Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acquired immunodeficiency syndrome (AIDS) was first diagnosed in burundi in 1983 when a large number of patients were registered with Kaposi's sarcoma, cryptococcal meningitis, and disseminated candidiasis. In the 1st phase of the disease the vi rus is dormant. In the 2nd phase seroconversion appears; and in the 3rd phase generalized adenopathy emerges. In the 4th phase the full-blown disease appears as a result of cellular immunity deficit with emaciation, fever, sweating, chronic diarrhea, asthenia, blood parameter changes (lymphopenia, thrombocytopenia, leukopenia, anemia, and specific immune disorders). The early phases can be diagnosed by serological tests. During 1989 a group of 155 patients with 1st signs of seropositivity were studied in the central hospital of Bugumbura. The available clinical diagnostic markers were: 56 cases of herpes, 26 cases of generalized adenopathy, 25 cases of inflammatory infiltration of paraganglionic zones, 13 abscesses and phlegmons, 8 cases of chronic proctitis, 8 prurigo cases, 7 cases of chronic pneumonia and bronchitis, 4 cases of paresis of the facial nerve, 4 cases of Kaposi's sarcoma, 2 cases of fresh syphilis, 2 cases of anemia, asthenia, dizziness, and weight loss. Tomo- and zonographical X-ray study of the thorax of 80 patients aged 20-65 (51 men and 29 women) was performed. In 62 patients changes in the lungs were evident. In 2 patients tuberculosis of the lungs was diagnosed: miliary TB in a 26-year woman and disseminated TB in a 31-year man. 2 chronic and 3 bronchial, and 10 interstitial pneumonia cases were diagnosed in 15 patients with average age of 30 years. 4 patients had peribronchial and pneumonic infiltrations. In a group of 45 patients magnified picture showed no deformation in the lungs; and only 5 had respiratory organ pathology. Interstitial pneumonia was the most often diagnosed ailment by X-ray inpatients infected with HIV.
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PMID:[X-ray pulmonary manifestations in patients infected with the human immunodeficiency virus]. 196 22

In a cross-sectional population study of Danish patients with AIDS 16 of 23 had clinical signs of neurological disease with muscle weakness or ataxia of the lower limbs as the dominant manifestation. Tibial and median nerve conduction was mildly slowed in a few patients and 15 had widening of cerebral ventricles at CT. However, all had prolonged latency of cortical evoked response following tibial nerve stimulation mainly due to slowing through the spinal cord. The prolongation of the latency of the evoked cortical responses was most pronounced in patients with lower limb ataxia and/or paresis. It is concluded that affection of the long tracts of the spinal cord are closely associated with the human immunodeficiency virus infection.
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PMID:Myelopathy in AIDS. A clinical and electrophysiological study of 23 Danish patients. 335 13

Few cases of MRI in neurosyphilis have been reported. We examined the value of MRI in patients with general paresis; MRI was performed on four HIV-negative patients with parenchymatous neurosyphilis. It demonstrated frontal and temporal atrophy, subcortical gliosis and, in one patient, increased ferritin in the basal ganglia. The progression of the lesions on MRI correlated well with the neuropsychiatric disturbances. The MRI findings correlated with the well-known neuropathological findings. This combination of pathological findings in neurosyphilis has not been described before and we suggest that MRI is of prognostic value in patients with general paresis.
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PMID:MRI in patients with general paresis. 869 19

