Kelemahan Virus AIDS Berhasil Terdeteksi

[Dark_Angel]

ya namanya penyakit mesti ada obatnya lah /swt

 

[Erica]

DBD aja mana ada obatnya tuh,padahal udah penyakit lama /wah

 

[T!T!~ch@/\/]

wew tp klo AIDS ntar d salah gunaian tuh /wah

 

[Erica]

buat apaan mbak /?

 

[Dark_Angel]

DBD aja mana ada obatnya tuh,padahal udah penyakit lama /wah

ada tu obatnya semprot obat nyamuk /e4 /e4 /e4

 

[tatoy_airsoft_maniac]

pertanyaanya adalah.... kapan vaksinnya ditemukan???

kita tanyakan pada...... galileo

 

[Thoeyenwen]

bener kata cc Titi chan tar disalah gunain yang ad tar jd pada free sex /pif

 

[Erica]

ada tu obatnya semprot obat nyamuk /e4 /e4 /e4

semprotin aja baygon seluruh rumah loe,palingan loe keracunan tuh /e4/e4/e4

 

[gokous]

/gg/gg/gg sekalian aja masukin ke tubuh kita/gg

 

[Erica]

^
^
virus hiv di masukin ke tubuh loe /?

 

[gokous]

baygonnya kita telen langsung aja/gg/gg

 

[Erica]

oh gue kirain loe mau di masukin virus hiv /e4/e4/e4

 

[Dark_Angel]

baygonnya kita telen langsung aja/gg/gg

skalian virus aidsnya di telen /e4 /e4

 

[Vas^Co]

Nih cara hadapin HIV ini potongan dari .pdf yg aku download

Treatment

According to the pathogenesis of HIVE, treatment should aim at suppressing the viral replication in the CNS. It is an unresolved issue whether the antiviral com- pounds need to penetrate into the CSF. A variety of clinical (Letendre 2004), vi- rological (de Luca 2002), pathological and electrophysiological studies suggest that substances reaching higher CSF concentrations are more effective. In contrast, we found no association of the number of CNS-penetrating substances and their CSF levels with the magnitude of CSF viral load suppression (Eggers 2003). HAART- induced neurocognitive improvement correlates more closely with viral load sup- pression in the CSF than in the plasma (Marra 2003).
In the absence of prospective, controlled, and randomized studies with clinical end points, we consider it important that any antiretroviral regimen in patients with HIVE includes as many as possible CNS-penetrating substances. We suggest any of the following: zidovudine, lamivudine (high concentrations in ventricular CSF; unpublished observations), nevirapine and indinavir. With the substances approved for clinical use in the recent years, CNS penetration is low or unknown.

650 HIV-1 associated Encephalopathy and Myelopathy



Table 4: Differential diagnoses of HIV encephalopathy and diagnostic workup
Condition adequate diagnostic step (commentary)
Neurosyphilis Antibody testing and CSF analysis (pleocytosis >15/µl)
(serological findings may be atypical for active neurosyphilis)
CMV encephalitis CSF (pleocytosis, potentially granulocytic; decreased glucose elevated total protein)
PCR for CMV in CSF, CMV antigen (pp65) in blood
antibody testing in blood and CSF (IgG and antibody index may be increased)
MRI (potentially subependymal hyperintensity and contrast en- hancement)
Occurs mostly in association with manifestation of other organs
(retinitis, colitis, pneumonitis, esophagitis)
Toxoplasmosis CT / MRI (single or multiple lesions found most frequently in basal ganglia or thalamus, space occupying effect, edema, frequently
with contrast enhancement (patchy or ring-shaped))
Presence of toxoplasma specific IgG in blood and CSF (rarely total seronegativity)
(may rarely pass as diffuse microglial nodule encephalitis)
Primary CNS lymphoma CT / MRI (single or multiple lesions most frequently adjacent to ventricles, space occupying effect, edema, almost invariably in- tense contrast enhancement (patchy more than ring-shaped))
CSF cytology
EBV PCR in CSF (HIV-associated CNS lymphomas EBV induced) PET or SPECT (tracer enhancement in lesion)
VZV encephalitis CSF (marked inflammatory signs)
VZV specific IgG in blood and CSF (IgM may be absent) VZV PCR in CSF
Mostly antecedent or accompanying cutaneous zoster lesions
Cryptococcal meningitis CSF (opening pressure frequently elevated, cell count and protein may be normal), India ink stain
Cryptococcal antigen in blood and CSF, fungal culture

Tuberculous meningitis and other bacterial in-
fections
Progressive multifocal leukoencephalopathy
(PML)

CSF, culture, PCR for mycobacteria appropriate tests

MRI (single or multiple lesions of white matter, no space occupy- ing effect, no edema, no contrast enhancement)
PCR for JC virus in CSF

Intoxication Determination of drug levels / screening for illicit drugs

Metabolic encepha- lopathy and impaired general physical condi- tion

Depression with
Ñpseudo dementiaì
Other Ñsubcorticalì de- mentia forms

Determination of electrolytes, renal and hepatic markers, hor- mones (thyroid, cortisol), blood count
Hypoxaemia? (blood gas analysis)
Reduced physical state? (bed ridden, wasting, pyrexia)
Psychiatric examination

