inhalation fever due to occupational or domestic exposure to fungi, or to other environmental causes, and for humoral or cellular immunological incompetence. These patients (one male, seven females) presented with recurrent episodes (mean 6, range 2-13) of a flu-like illness, often with cough, wheezing and pleuritic chest pain, but without systemic involvement. Previous medical histories were unremarkable. There was no relation with smoking habits, occupation, drug use or other possible exposures. Biochemical data were non-specific. There was no peripheral nor pulmonary eosinophilia; total IgE was normal, with negative RASTs and precipitins to a variety of antigens. Cultures and serological tests for bacteria, viruses, fungi, etc were non-contributory. Chest X-ray and computed tomography (CT) scan showed bilateral migratory pulmonary infiltrates, with a predilection for the middle and lower lung zones, often with a minor-to-moderate pleural effusion. Lung function tests were usually normal; at the most a slight decrease in diffusing capacity was noted in some patients. There was no or only a slight response to antimicrobials; systemic corticosteroids were not given. Further evolution was benign with patients being asymptomatic between the episodes. Despite elaborate investigations, the cause of these 'pneumonias' remains frustratingly unknown.
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6/112. Acute lupus pneumonitis mimicking pulmonary tuberculosis: a case report.

    We report a case of systemic lupus erythematosus in a 15-year-old girl with initial presentation as acute lupus pneumonitis. A fulminant course with pancytopenia and respiratory distress were developed 3 weeks after symptom onset. Chest radiographs revealed an interstitial pattern with miliary nodules over bilateral lower lung fields that mimics miliary tuberculosis. The patient was treated with intravenous immunoglobulin and antituberculosis drugs because the infection-associated hemophagocytic syndrome and pulmonary tuberculosis could not be excluded from the clinical course. The response to antituberculosis treatment, however, was poor and her respiratory condition deteriorated rapidly to impending respiratory failure 1 week after admission. Systemic lupus erythematosus with acute lupus pneumonitis was then diagnosed based on the fulminant clinical course and accordant laboratory results. Corticosteroid (methylprednisolone) and cytotoxic agent (cyclophosphamide) pulse therapies were applied twice and once, respectively. She recovered gradually after receiving the immunotherapy.
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7/112. Drug-induced linear IgA bullous disease following antibiotics.

    A 69-year-old woman presented with pneumonia and subacute bacterial endocarditis. Nine days after intravenous vancomycin and ciprofloxacin were commenced, the patient developed a bullous mucocutaneous eruption. Clinical presentation and histopathology were consistent with drug-induced linear IgA bullous disease (LABD). The patient's lesions resolved with cessation of antibiotics. A review of the features of drug-induced LABD and the drugs that have been implicated are presented.
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8/112. disopyramide-induced pneumonitis, diagnosed by lymphocyte stimulation test using bronchoalveolar lavage fluid.

    A 72-year-old man was admitted to our hospital with fever and cough. He had been on disopyramide treatment for nine days to control cardiac arrhythmia. On admission, chest X-ray examination revealed reticulonodular opacities in both lungs, and impending respiratory failure was evident. A differential cell count of the bronchoalveolar lavage fluid (BALF) showed a marked increase of lymphocytes. A lymphocyte stimulation test (LST) for disopyramide using BALF was positive, although the test using peripheral blood was negative. This case suggests that LST using BALF is useful for the diagnosis of drug-induced pneumonitis.
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9/112. Pulmonary toxicity secondary to procarbazine.

    procarbazine is a chemotherapy methylating agent that has been used in combination with other drugs, perhaps most successfully in the treatment of Hodgkin's disease. There are several side effects that it is commonly associated with; however, it has only rarely been reported to cause lung injury. The resulting pneumonitis may be severe and irreversible. There are eight reported cases in the literature. Here, we report another such case.
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10/112. 3: Community-acquired pneumonia.

    Community-acquired pneumonia is caused by a range of organisms, most commonly streptococcus pneumoniae, mycoplasma pneumoniae, chlamydia pneumoniae and respiratory viruses. Chest x-ray is required for diagnosis. A risk score based on patient age, coexisting illness, physical signs and results of investigations can aid management decisions. patients at low risk can usually be managed with oral antibiotics at home, while those at higher risk should be further assessed, and may need admission to hospital and intravenous therapy. For S. pneumoniae infection, amoxycillin is the recommended oral drug, while benzylpenicillin is recommended for intravenous use; all patients should also receive a tetracycline (eg, doxycycline) or macrolide (eg, roxithromycin) as part of initial therapy. Flucloxacillin or dicloxacillin should be added if staphylococcal pneumonia is suspected, and gentamicin or other specific therapy if gram-negative pneumonia is suspected; a third-generation cephalosporin plus intravenous erythromycin is recommended as initial therapy for severe cases. Infections that require special therapy should be considered (eg, tuberculosis, melioidosis, legionella, acinetobacter baumanii and pneumocystis carinii infection).
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