News HIV/AIDS News & Information - Part 184

11 Mar

Neurologic Manifestations of HIV Infection

Involvement of the nervous system in HIV infection is common, manifesting in about half of patients.

Neurologic complications

Aseptic meningitis. At the time of HIV seroconversion or primary infection, patients may present with symptoms of aseptic meningitis, such as fever, headache, stiff neck, and a lymphocytic pleocytosis.

AIDS dementia complex

AIDS dementia complex is reported in about 6% to 7% of patients with AIDS. Clinical features include cognitive dysfunction, impaired motor performance, and behavioral changes. Subclinical cognitive and motor impairment may occur at all stages of HIV infection.

Progressive symptoms may include mental slowing, forgetfulness, poor concentration, apathy, social withdrawal, loss of spontaneity, and reduced libido. Patients display personality changes, including reduced emotional expression, increased irritability, mania, and disinhibition. Loss of fine motor control (deterioration in handwriting), slowing of gait, unsteadiness, urinary incontinence, and may be seen. Seizures occur in 10% of patients.

AIDS dementia complex is a diagnosis of exclusion because depression, metabolic disorders, and other infectious causes of encephalitis may present in a similar manner. Clinical diagnosis may be aided by neuropsychologic testing.

Central nervous system (CNS) computed tomography (CT) and magnetic resonance imaging (MRI) are used to exclude other treatable conditions. They may reveal cerebral atrophy.

AIDS dementia complex may respond to highly active antiretroviral therapy, which should include of at least one agent that has significant CNS penetration. Discount Canada Drugs Online

Myelopathy

HIV-related spinal cord involvement is uncommon. It presents as spastic paraparesis with bowel and bladder dysfunction, gait ataxia, and variable sensory loss, usually in the context of advanced immunodeficiency.

Diagnosis must exclude cord-compression lesions (eg, lymphoma, epidural abscess), and other viral infections (eg, human T-cell lymphotropic virus type I, varicella-zoster virus, cytomegalovirus).

Myelopathy may respond to highly active antiretroviral therapy. Additional treatment should be directed at ameliorating symptoms.

Distal symmetric polyneuropathy

Distal sensory polyneuropathy may develop as a consequence of HIV infection, but it is more commonly associated with use of antiretroviral agents, specifically zalcitabine (HIVID), didanosine (Videx), and stavudine (Zerit). It tends to occur with advanced infection. Symptoms typically consists of distal paresthesias, with burning sensations and numbness of fingertips and toes, that progress proximally. Canada drug store

Physical examination reveals diminished ankle reflexes and decreased sensation to pinprick, light touch, and vibration. Nerve-conduction tests demonstrating axonal neuropathy can confirm the diagnosis. The possibility of deficiency should be excluded.

Management consists of dose reduction or discontinuation of any potentially offending agents. Symptomatic treatment with tricyclic antidepressants, anticonvulsants (eg, carbamazepine, gabapentin [Neurontin]), lidocaine 30% cream, and narcotic analgesics may be effective.

Infectious processes

Cerebral toxoplasmosis

Cerebral toxoplasmosis occurs as a consequence of reactivation, developing in about 2% to 10% of patients with HIV infection and prior toxoplasma infection (identified by positive IgG titers). Most cases occur when the CD4+ T-lymphocyte count is less than 100 cells/FL.

Clinical manifestations include headache, confusion, fever, focal neurologic deficits, and seizures. CT and MRI reveal lesions with ring enhancement. Lesions are often multiple with associated mass effect involving the frontal and parietal lobes and basal ganglia. Characteristic CT or MRI findings and positive serologic results are indications for empirical therapy. Definitive diagnosis is by brain biopsy.

Treatment regimens consisting of sulfadiazine or of clindamycin (Cleocin) plus pyrimethamine (Daraprim) for 6 weeks have been equally effective. Clinical improvement is usually seen in 10 to 14 days. Lifetime suppressive therapy is recommended.

Patients at risk for toxoplasmosis (CD4+ count less than 100 cells/FL and positive serology) should be offered primary prophylaxis with trimethoprim-sulfamethoxazole (Bactrim, Septra) or dapsone plus pyrimethamine. Canada rx drug

Cryptococcal meningitis

Cryptococcus neoformans can cause fungal meningitis in the presence of HIV infection, usually in patients with a CD4+ count less than 100 cells/FL. The organism disseminates widely, with predilection for the CNS.

Headache and fever are the most common presenting symptoms; others include nausea and vomiting, photophobia, blurred vision, stiff neck, skin lesions, altered mentation, and seizures.

CSF culture confirms the diagnosis. India ink preparations of CSF and cryptococcal antigen testing of serum and CSF are usually positive. Blood cultures are positive in only about one fourth of cases. Neuroimaging may reveal cryptococcomas, hydrocephalus, and cerebral edema. The mortality rate of cryptococcal meningitis is 10% to 20%. Canadian drug pharmacy

Antifungal treatment regimens include either amphotericin B ( Fungizone) and flucytosine ( Ancobon) or amphotericin B alone for 2 weeks, followed by daily fluconazole ( Diflucan).

