Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report here two cases of Legionella pneumophila pneumonia that were markedly improved by parenteral ciprofloxacin administration. A 69-year-old man who had previously visited a hot spring was admitted to our hospital with severe pneumonia and a 48-year-old man with dilated cardiomyopathy as an underlying disease was also hospitalized because of heart failure and pneumonia. In both cases a urinary antigen test for L. pneumophila was negative at the incipient stage, and the initial treatment with a beta-lactam agent was ineffective. However, the high titer of L. pneumophila serogroup 6 antigen in the serum at the convalescent stage revealed that these two pneumonia cases were caused by L. pneumophila, and the following intravenous administration of ciprofloxacin was highly effective. We concluded that intravenous treatment with ciprofloxacin could be effective against L. pneumophila pneumonia, which is sometimes hard to diagnose in the acute phase.
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PMID:[Two cases of Legionella pneumophila pneumonia improved by parenteral ciprofloxacin administration]. 1277 3

Myocarditis is inflammation of cardiac muscle, which may be acute, subacute, or chronic with either focal or diffuse involvement of the myocardium. This leads to a cardiomyopathy with clinical features of heart failure as well as echocardiographic evidence of global dilation of the cardiac chambers. There are numerous reports in the literature of viral myocarditis causing dilated cardiomyopathy; however, there are no reports of recurrent viral myocarditis and vaccine-associated myocarditis in a single patient with complete reversal of the cardiomyopathy and return to normal cardiac function. We present a case of recurrent myocarditis in a female patient caused by a viral upper respiratory infection and streptococcal pneumonia vaccination who presented with recurrent episodes of reversible cardiomyopathy.
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PMID:Recurrent reversible dilated cardiomyopathy secondary to viral and streptococcal pneumonia vaccine-associated myocarditis. 1678 23

A 44-year-old man was treated with amiodarone for dilated cardiomyopathy. After 53 months, he developed amiodarone-induced interstitial pneumonia. Amiodarone treatment was terminated, and the patient was given corticosteroids. These treatments were effective. However, pneumonitis recurred whenever prednisolone was reduced to less than 5 mg per day. Considering the patient's background characteristics, we considered his body mass index (BMI, kg/m(2)) and found his to be high. When four additional patients with amiodarone pulmonary toxicity were reviewed at our institute, a correlation between BMI and the duration of shadow disappearance was found (R(2)=0.8695). Because amiodarone is lipophilic, the patient's high BMI might have influenced the repeated appearance of pulmonary toxicity.
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PMID:Amiodarone pulmonary toxicity: a patient with three recurrences of pulmonary toxicity and consideration of the probable risk for relapse. 1717 May 5

An 82-yr-old man was presented with fever and cough accompanied by generalized erythematous rash. He had taken mexiletine for 5 months, as he had been diagnosed with dilated cardiomyopathy and ventricular arrhythmia. Laboratory studies showed peripheral blood eosinophilia and elevated liver transaminase levels. Chest radiographs showed multiple nodular consolidations in both lungs. Biopsies of the lung and skin lesions revealed eosinophilic infiltration. After a thorough review of his medication history, mexiletine was suspected as the etiologic agent. After discontinuing the mexiletine and starting oral prednisolone, the patient improved, and the skin and lung lesions disappeared. Subsequently, mexiletine was confirmed as the causative agent based on a positive patch test. Drug-induced hypersensitivity syndrome is a severe adverse reaction to drugs and results from treatment with anticonvulsants, allopurinol, sulfonamides, and many other drugs. Several cases of mexiletine-induced hypersensitivity syndrome have been reported in older Japanese males with manifestation of fever, rash, peripheral blood eosinophilia, liver dysfunction without other organ involvement. Here, we report a case of mexiletine-induced hypersensitivity syndrome which presented as eosinophilic pneumonia in a Korean male.
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PMID:A case of mexiletine-induced hypersensitivity syndrome presenting as eosinophilic pneumonia. 2005 62

Infections in solid-organ transplant recipients are the most important causes of morbidity and mortality. A primary goal in organ transplant is the prevention or effective treatment of infection, which is the most common life-threatening complication of long-term immunosuppressive therapy. A 21-year-old woman who underwent heart transplant 3 years previous owing to dilated cardiomyopathy was referred to our hospital with symptoms of high fever and cough. The patient's history revealed that she had received a trimethoprim-sulfamethoxazole double-strength tablet each day for prophylactic purposes. On chest radiograph, pneumonia was detected, and in broncho-alveolar lavage sample, Pneumocystis jiroveci cysts were found. After diagnosing P. jiroveci pneumonia, trimethoprim-sulfamethoxazole was initiated at 20 mg/kg/d including intravenous trimethoprim in divided dosages every 6 hours. On the sixth day of therapy, she died in intensive care unit. In solid-organ transplant recipients, although antipneumocystis prophylaxis is recommended within the first 6 to 12 months after transplant, lifelong prophylaxis is also used in several settings. In addition, the physician should keep in mind that P. jiroveci pneumonia may develop in solid organ recipients, despite trimethoprim-sulfamethoxazole prophylaxis.
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PMID:A heart transplant recipient lost due to Pneumocystis jiroveci pneumonia under trimethoprim-sulfamethoxazole prophylaxis: case report. 2114 1

