Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 32-year-old male was admitted to our hospital complaining of fever and dyspnea on effort. Laboratory data on admission indicated leukocytosis and elevation of C-reactive protein. A chest radiograph showed diffuse reticulonodular shadows in both lower lung fields, and a chest computed tomography showed centrilobular reticulonodular opacity. Bronchoscopic findings revealed a large amount of slightly yellowish secretion in all bronchi. Cells found in the bronchoalveolar lavage fluid (BALF) included 61% neutrophils. Haemophilus influenzae was isolated from cultures of the BALF and sputum. Transtracheal lung biopsy specimens showed focal infiltration of neutrophils in the alveoli, and the pathological findings in the lung were compatible with bronchiolopneumonia. Since the CD4/CD8 ratio was 0.09 and a positive reaction was obtained for anti-human immunodeficiency virus (HIV) antibody, HIV-associated pneumonia due to H. influenzae was diagnosed. Seven days' administration of cefozopran improved the patient's condition. It is interesting that radiological findings are often unusual in HIV-infected patients with H. influenzae pneumonia.
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PMID:[A case of AIDS-associated Haemophilus influenzae pneumonia with diffuse reticulonodular shadows]. 1264 13

A 41-year-old man was hospitalized, presenting increasing dyspnea and extensive ground-glass opacities on chest X-ray. Infection by human immunodeficiency virus was confirmed. Cytologic examination of bronchoalveolar lavage fluid revealed numerous trichomonads and aggregates of Pneumocystis sp. Treatment was followed by rapid improvement of respiratory symptoms and chest X-ray. The trichomonad species found in the lungs was identified as Trichomonas vaginalis by small-subunit rRNA gene amplification and sequencing. With the exception of rare cases of contamination of newborn babies during delivery, T. vaginalis has never been found in lungs in healthy or immunocompromised adults. In the present case, T. vaginalis is found as coinfecting agent. Our data, like those found in the literature, suggest that trichomonads are overlooked parasites that may be regularly implicated in diverse human pathologies.
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PMID:Pulmonary coinfection by Trichomonas vaginalis and Pneumocystis sp. as a novel manifestation of AIDS. 1279 27

The characteristics of cardiac tamponade in patients with human immunodeficiency virus (HIV) disease were examined by evaluating the cases, case series, and related articles, including autopsy series, identified through a comprehensive literature search. One-hundred eighty-five cases of cardiac tamponade have been reported in patients with HIV disease. Sex data were available in 176 patients, of whom 154 (87%) were males. The mean age was 34.7 +/- 10.4 years (range, 11 months to 61 years). Mean CD4 cell count was 98 +/- 95 cells/mm3 (range, 3 to 430 cells/mm3). The most common etiology of pericardial tamponade was mycobacterial infection (78 patients), including Mycobacterium tuberculosis, Mycobacterium avium-intracellulare, and Mycobacterium kansasii. A bacterial cause was found in 20 patients (11%). Staphylococcus aureus was the predominant bacteria, followed by streptococci, Pseudomonas aeruginosa, Listeria monocytogenes, Klebsiella pneumoniae, and Rhodococcus equi. Lymphoma was found in 15 (8%) patients and Kaposi sarcoma in 13 (7%) patients. Numerous unusual organisms, including Cryptococcus neoformans, Nocardia asteroides, Aspergillus species, cytomegalovirus, and herpes simplex were also associated with cardiac tamponade in HIV patients. Occasionally, HIV itself was involved in the pathogenesis. In 48 patients (26%), no cause was found or reported. The most common clinical presentation was dyspnea, followed by fever, cough, chest pain, and cardiac arrest. The predominant pericardial fluid color composition was serosanguineous. The majority of patients died during hospitalization or in the immediate follow-up period. Vigilance for cardiac tamponade in patients with HIV disease, especially in those with opportunistic infections and/or malignancies, and cardiac symptoms, may result in early and proper management of cardiac tamponade in these patients.
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PMID:Cardiac tamponade in patients with human immunodeficiency virus disease. 1293 67