Normal pressure hydrocephalus, Parkinsonian syndroms, other neurodegenerative conditions, subcortical arteriosclerotic en- cephalopathy

HIV-associated myelopathy 651



A number of small studies investigated the effect of Selegelin, Nimodipin, Lexipa- fant, and valproic acid for treatment of HIVE. These drugs act on the molecular pathogenesis of HIVE and are used in conjunction with antiretroviral treatment. Although a trend for clinical and neuropsychologic improvement was seen with some substances, none of them can be recommended for clinical routine.
Prognosis: An optimal HAART may lead to significant clinical improvement of HIVE. The extent of improvement includes restoration of working ability in pa- tients previously dependent on caregivers. This effect can be observed for up to four years, in parallel with sufficiently suppressed plasma viraemia (Cysique 2006). During the first months of treatment, the radiological signs of leukoencephalopathy may become more prominent, but eventually regress over the following one to two years.
Autopsy studies and clinical case series show, however, that some patients develop
a clinically apparent CNS disease despite effective HAART-induced suppression of plasma viral load (Brew 2002; own unpublished observations). Even with rapid decrease of plasma viraemia during HAART, many HIVE patients show a signifi-
cantly protracted decrease of the CSF viral load (Eggers 2003). On these grounds
we recommend that in patients with HIVE, the CSF viral load should be determined during the first one or two years of HAART. Modification of the antiviral regimen should be considered when clinical and virologic studies suggest ongoing CNS viral replication with complete suppression of plasma viraemia.


HIV-associated myelopathy

Clinical characteristics

HIV-infected patients may develop a myelopathy without the neuropsychological signs and symptoms of HIVE, labelled HIV associated myelopathy (HIVM). The histopathological hallmark are vacuoles most prominent in the cervical and thoracic parts of the spinal cord and lipid-laden macrophages, hence the term ìvacuolar myelopathyî (Petito 1985). These changes are reminiscent of severe combined de- generation and may occur with HIV-negative patients. As HIV viral products have only inconsistently been shown to be part of the lesions, the role of the virus for the disease is uncertain. Pathogenetically, a disturbance of cobalamin-dependent trans- methylation has been discussed. Like HIVE, HIVM occurs mainly with advanced immunosuppression. Only a proportion of patients with the autoptic finding of vacuolar myelopathy shows clinically apparent myelopathy during life (dal Pan
1994).

Diagnostic workup

A patient may be suspected of having HIVM if he has a spastic-atactic gait, hyper- reflexia with positive Babinski sign, disturbance of sphincter control, erectile dys- funtion, and slight signs of sensory dysfunction in a glove and stocking distribu- tion. The diagnosis of an independent HIVM should only be made when a con- comittant cognitive impairment is significantly less prominent than the myelopathy. Electrophysiological tests which show increased latencies of somatosensory evoked

652 HIV-1 associated Encephalopathy and Myelopathy


potentials (SEP) and the motor evoked potentials on transcranial magnetic stimula- tion are compatible with the diagnosis. CSF, microbiological and spinal imaging studies are inconspicuous or unspecific, and they have their importance in the ex- clusion of differential diagnosis, as listed in Table 4. Spinal imaging should include MRI of the cervical and, possibly the thoracic cord.


Table 5: Differential diagnoses of HIV myelopathy and diagnostic workup
condition adequate diagnostic step (commentary)

Mechanic compresssion of the myelon (cervical myelopathy, disk herniation)

degenerative changes of the cervical spine
MRI shows reduced CSF spaces around the spinal cord with hyperintense lesions of the cord parenchyma

Neurosyphilis Antibody testing and CSF analysis (pleocytosis >45/3)
(serological findings may be atypical for active neurosyphi- lis)
CMV myelopathy CSF (signs of inflammation) PCR for CMV in CSF
antibody testing in blood and CSF (IgG and antibody index
may be increased)
Toxoplasmosis contrast enhancing cord lesion on MRI
VZV myelitis CSF (marked inflammatory signs)
VZV specific IgG in blood and CSF (IgM may be absent) VZV PCR in CSF
Mostly antecedent or accompanying cutaneous zoster lesions
HSV myelitis CSF (inflammatory signs may be absent), HSV PCR in
CSF

HTLV-1
(tropical spastic paraparesis)

Severe combined degenera- tion
heredo-degenerative diseases
(hereditary spastic parapa- resis, adrenoleukodystrophy,
Friedreich ataxia etc.)

travel to the Carribean, West Africa or East Asia
slow evolution of symptoms, bladder dysfunction charac- teristic, CSF inflammation, HTLV-1 specific antibodies
Vitamin B12 levels, increased erythrocyte volume

appropriate tests

 

[Erica]

^
^
nice info,/no1

 

[bot]

apan tuh
gw gak ngerti ada yang bisa translate /e4 /e4 /e4

 

[T!T!~ch@/\/]

iya nih translate plssss males mikir ah /gg /heh

 

[gokous]

sip deh/no1/no1
goodgood/no1

 

[Erica]

^
^
translate kan tuh kata atasnya loe /e4/e4/e4

 

[Dark_Angel]

ayo yg py transtool translate dunk /pif
males baca panjang2 gitu bhs inggris kedokteran lagi /swt