FIV is a lentivirus of domestic cats that causes a spectrum of diseases that is remarkably similar to the clinical syndrome produced by HIV infection in people. Both HIV and FIV has been shown to cause neurologic dysfunction. Specific Pathogen-Free (SPF) cats were placed into one of three groups: FIV-PPR infected; DU-FIV-PPR (a dUTPase mutant of the FIV-PPR clone) infected; or an age-matched control group. In both infected groups, the general clinical signs of infection included lymphadenopathy, oral ulcerations, rough hair coat, and conjuntivitis. Specific neurological changes in the FIV-PPR infected cats included hind limb paresis; delayed righting and pupillary reflexes; behavioral changes; delayed visual and auditory evoked potentials; decreased spinal and peripheral nerve conduction velocities; and marked alterations in sleep patterns. Most of these changes were also observed in the DU-FIV-PPR infected cats. However, these cats tended to have a slightly less severe disease. In this study, we have demonstrated that an infectious molecular clone of FIV closely parallels the disease course of wild type FIV-infected cats. By using a knockout gene mutant of this clone, we were able to demonstrate that the dUTPase gene is not essential for neuropathogenesis. Further use of the FIV-PPR clone should prove useful in determining the essential viral elements that are important in the neuropathogenesis of lentiviral infections.
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PMID:Neurologic dysfunctions caused by a molecular clone of feline immunodeficiency virus, FIV-PPR. 897 20

The primary HIV infection is the period of time following HIV inoculation. Its manifestations are diverse. We present here some clinical cases: a mononucleosis-like syndrome with fever, angina, lymphadenopathy and skin rash, a frequent picture, with among other signs, flu-like symptoms, lymphocytic meningitis and facial paresis. In presence of those nonspecific clinical pictures, it is important for the primary health care physician to consider primary HIV infection, detect a history of exposure and order HIV-tests including p24-antigenemia. On one side, an early treatment blocks replication and dissemination of HIV in the body and brings an amelioration of prognosis. On the other side, the patient is particularly infectious during this phase and should take appropriate preventive measures.
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PMID:[Primary HIV infection, how to recognize it?]. 1068 11

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

This study reported on 53 cases of neurosyphilis which were seen in the Dermatovenerology Department of the Ibn Rochd University Hospital Center in Casablanca from January 1983 to December 1988. The classification was as follows: 26 general paresis, 8 tables, 6 myelitis and cerebral syphilitic arteritis, 7 optic atrophy, 2 early syphilitic meningoencephalitis, 2 unclassifiable forms, and 1 asymptomatic neurosyphilis. A history of syphilis was found in 43 or 3% of the cases. Patients ranged in age from 22 to 61 years, with an average of 40.8 years. There was a clear predominance of males (81.1%). All of the patients were negative for HIV. The diagnosis of neurosyphilis was highlighted along with the clinical manifestations associated with a positive serology (VDRL, TPHA) in the serum and the cerebrospinal fluid (CSF). There was a pleocytosis of CSF in 52.8% of the cases and increased CSF protein in 35.8% of the cases. Treatment consisted of intravenous aqueous penicillin G in 52 patients with a follow up of between 2-66 months. Improvement of lesions was noted in 48% of the cases and sequelae were definitive in 50% of the cases. 1 patient (2% of the cases) died. (author's modified)
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PMID:[Neurosyphilis: 53 cases]. 1231 17

Acute invasive external otitis is an uncommon life-threatening infection of the external auditory canal (EAC), most often affecting the elderly diabetic patients. Although few reports have been made in HIV-positive/Aids patients among the caucasians. We present here a 25 year old nursing mother with a month history of fever, persistent otalgia with acutely inflammed EAC, gross facial cellulitis, mastoid abscess and facial paresis, following a minor left ear trauma with a matchstick. This unusual course of ear infection in an otherwise healthy young adult prompts a search for an immunodepressing factor which was confirmed to be Human Immunodeficiency Virus (HIV). This article highlights the clinical peculiarities and the management of invasive external otitis in an HIV-positive patient.
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PMID:Human immunodeficiency virus and invasive external otitis--a case report. 1276 21