PRESENTING FEATURES: A 53-year-old man who had human immunodeficiency virus (HIV) presented to the Johns Hopkins Hospital with a 3-month history of increasing dysphagia, cough, dyspnea, chest pain, and an episode of syncope. His past medical history was notable for oral and presumptive esophageal candidiasis that was treated with fluconazole 6 months prior to presentation. Three months prior to presentation, he discontinued his medications, and his symptoms of dysphagia recurred. During that time he developed intermittent fevers and chills, progressively worsening dyspnea on exertion, and a cough productive of white sputum. He also reported a 40-lb weight loss over the past 3 months. On the day prior to presentation, he had chest pain and shortness of breath followed by weakness, dizziness, and a brief syncopal episode. He denied orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, jaundice, hemoptysis, hematemesis, melena, hematochezia, or diarrhea. There was no history of alcohol use, and he stopped smoking tobacco approximately 1 month previously. He smoked cocaine but denied injection drug use. The patient had never been on antiretroviral therapy and had never had his CD4 count or viral load measured. On physical examination, the patient was a thin, cachectic man who appeared older than his stated age. His vital signs were notable for blood pressure of 102/69 mm Hg, resting tachycardia of 102 beats per minute, resting oxygen saturation of 92% on room air, normal resting respiratory rate, and a temperature of 38.1 degrees C. His oropharynx was clear, with no signs of thrush or mucosal ulcers. His pulmonary examination was notable for diminished breath sounds in the lower lung fields bilaterally. Cardiac, abdominal, and neurologic examinations were normal. His skin was intact, with no visible petechiae, rashes, nodules, or ulcers. Laboratory studies showed a total white blood cell count of 3.2 x 10(3)/microL, with a total lymphocyte count of 330/microL, hematocrit of 30.2%, a serum sodium level of 129 mEq/L, and a serum lactate dehydrogenase level of 219 IU/L. The patient had an absolute CD4 count of 8 cells/mm3 and a HIV viral load of 86,457 copies/mL. His arterial blood gas on room air had a pH of 7.51, a PCO2 of 33 mm Hg, and a PO2 of 55 mm Hg. Electrocardiogram and serial serum cardiac enzymes were normal. A chest radiograph showed bilateral upper lobe patchy infiltrates with left upper lobe consolidation. Computed tomographic (CT) scan of the chest with contrast showed bilateral ground glass infiltrates with focal consolidation (Figure 1) and no evidence of pulmonary embolism. Induced sputum was negative for Pneumocystis carinii, fungi, or acid-fast bacilli. A bronchoalveolar lavage was performed. What is the diagnosis?
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PMID:Cases from the Osler Medical Service at Johns Hopkins University. Diagnosis: P. carinii pneumonia and primary pulmonary sporotrichosis. 1533 85

A 11-year-old female admitted to our hospital because of erythema of the face and the trunk, and a wide and dense cluster of verruca vulgaris on the right sole. She had no family history of immunodeficiency, no perinatal abnormality, no growth abnormality, or no history of severe infections. From the age of 4 years, she noticed erythema around her nose. At the age of 9 years, small erythema and papules appeared on her chest. In January, 2003, erythema around her nose and papules of the trunk spread rapidly, and she also felt fatigue and effort dyspnea. Laboratory examinations revealed near absence of serum IgG, and IgE, high serum IgM (525 mg/dl), and normal IgA and IgD. Thl/Th2 ratio was 36.9. We diagnosed her as having hyper-IgM syndrome. Histological examinations of a skin biopsy showed the infiltration composed of mainly histiocytes,and mildly atypical CD8 + T cells around the blood vessels in the dermis. We concluded her skin manifestations as reactive lymphohistiocytic infiltration at the base of immunodeficiency and durable stimulation of various antigens. Her skin manifestations improved transiently by the intravenous immunogrobulin and corticosteroids therapy.
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PMID:[A female case of hyper-IgM immunodeficiency syndrome with uncommon skin manifestations]. 1555 25

Heart failure is a common, progressive, complex clinical syndrome with high morbidity and mortality. Coronary artery disease is its most common cause. The evaluation of symptomatic patients with suspected heart failure is directed at confirming the diagnosis, determining the cause, identifying concomitant illnesses, establishing the severity of heart failure, and guiding therapy. The initial evaluation should include a focused history and physical examination, a chest radiograph, and an electrocardiogram. The presence of heart failure can be confirmed by an echocardiogram. Heart failure is highly unlikely in the absence of dyspnea and an abnormal chest radiograph or electrocardiogram. Radionuclide angiography or contrast cineangiography may be necessary when clinical suspicion for heart failure is high and the echocardiogram is equivocal. Patients with confirmed heart failure should undergo additional testing, including a more detailed history and physical examination; a complete blood count; blood glucose measurement; liver function tests; serum electrolyte, blood urea nitrogen, and creatinine measurements; lipid panel; urinalysis; and thyroid-stimulating hormone level. A serum ferritin level, human immunodeficiency virus test, antinuclear antibody assays, rheumatoid factor test, or metanephrine measurements may be required in selected patients. Patients with coronary artery disease, hypertension, diabetes mellitus, exposure to cardiotoxic drugs, alcohol abuse, or a family history of cardiomyopathy are at high risk for heart failure and may benefit from routine screening.
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PMID:Diagnosis of heart failure in adults. 1560 63

Nucleoside reverse-transcriptase inhibitors (NRTIs) have been associated with functional and structural mitochondrial abnormalities, leading to several adverse events, such as increased serum lactic acid levels and lactic acidosis. Mild-to-moderate, asymptomatic hyperlactataemia has been frequently reported in human immunodeficiency virus (HIV)-infected patients treated with NRTIs, with an estimated prevalence between 15% and 35%. On the contrary, symptomatic, severe hyperlactataemia and lactic acidosis are less common, with an incidence ranging from 1.7 to 25.2 cases per 1000 person-years of antiretroviral treatment, and are associated with a remarkable mortality rate, which varies from 30% to 60% in different studies. The clinical presentation of lactic acid syndrome is non-specific and includes asthenia, malaise, nausea, vomiting, abdominal pain, weight loss, tachypnoea, dyspnoea, liver steatosis and increased transaminase levels, and risk factors include previous or concurrent therapy with stavudine or didanosine. Management of symptomatic lactic acid alterations involves NRTI-therapy interruption and supportive care, while natural history of hyperlactataemia is still unknown, and it is uncertain whether asymptomatic patients with increased lactate concentrations are at increased risk of developing lactic acidosis.
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PMID:Hyperlactataemia and lactic acidosis in HIV-infected patients receiving antiretroviral therapy. 1568 Oct 97

