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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Shortness of breath is a common complaint encountered in both the ambulatory and acute care setting. In patients infected with the human immunodeficiency virus, dyspnea often heralds the onset of a potentially life-threatening opportunistic infection. We present a case of a rare cause of dyspnea in the general population and to our knowledge the first such case reported in the setting of human immunodeficiency virus infection in the United States.
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PMID:Dyspnea in a woman infected with the human immunodeficiency virus. 1178 54

In a 37-year-old patient HIV infection was diagnosed in June 1986. Eight years later the patient complained of increasing shortness of breath and occasional syncopes on exertion. He developed peripheral oedema and ascites. Echocardiography revealed severe pulmonary hypertension. Right ventricular systolic pressure (RVSP) was 77 mm Hg. There was no evidence of left ventricular dysfunction, valvular heart disease, thromboembolic disease or obstructive or restrictive lung disease, nor were there other known causes or risk factors of pulmonary hypertension. HIV-associated pulmonary arterial hypertension was diagnosed. Oral anticoagulation and zidovudine were begun, but RVSP rose to 96 mm Hg. After the introduction of lamivudine, and later stavudine and nelfinavir, HIV-RNA copies decreased from 133 400 to below 50 copies per mL. Six years after the diagnosis of HIV-associated pulmonary arterial hypertension RVSP had continually fallen to 49 mm Hg and the grossly enlarged right heart dimensions had nearly normalised without vasodilator treatment. The patient remains in excellent health and his sole complaint is of mild dyspnoea on exertion.
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PMID:Regression of HIV-associated pulmonary arterial hypertension and long-term survival during antiretroviral therapy. 1197 Dec 5

A 48-year-old male patient with AIDS presented with postinfarct unstable angina, decreased left ventricular function (EF 35%), significant left main coronary artery disease, and total occlusion of the proximal left anterior descending and right coronary arteries. In order to avoid the potential immunosuppressive effect of cardiopulmonary bypass (CPB) in an already compromised host with an already low CD4+ helper/inducer T cell count (180/microL) and high retroviral load (165,000 copies/mL), the application of beating-heart technology and off-pump coronary bypass grafting was an ideal indication. The patient underwent successfully off-pump/CPB coronary revascularization. The triple drug combination of highly active antiretroviral therapy (HAART) was resumed postoperatively. The patient was discharged from the hospital on the 7(th) postoperative day. The CD4+ count was 142/microL and the viral load decreased to 450 copies/mL. Seven months post-operatively the patient was free of angina and without shortness of breath. The CD4+ count was 160/(m)L and the viral load undetectable. Improved survival of HIV positive patients has resulted in a shift from caring for terminally ill patients to caring for patients with chronic illness. While protease inhibitors have positively affected survival, they may also cause plasma lipid abnormalities, which can lead to severe premature coronary artery disease. Therefore, an increasing population of AIDS and HIV positive patients with coronary artery disease may require cardiac interventions in the near future. Coronary revascularization without CPB and its potential immunocompromising effect may play an important role in patients with severe coronary artery disease and AIDS.
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PMID:Off-pump coronary artery bypass grafting in a patient with AIDS, acute myocardial infarction, and severe left main coronary artery disease. 1262 72

Microsporidia are ubiquitous spore-forming parasites that are important worldwide pathogens in the HIV/AIDS pandemic. They are also increasingly being seen in HIV(-) individuals. Infection has been documented in almost every tissue and organ in the body and in a broad spectrum of cell types, including epithelial, mesenchymal, and neural. Microsporidia elicit a wide range of pathology, e.g., inflammation and cell death, and symptoms, e.g., shortness of breath, sinusitis, and diarrhea with wasting. Untreated, microsporidiosis has been documented as a cause of death.
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PMID:Diagnostic pathology of microsporidiosis. 1277 4

Symptoms serve as intervention foci for patients and health care providers. Research has established a relationship between symptoms and quality of life for persons living with HIV/AIDS. This article reports symptom prevalence and intensity data that include gynecological and cognitive symptoms self-reported by HIV-infected women (N = 118). Using a cross-sectional, descriptive design, data were obtained using the Center for Epidemiological Studies-Depression Scale (CES-D), Medical Outcomes Study Short Form-36 (MOS SF-36), and the revised Sign and Symptom Check-List for Persons Living with HIV/AIDS (SSC-HIV). Prevalent symptoms were depression (83%), muscle aches (84%), weakness (80%), and painful joints (71%). Symptoms with the highest mean intensity, however, were headaches, rash, insomnia, vaginal itching, and shortness of breath at rest. Symptoms also significantly predicted role functioning. This study contributes to our understanding the nature of symptoms and the influence of symptoms on role and physical functioning among HIV-infected women.
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PMID:The influence of symptoms on quality of life among HIV-infected women. 1498 39

