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

Peripheral neuropathy is common in human immunodeficiency virus type-1 (HIV-1) infection. Peripheral neuropathies complicate all stages of the HIV-1 disease and cause considerable morbidity and disability in HIV-1 infected individuals and acquired immunodeficiency syndrome (AIDS) patients. Whereas symptomatic neuropathies occur in approximately 10% to 15% of HIV-1-infected patients overall, pathologic evidence of peripheral nerve involvement is present in virtually all end-stage AIDS patients. There are 6 major clinical types of HIV-associated neuropathies that are regularly seen in large HIV-1 clinics. Distal sensory polyneuropathy (DSP) is the most common among the HIV-1-associated neuropathies. DSP generally occurs in later stages of HIV-1 infection and it follows an indolent and protracted clinical course. The dominant clinical features in DSP include distal pain, paresthesia and numbness in a typical length-dependent fashion with proximal to distal gradient. Whereas toxic neuropathies--secondary to certain antiretroviral agents--are clinically similar to DSP, their temporal relation to neurotoxic medication helps distinguish them from other HIV-1-associated neuropathies. DSP and toxic neuropathy may coexist in a single patient. Acute and chronic inflammatory demyelinating polyradiculoneuropathies (AIDP and CIDP) produce global limb weakness. AIDP may occur at seroconversion and it can therefore be the initial manifestation of HIV-1 infection. CIDP generally occurs in the mid to late stages of HIV-1 infection. Progressive polyradiculopathy (PP) occurs in patients with advanced immunodeficiency and is generally caused by the opportunist cytomegalovirus (CMV) infection. Mononeuropathy multiplex (MM) in early stages of HIV-1 infection is immune mediated, whereas in advanced AIDS it is caused by the CMV infection. Finally, subclinical autonomic nervous system involvement is common in all stages of HIV-1 infection. Because HIV-1-associated neuropathies are diverse in their etiology and pathogenesis, a precise clinical diagnosis is required to formulate a rational therapeutic intervention.
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PMID:Epidemiology and clinical features of HIV-1 associated neuropathies. 1129 7

An axonal sensory neuropathy is a frequent complication in the course of HIV infection; more than 30% of all HIV-infected individuals will develop a polyneuropathy. Low CD4 cell counts and high HIV RNA loads increase the risk. This neuropathy causes pain, paresthesias and burning sensations and/or numbness in the feet, which sometimes occurs in the hands as well. Neurological examination reveals sensory deficits in a stocking and glove distribution and depressed or absent ankle reflexes, without severe paresis. The cause of the sensory neuropathy is unknown. Either the HIV infection or certain other infections, for example cytomegalovirus, may play a role in the pathogenesis; vasculitis may be a process associated with this. Some antiretroviral drugs within the nucleoside analogue group cause a neuropathy but the pathogenesis of this remains unclear. Amitriptyline, tramadol and carbamazepine can be used for symptomatic treatment. The efficacy of lamotrigine and gabapentin has yet to be confirmed.
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PMID:[Sensory neuropathy in HIV infection: pathogenesis and therapy]. 1133 55

HIV-positive individuals are at high risk of developing an anxiety disorder, with a prevalence rate as high as 38 percent. The symptoms may occur anytime during the course of the infection, and can become excessive in some patients, impairing the person's ability to cope with their circumstances. Signs and symptoms include chest pain, headache, numbness, and insomnia. HIV treatments that may cause anxiety symptoms include ddI, d4T, AZT, fluconazole, foscarnet, and isoniazid. Health care providers need to thoroughly evaluate anxiety symptoms during an initial evaluation to rule out substance abuse and pre-existing anxiety. Treatment of anxiety in HIV/AIDS ranges from benzodiazepines to alternative therapies such as massage and acupuncture. A chart lists potential drug interactions between common antidepressive and HIV antiretroviral drugs.
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PMID:Anxiety and HIV infection. 1136 9

A case study is presented on the therapeutic dilemmas surrounding the introduction of antiretroviral therapy. Such dilemmas can include a patient's willingness to understand and adhere to a prescribed regimen or how to deal with side effects that may occur as a result of a regimen. This case involves a 38-year-old, HIV-positive male who, in response to numbness in his left foot, reduced his dosage of d4T by half, without consulting his physician. Now that the numbness has disappeared, the patient opposes returning to the original dosage of d4T. Opinions on this case are provided by two medical professionals, along with their suggestions for accommodating the patient.
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PMID:Too little of a good thing. 1136 60