Cerebral aspergillosis is a rare cause of brain expansive lesion in AIDS patients. We report the first culture-proven case of brain abscess due to Aspergillus fumigatus in a Brazilian AIDS patient. The patient, a 26 year-old male with human immunodeficiency virus (HIV) infection and history of pulmonary tuberculosis and cerebral toxoplasmosis, had fever, cough, dyspnea, and two episodes of seizures. The brain computerized tomography (CT) showed a bi-parietal and parasagittal hypodense lesion with peripheral enhancement, and significant mass effect. There was started anti-Toxoplasma treatment. Three weeks later, the patient presented mental confusion, and a new brain CT evidenced increase in the lesion. He underwent brain biopsy, draining 10 mL of purulent material. The direct mycological examination revealed septated and hyaline hyphae. There was started amphotericin B deoxycholate. The culture of the material demonstrated presence of the Aspergillus fumigatus. The following two months, the patient was submitted to three surgeries, with insertion of drainage catheter and administration of amphotericin B intralesional. Three months after hospital admission, his neurological condition suffered discrete changes. However, he died due to intrahospital pneumonia. Brain abscess caused by Aspergillus fumigatus must be considered in the differential diagnosis of the brain expansive lesions in AIDS patients in Brazil.
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PMID:Cerebral aspergillosis due to Aspergillus fumigatus in AIDS patient: first culture-proven case reported in Brazil. 1602 Dec 91

Human immunodeficiency virus (HIV) and acute immunodeficiency syndrome are known to be associated with cardiac involvement. In this respect, a relation between HIV and dilated cardiomyopathy has been described. Additionally, highly active antiretroviral therapy (HAART) may independently contribute to cardiac impairment. We here report two cases of severely reduced left ventricular function detected in the context of a recent standardized screening of 132 HIV+ individuals of the German heart failure network. Both patients presented in a poor overall condition and progressive exercise-induced dyspnea accompanied by edema or angina pectoris, respectively. Subsequent examinations revealed left bundle-branch blockade, ventricular arrhythmia, elevated serum BNP-levels as well as pathologic transthoracic echocardiography, left ventricular angiography, electron beam tomography and cardiac magnetic resonance imaging without significant coronary stenoses or immunohistological signs of an ongoing or prior myocarditis. Clinical signs of progressive chronic heart failure developed slowly but constantly following initiation of the HAART regimen. Patients were treated by an implantation of a biventricular implantable cardioverter defibrillator beside conventional conservative standard therapy followed by a significant improvement of clinical symptoms. Antiviral medication could be maintained in both patients. Taking all data into account, the diagnosis of a HAART-associated dilated cardiomyopathy could be assessed. Even though the pathogenesis of secondary heart failure after HAART is still object of investigation a mitochondrial impairment by antiviral drugs is thought to contribute the development of dilated cardiomyopathy. However, due to the coexistence of an eminent HIV infection, a direct effect of the HI virus itself can not be completely excluded.
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PMID:Dilated cardiomyopathy in two adult human immunodeficiency positive (HIV+) patients possibly related to highly active antiretroviral therapy (HAART). 1618 52

Pulmonary arterial hypertension (PAH) is a pathological condition of the small pulmonary arteries. PAH is characterized histopathologically by vasoconstriction, vascular proliferation, in situ thrombosis, and remodeling of all 3 levels of the vascular walls. These pathologic changes result in progressive increases in the mean pulmonary-artery pressure and pulmonary vascular resistance, which, if untreated, leads to right-ventricular failure and death. PAH can be associated with multiple conditions or risk factors (eg, collagen vascular diseases, liver disease, human immunodeficiency virus, congenital heart disease, or ingestion of certain medications or toxins) or it can be idiopathic. Up to 10% of the idiopathic cases are familial. Regardless of the etiology, the clinical presentation, histopathologic lesions, and response to therapy are all similar. Early in the disease process, the signs and symptoms of PAH are often subtle and nonspecific, making diagnosis challenging. Patients most often present with progressively worsening dyspnea and fatigue. An extensive evaluation is indicated to diagnose PAH, decipher its etiology, and determine long-term treatment goals. Transthoracic echocardiogram is an excellent screening tool to evaluate PAH, but every patient requires a right-side heart catheterization to help stage the disease and guide therapy. Prior to a decade ago, clinicians were only able to offer symptomatic therapy to this challenging group of patients. Earlier diagnosis, rapidly advancing understanding of the pathogenesis, and an increasing number of treatment options have changed the course of PAH, which was once thought to be invariably fatal.
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PMID:Diagnosis and management of pulmonary arterial hypertension: Implications for respiratory care. 1656 91


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