A 50-year-old man who underwent hemodialysis (HD) at local outpatient HD center due to end-stage renal disease (ESRD) was transferred to our hospital because of pneumonia. He had severe emaciation and past history of congestive heart failure. Presenting symptoms almost consistently involved difficulty in hearing and recurrent attacks of migraine-like headaches. He was diagnosed with dilated cardiomyopathy, showing diastolic mechanical dyssynchrony by tissue Doppler echocardiography. On the day of death, he had hematemesis and hemorrhagic shock. Autopsy revealed perforation of duodenum, and genetic analysis using mitochondrial DNA from cardiac muscle and iliopsoas muscle revealed a 3243A > G mutation in the mitochondrial tRNA(Leu(UUR)) gene, which is related to mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). Multiple organ failure due to the mutation of mitochondrial DNA with gastrointestinal bleeding is not a common.
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PMID:An autopsy case of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) with intestinal bleeding in chronic renal failure. 2163 Dec 36

The patient presented himself at the primary practitioner with dyspnoea and chest pain, and was initially misdiagnosed as having pneumonia. Two weeks later the patient developed universal oedema and was hospitalized. Echocardiography showed dilated cardiomyopathy. The initial diagnosis was delayed because the patient was not asked about his possible drug abuse. Remember to ask about drug abuse in younger patients with dyspnoea and uncharacteristic chest pains.
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PMID:[Dilated cardiomyopathy in an amphetamine user]. 2167 69

A 49-year-old man with an 11 year history of dilated cardiomyopathy presented with a worsening of symptoms associated with an upper respiratory tract infection. During his hospitalisation, a central venous catheter (CVC) was inserted and this was complicated by pulmonary infarct from an air embolism. The infarct had the appearance of a round pneumonia on radiography. The patient died one week after the CVC insertion from cardiogenic shock and multi-organ failure.
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PMID:Pulmonary infarction from central venous air embolism mimicking round pneumonia. 2168 80

It has been suggested that oseltamivir-resistant influenza viruses harboring the H274/275Y mutation are less virulent than are those that are oseltamivir-sensitive, and fatality attributed to infection with an oseltamivir-resistant virus is very rare. Here we report the first fatal adult case of oseltamivir-resistant 2009 pandemic influenza A (H1N1) in Korea. A 60-year-old Korean male who had hypertension, diabetes mellitus, chronic kidney disease, and dilated cardiomyopathy visited Chonnam National University Hospital because of a 7-day history of chest pain and dyspnea. The patient was at another clinic and had been medicated with oseltamivir (75 mg twice daily) beginning 7 days before admission. Empirical antibiotics were started on the first day of hospitalization. Reverse-transcriptase polymerase chain reaction for 2009 pandemic influenza A (H1N1) was reported to be positive, and a double dose of oseltamivir (150 mg twice per day) was started on day four of hospitalization. However, the pneumonia worsened and the patient died, despite 3 days of high-dose antiviral therapy and 6 days of antibacterial therapy. An H275Y mutation was detected in the neuraminidase gene sequence. This case shows that oseltamivir resistance after short-term drug exposure is possible and can be fatal, emphasizing that early use of zanamivir should be considered in suspicious cases.
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PMID:First Fatal Oseltamivir-Resistant 2009 Pandemic Influenza A (H1N1) Case in an Adult in Korea. 2211 Oct 74

A 43-year-old man with a cardiac device for dilated cardiomyopathy presented with fever, night sweats, and weight loss. Investigations revealed pancytopenia, acute renal failure, abnormal lung function, and raised inflammatory markers. A renal biopsy demonstrated pauci-immune necrotizing crescentic glomerulonephritis. He was diagnosed with pulmonary-renal antineutrophil cytoplasmic antibody-negative systemic small vessel vasculitis. He commenced immunosuppression with prednisolone and cyclophosphamide with recovery from pancytopenia and improvement in renal function 3 months later. Subsequently, a bone marrow culture grew Mycobacterium fortuitum. Isolation on repeat peripheral mycobacterial blood cultures prompted treatment with ciprofloxacin and clarithromycin. Four months later, he presented with neutropenic sepsis, influenza A/H1N1, and Aspergillus flavus pneumonia. Despite treatment he deteriorated. A transthoracic echocardiogram revealed a vegetation on the right ventricular pacing wire. The device was removed. The vegetation revealed acid and alcohol fast bacilli on Ziehl-Neelsen staining and grew M. fortuitum on culture, sensitive to ciprofloxacin and clarithromycin. Despite device removal and antimicrobial therapy, the patient succumbed to treatment-related complications. The association between glomerulonephritis and endocarditis is well known; however, this is the first case to our knowledge describing pauci-immune necrotizing crescentic glomerulonephritis in the context of M. fortuitum endocarditis. Clinicians should maintain a high index of suspicion for endocarditis in patients with a cardiac device who present with fever and pauci-immune necrotizing crescentic glomerulonephritis. Patients should be investigated with mycobacterial blood cultures, at least three sets of standard blood cultures and transthoracic and transesophageal echocardiography. Clinicians should beware the perils of immunosuppression in the face of an occult sepsis.
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PMID:Fortuitous vasculitis. 2225 Jul 55


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