The aim of the study was to assess adherence with antiretroviral medication in a sample of HIV patients in Hong Kong and identify predictors of adherence. The study used a cross-sectional correlational design. Adherence behaviour was assessed with the use of self-reports. Other scales assessed knowledge with HIV medication, coping, health locus of control, anxiety, depression and fatigue. A blood sample was also obtained to assess CD4+ counts and viral load. Sociodemographic characteristics and medical information were obtained from the medical records. A high adherence rate was found in this sample of 136 predominantly Chinese patients. There were only 13.7% of the patients being classified as non-adherent. Predictors of adherence included high self-efficacy in terms of being certain that the medication schedule will be followed all or most of the time as directed, low tension-anxiety scores, and low intensity of nausea and vomiting (R2=0.304). An expanded regression model revealed additional factors influencing adherence, including coping variables, pain and numbness in the hands and feet, age, disease stage, internal locus of control, fatigue, family support and taking medication twice daily. This model explained 49% of the variance in adherence. The results suggest that adherence is a multidimensional concept. Every effort should be made to assess in individuals those variables found to affect adherence and alter them whenever possible. Continuous support of patients and individualized medication programmes that will help patients adjust their treatment to their lifestyle are recommended.
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PMID:Factors associated with adherence to antiretroviral medication in HIV-infected patients. 1197 33

Informal caregivers of people with AIDS provide practical help and nursing care at home. They are often the lovers, spouses, friends, or family of someone with AIDS and are not professional care providers. They provide essential care, saving society considerable expense. Caregivers provide practical support such as shopping, housekeeping, and transportation to clinics, as well as basic assistance such as help with bathing, going to the bathroom, and feeding. As symptoms worsen, caregivers are also likely to adopt the more clinical roles of keeping track of medications, giving injections, inserting catheters, and cleaning wounds. Caregivers also often assess medical and mental conditions, being the first to notice changes in health and to decide when to seek help. Caregivers, however, can suffer considerable care-related stress, leading to numbness, compassion fatigue, or burnout. Caregivers may also fear social rejection, loss of job and/or housing and may therefore hide their caregiving status from family, friends, and co-workers. For women with HIV, being responsible for children at home may make it difficult or impossible to obtain caregiving support for themselves. Helping caregivers benefits both the caregiver and the patient. Professional clinicians can include the caregiver in the triad of care comprised of the doctor, caregiver, and patient. Participating in support groups can also help caregivers.
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PMID:Are informal caregivers important in AIDS care? 1229 55

Whereas small-fibre sensory neuropathies might ultimately lead to cell death and loss of sensation, they first progress through a phase, which might last for years, characterized by the presence of analgesia-resistant neuropathic dysesthesias and pain. Much previous research has addressed these two phases as separate phenomena mediated by presumably discrete biochemical mechanisms. We hypothesized that activity in signalling pathways that ultimately lead to apoptosis plays a critical role in the generation of neuropathic pain, before death of sensory neurons becomes apparent. We have tested the hypothesis that activator and effector caspases, defining components of programmed cell death (apoptosis) signalling pathways, also contribute to pain-related behaviour in animals with small-fibre peripheral neuropathies and that the death receptor ligand, tumour necrosis factor-alpha, and its downstream second messenger, ceramide, also produce pain-related behaviour via this mechanism. In two models of painful peripheral neuropathy, HIV/AIDS therapy (induced by the nucleoside reverse transcriptase inhibitor, dideoxycytidine), and cancer chemotherapy (induced by vincristine) peripheral neuropathy, and for pain-related behaviour induced by tumour necrosis factor-alpha and its second messenger, ceramide, inhibition of both activator (1, 2, 8 and 9) and effector (3) caspases attenuates neuropathic pain-related behaviour, although has no effect in streptozotocin-diabetic neuropathy and control rats. We conclude that during a latent phase, before apoptotic cell death is manifest, the caspase signalling pathway can contribute to pain in small-fibre peripheral neuropathies, and that inflammatory/immune mediators also activate these pathways. This suggests that these pathways are potential targets for novel pharmacological agents for the treatment of inflammatory as well as neuropathic pain.
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PMID:Caspase signalling in neuropathic and inflammatory pain in the rat. 1557 43