PRESENTING FEATURES: An 18-year-old white man was admitted to the Osler Medical Service with the chief complaint of back pain. Two weeks prior to admission, the patient developed diffuse and aching upper back pain. Over the next couple of days, he also developed severe anterior chest pain that was somewhat pleuritic in nature but diffuse and extending bilaterally into the shoulders. One week prior to admission, he developed intermittent fevers and night sweats. The patient denied any lymphadenopathy, pharyngitis, sick contacts, shortness of breath, rash, or bleeding. He was seen by a physician and told that he had thrombocytopenia. There was no history of recent or remote unusual bleeding episodes. His medical history was unremarkable except for a childhood diagnosis of attention deficit/hyperactivity disorder. He was not taking any medications and had no history of tobacco, alcohol, or illicit drug use. He had no risk factors for human immunodeficiency virus infection. Physical examination showed that he was afebrile and had normal vital signs. He was a well-appearing man who was lying still because of pain. HEENT examination was unremarkable. There was no pharyngeal erythema or exudates. His lungs were clear. His neck was supple and without lymphadenopathy. Examination of his back and chest revealed no focal tenderness. There was no hepatosplenomegaly, and his skin was without petechiae or rashes. Examination of the patient's joints showed pain on passive and active movement of his shoulders bilaterally, but no frank arthritis. There was no rash, petechiae, or echymoses. Chest radiograph and electrocardiogram were unremarkable. On admission, the laboratory examination was notable for a hematocrit level of 32.5%, with a mean corpuscular volume of 79 fL, and white blood cell count of 2.8 x 10(3)/microL. Platelet count was 75 x 10(3)/microL. A white blood cell differential revealed 7% bands, 53% polys, 34% lymphs, 5% atypical lymphocytes, 2% nucleated red cells, and a few young unidentified cells. His chemistry studies were unremarkable. What is the diagnosis?
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PMID:Cases from the Osler Medical Service at Johns Hopkins University. 1521 Mar 89

A 31-year-old, previously healthy white man presented to the emergency department with complaints of malaise, fevers, shortness of breath, a non-productive cough, and a "rash." His physical exam revealed a temperature of 100.2F, a pulse of 129 bpm, respiratory rate of 14 BPM, and blood pressure of 140/74 mm Hg. He was alert, oriented, and in no distress. His oropharynx was dry, his neck was supple, and cervical lymphadenopathy was absent. He had tachycardia, bilateral wheezes, and rhonchi with prolonged expirations. There was a diffuse vesicular eruption enveloping his entire body with involvement sparing his palms and soles (Figures 1 and 2). Laboratory values showed a hemoglobin of 16.0 g/dL and a white blood cell count of 7100 cells/pL, with 39%neutrophils, 23% bands, and 35% lymphocytes. His platelet count was mildly decreased to 86,000 x 103/pL. Chest radiograph revealed bilateral diffuse interstitial infiltrates. A diagnosis of acute varicella-zoster virus pneumonia (varicella pneumonia) was made, and the patient was started on IV acyclovir (10 mg/kg every 8 hours). Upon further questioning, the patient stated that his daughter had been diagnosed with "chickenpox" 7 days ago. The patient had numerous exposures to chickenpox in the past but had never developed clinical expressions of varicella. He was not at risk for HIV infection, not having multiple sexual partners, IV drug abuse, or blood transfusions. During the 1 day of in-hospitalization, his fever abated and the pulmonary signs diminished. Following discharge, IV acyclovir was replaced by valacyclovir to complete a 7-day course of therapy.
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PMID:Infectious disease capsules: a pox on your house. 1524 83