Our objective is to assess the relevance of the different laboratory findings in cerebrospinal fluid (CSF) and serum for the diagnosis and survey of active neurosyphilis. A retrospective study of six hospitalized neurosyphilitic patients at Neurological Hospital of Lyon from 1987 to 2002 was carried out. Six males were found, aged from 29 to 72 years. Neurosyphilis can be group in two categories: early (meningeal and meningovascular neurosyphilis) and late (progressive general paralysis and tabes dorsalis). All were tertiary stage and HIV negative. We performed in CSF, white and red cell count, cytology, total protein, glucose levels, in CSF and serum, albumin, total IgG, IgA, IgM for calculation of albumin quotient and IgG, IgA and IgM index. Serological tests for syphilis in CSF and serum are VDRL and TPHA. To increase the reliability of treponema antibody tests, the ratio of serum-to-CSF content of albumin is used to assess intrathecal production of treponema antibodies, especially the treponema pallidum hemagglutination assay (TPHA index). The CSF changes in neurosyphilis included elevated cell count with lymphocytic-plasmocytic cell reaction, increased protein content, strongly positive IgG index, numerous positive IgG oligoclonal bands, positive blood and CSF serology. Serological tests are difficult to interpret. Examination of CSF played a major role in the diagnosis and treatment of all forms of neurosyphilis. The CSF abnormalities improved with clinical improvement, especially in meningeal and vascular neurosyphilis, but the response in paresis and tabes was slower or nonexistent. Pleocytosis and protein are indicators of inflammatory activity in the central nervous system and are used as a clinical guide in the diagnostic, for treatment and re-treatment.
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PMID:[Diagnosis and biological monitoring of 6 neurosyphilis cases: value of cerebrospinal fluid analysis]. 1467 54

Herpes zoster (HZ) results from recrudescence of varicella zoster virus latent since primary infection (varicella). The overall incidence of HZ is approximately 3/1000 of the population per year rising to 10/1000 per year by 80 years of age. Approximately 50% of individuals reaching 90 years of age will have had HZ. In approximately 6%, a second attack may occur (usually several decades after the first). Patients with HZ can transmit the virus to a non-immune individual causing varicella. HZ is not contracted from individuals with varicella or HZ. Reduced cell-mediated immunity to HZ occurs with ageing, explaining the increased incidence in the elderly and from other causes such as tumours, HIV and immunosuppressant drugs. Diagnosis is usually clinical from typical unilateral dermatomal pain and rash. Prodromal symptoms, pain, itching and malaise, are common. The most common complication of HZ is postherpetic neuralgia (PHN), defined as significant pain or dysaesthesia present >or= 3 months after HZ. PHN results from damage and secondary changes within components of the nervous system subserving pain. Some motor deficit is common; severe and long-lasting paresis may rarely accompany HZ. More than 5% of elderly patients have PHN at 1 year after acute HZ. Predictors of PHN are, greater age, acute pain and rash severity, prodromal pain, the presence of virus in peripheral blood as well as adverse psychosocial factors. Therapy for acute HZ is intended to reduce acute pain, hasten rash healing and reduce the risk of PHN and other complications. Antiviral drugs are close to achieving these aims but do not entirely remove risk of PHN. Oral steroids show no protective effect against PHN. Adequate analgesia during the acute phase may require strong opioid drugs. Nerve blocks and tricyclic antidepressants (TCAs) may reduce the risk of PHN although firm evidence is lacking. PHN requires thorough evaluation and development of a management strategy for each individual patient. Initial therapy is with TCAs (e.g., nortriptyline) or the anticonvulsant gabapentin. Topical lidocaine patches frequently reduce allodynia. Strong opioids are sometimes required. Topical capsaicin cream is beneficial for a small proportion of patients but is poorly tolerated. NMDA antagonists have not proved beneficial with the exception of ketamine. Transcutaneous Electrical Nerve Stimulation (TENS) may be effective in some cases. HZ is a common condition. Severe complications such as stroke, encephalitis and myelitis are relatively rare whereas sight threatening complications of ophthalmic HZ are more common. PHN is common, distressing and often intractable. Good management improves outcome.
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PMID:Management of herpes zoster (shingles) and postherpetic neuralgia. 1501 24


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