Despite the introduction of highly active antiretroviral therapy (HAART), diffuse large B-cell lymphoma (DLBCL) remains a common malignancy in human immunodeficiency virus (HIV)-infected patients, especially the plasmablastic variant. About 50% of lymphomas in HIV patients are extranodal and half of them occur in the head and neck area. The main oral symptoms are pain, swelling, numbness and tooth mobility. We report the case of a 52-year-old patient with a known HIV infection and fracture of the angular region of the mandible. The fracture did not unite following open reduction and osteosynthesis. A biopsy performed at the time of revision revealed the diagnosis of a primary lymphoma in the mandible. After chemotherapy had induced complete remission of the lymphoma and autogenous iliac crest bone grafting had been performed the fracture united. Primary lymphoma in the mandible is a disease that presents with a nonspecific radiological appearance which may mimic osteomyelitis or periodontal pathology. A rapid and accurate diagnosis is critical for the appropriate treatment. In our experience HIV-positive patients with mandibular fracture should be treated according to the guidelines established for HIV-negative patients. However, risky compromises such as intraoral approach or hazardous fracture fixation should be avoided.
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PMID:[HIV-associated lymphoma -- an unusual cause of pathological mandibular fracture]. 1568 41

A 39-year-old man presented with a chronic nonhealing toe ulcer and multiple skin-colored papules on the back, arms, and knees. From an initial small erosion, the toe lesion ulcerated over a 1.5-year period, while the papules progressed over a 6-month period, first appearing on the back and then spreading to the arms and knees. The past medical and family history were non-contributory. Pertinent findings included the aforementioned well-defined, asymmetric, shiny papules (Fig. 1). There were multiple, discrete, erythematous, pedunculated, tumor-like masses of various sizes over the right thigh (Fig. 2) and a well-defined 4 cm x 3 cm ulcer on the second toe of the left foot, the floor of which was covered by necrotic slough. There was distal loss of sensation to temperature, touch, and pain. The greater auricular, ulnar, radial cutaneous and common peroneal nerves were thickened bilaterally, but non-tender. A clinical diagnosis of histoid leprosy was made. The differential diagnosis for the tumor-like thigh masses included dermatofibroma, neurofibroma, and Kaposi's sarcoma. The hemogram, liver/renal function tests, chest X-ray, and abdominal ultrasound were normal. Human immunodeficiency virus enzyme-linked immunosorbent assay (HIV ELISA) was negative. The ear lobe smear (ELS) for acid-fast bacilli showed a bacterial index (BI) of 6+[> 1000 organisms/oil immersion field (oif)] and a morphological index (MI) of 50%. The skin-colored papules on the back and the pedunculated masses showed a BI of 5+ (100-1,000 organisms/oif) and an MI of 50%. The normal skin showed a BI of 4+ (10-100 organisms/oif) and an MI of 5%. Biopsy of the papules and pedunculated tumors showed a well-circumscribed area of the dermis packed with many acid-fast organisms and foamy macrophages, consistent with histoid leprosy (Fig. 3). Fite-Faraco stain demonstrated cells packed with lepra bacilli. A final diagnosis of lepromatous leprosy, histoid variant, was made. Dapsone, clofazimine, rifampicin, and, later, ofloxacin were started.
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PMID:Histoid leprosy - unusual presentation. 1665 Jan 72

Peripheral nerve disorders are frequent complications of HIV disease. Distal symmetrical polyneuropathy (DSP) is the most common peripheral nerve disorder associated with HIV and occurs in over one third of infected patients but may occur in up to 67% if asymptomatic patients are included. Risk factors for DSP include increased age, advanced HIV disease, and history of "d-drugs" or other neurotoxic drugs. The primary manifestations of polyneuropathy are slowly progressive numbness and paresthesias, with burning sensations in the feet usually in a symmetrical pattern. The etiology of HIV-associated DSP is unknown, although neurotoxic effects of cytokines, toxicity of HIV proteins, and mitochondrial damage have been implicated. The current treatment for HIV-associated DSP is symptomatic, with pain modifying medications, including anti-inflammatory agents, opioids, antidepressants, antiepileptics, topical anesthetics, and capsaicin. Sustained virologic control may improve DSP. Novel therapies such as -acetyl-l-carnitine or neurotrophic factors are being studied for treatment of DSP.
Curr HIV/AIDS Rep 2007 Aug
PMID:Managing HIV peripheral neuropathy. 1788 96


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