Lactic acidosis is an uncommon but potentially life-threatening adverse effect of didanosine. When given concomitantly with tenofovir disoproxil fumarate (DF), the area under the concentration-time curve of didanosine is increased by 48-60%. A 63-year-old man with human immunodeficiency virus (HIV) infection tolerated several didanosine-containing antiretroviral regimens. He developed generalized weakness, loss of appetite, weight loss, nausea, and vomiting 1.5 years after tenofovir DF was added to his didanosine-containing regimen. He was diagnosed with lactic acidosis and died after a 13-day hospital stay, when his lactate level increased to 189.7 mg/dl and his arterial blood gas pH value fell to 6.75. Health care providers should maintain a high index of suspicion for lactic acidosis in patients with HIV infection who receive didanosine and tenofovir DF concurrently. For patients receiving antiretroviral regimens containing this drug combination, it would be prudent to monitor lactate levels periodically. This is especially important when patients experience symptoms suggestive of lactic acidosis, such as weakness, abdominal pain, weight loss, nausea and vomiting, and shortness of breath.
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PMID:Fatal lactic acidosis associated with coadministration of didanosine and tenofovir disoproxil fumarate. 1533 57

A 52-year-old black woman presented with a 2-day history of lower lip swelling 5 days after starting a new medication, lisinopril. She had never experienced similar episodes in the past. She denied shortness of breath, tightening of the throat, swelling of the tongue, generalized cutaneous eruption, urticaria, or pruritus. She also denied symptoms consistent with facial paresis. Her past medical history was significant for hepatitis C infection, coronary artery disease, and hypertriglyceridemia. She had a 15 pack-year smoking history and denied both alcohol and drug abuse. She had never received a blood transfusion and was HIV negative. Physical examination disclosed a tender, swollen, and erythematous lower lip with induration, oozing, and crusting (Figure 1). Pinpoint openings evident throughout the lip surface exuded a clear, sticky, mucoid secretion. Tongue, parotid glands, and regional lymph nodes were normal. The working diagnosis was angioedema secondary to lisinopril. The presumptive offending drug was discontinued, and conservative therapy (topical clobetasol ointment, oral ranitidine, and oral fexofenadine) was initiated. Despite treatment, signs and symptoms persisted unabated. One week after initial presentation, a punch biopsy of her lower lip was taken to rule out granulomatous cheilitis and sarcoidosis. Histopathology included diffuse lymphohistiocytic infiltrate, minimal microabscess formation, and notable absence of granulomata. There was neither hypertrophy nor detectable abnormality of the salivary glands, with the exception of infiltrating mononuclear cells. Based on the clinical history and compatible pathologic findings, a diagnosis of cheilitis glandularis was made. Specifically, crusting and erosion clinically suggested a diagnosis of the superficial suppurative subtype of cheilitis glandularis. The patient received oral penicillin (dicloxacillin, 1.0 g/d) combined with oral fluoroquinolone (ciprofloxacin, 1.0 g/d). Within 2 weeks of starting the antibiotics, the lip swelling significantly decreased (Figure 2) and the patient was left with a mildly indurated nodule at the labial commissure. Following a 4-week course of continued antibiotic treatment, the lip returned to near baseline state. At both 6-month and 1-year follow-up visits, the lip remained normal.
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PMID:Cheilitis glandularis in an African-American woman: response to antibiotic therapy. 1627 62

Pulmonary arterial hypertension (PAH) is a rare and debilitating disease characterized by abnormal proliferation and contraction of pulmonary vascular smooth muscle cells. The resulting increase in pressure and pulmonary vascular resistance results in progressive right heart failure, low cardiac output, and ultimately death if left untreated. PAH is defined by a persistent elevation in pulmonary artery pressure with normal left-sided pressures, differentiating it from left-sided heart disease. Symptoms progress from shortness of breath and decreasing exercise tolerance to right heart failure, with peripheral edema and marked functional limitation. Exercise-induced syncope, worsening symptoms at rest, and intractable right heart failure indicate critical disease. PAH may be idiopathic with no identifiable cause or associated with collagen vascular diseases, drugs, HIV, liver disease, and/or congenital heart disease. Familial or genetically mediated PAH accounts for a small percentage of cases. Advances in the understanding of pathobiological pathways that contribute to vascular proliferation and remodeling have resulted in new therapies that improve quality of life and survival. Emerging therapies focus on the nitric oxide, prostacyclin, and endothelin pathways. Nursing interventions are critical to ensure patients' success with these expensive and complex treatments and their optimal adjustment to living with PAH.
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PMID:Pulmonary arterial hypertension. 1719 34


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