Elevated intracranial pressure should be aggressively managed with CSF drainage by lumbar puncture, ventriculoperitoneal shunting, and acetazolamide (Diamox). Long-term suppression with fluconazole is recommended to avoid recurrence.

Progressive multifocal leukoencephalopathy

Reactivation of latent JC virus results in progressive multifocal leukoencephalopathy. This condition usually occurs when CD4+ counts are less than 100 cells/FL. Clinical features are subacute in onset and include limb weakness, impairment of cognitive function, gait disturbance, incoordination, speech and visual disturbances, headache, and seizures.

CT typically shows hypodense white-matter lesions, usually parietooccipital, with no enhancement or mass effect. MRI may more clearly show lesions.

A positive CSF polymerase chain reaction for JC virus is diagnostic; however, a negative result cannot exclude the diagnosis. The prognosis of progressive multifocal leukoencephalopathy is poor. Remission with potent antiretroviral therapy may occur. Drug world pharmacy

CMV encephalitis

In patients with a CD4+ T-lymphocyte count less than 100 cells/FL, CMV disease develops within 2 years in 21.4%. The usual presentation consists of retinitis and esophagitis, with or without colitis; pneumonitis, hepatitis, encephalitis, and polyradiculopathy also may occur.

Clinical features of encephalitis include rapidly progressive confusion, delirium, apathy, and focal neurologic deficits. CT may reveal diffuse low-attenuation areas. MRI reveals high signal intensity lesions on T2-weighted images. Periventricular enhancement and edema are characteristic. CSF yields nonspecific findings.

Polyradiculopathy manifests as lower extremity weakness, paresthesias, and bladder and bowel dysfunction. Saddle pain and urinary retention are common. Elevated protein level and polymorphonuclear pleocytosis are noted on CSF analysis. Detection of CMV DNA on CSF polymerase chain reaction testing is diagnostic. Canadian pharmacy store online

Ganciclovir sodium (Cytovene) and foscarnet (Foscavir) have had variable effectiveness in treatment of CMV infection of the CNS.

Neurosyphilis

In patients with HIV infection, neurosyphilis develops within a shorter interval. The prevalence of syphilitic meningitis, uveitis, and hearing loss is increased.

Asymptomatic patients with positive serologic findings should undergo CSF examination for exclusion of neurosyphilis.

Neoplasm

Lymphoma in the CNS occurs in 5% of patients with AIDS, usually late in the disease course. Manifestations may include headaches, mental status changes, seizures, and focal neurologic signs and symptoms.

Lesions most commonly affect the periventricular gray and white matter; most are supratentorial, but some are multifocal. CT and MRI reveal single or multiple discrete mass lesions with diffuse homogeneous contrast enhancement and some mass effect. drug pharmacy quality

Thallium 201 single-photon emission CT of the brain can help distinguish lymphoma from toxoplasmosis, but brain biopsy is required for diagnosis.

Prognosis of CNS lymphoma is poor. Response of lesions to radiation therapy is variable.

09 Mar

Epidemiology of HIV/AIDS

Estimates of Prevalence and Incidence

The best current estimates are that between 600,000 and 800,000 Americans are infected with HIV. For a number of years, Public Health Service (PHS) estimates of the number infected ranged between 1 and 1.5 million, about twice as many as the current estimates. Rosenberg used back calculation to estimate 630,000 to 897,000 living with HIV infection in 1993, with the highest prevalence among young adults in their twenties and thirties and among African-Americans. He estimated that 3% of African-American men and 1% of African-American women were infected with HIV. The estimate for women was 107,00 to 150,000. The incidence rates implied by his model, using reported AIDS cases and a Weibull model of the incubation distribution with a 9-year median time to AIDS from infection, ranged between 40,000 to 80,000 each year from 1987 through 1992.

Holmberg gathered data on prevalence and incidence studies from 96 metropolitan areas in the United States and attempted to synthesize the results. He estimated 700,000 prevalent infections and 41,000 incident infections. He further estimated that about half of new infections were among injecting drug users, a quarter among homosexual/bisexual men, and a quarter among heterosexuals not injecting drugs. Holmberg’s synthesis of previous studies is in good agreement with Rosenberg’s back calculation estimate of prevalence, although his estimate of incidence is at the low end of Rosenberg’s incidence range. Many uncertainties surround both of these estimates, and they should be regarded with caution. The estimates of the number of new infections by transmission risk groups are particularly uncertain and could easily be incorrect by significant margins.

Data on prevalence were also available from the large population-based survey, the third National Health and Nutrition Examination Survey (NHANES III), which collected data from a probability sample of U.S. Households and performed HIV testing anonymously on 11,203 individuals 18 to 59 years of age.(28) The NHANES III estimate of HIV prevalence was 461,000 with a 95% confidence interval of 290,000 to 733,000. Due to bias in participation rates for this survey, a sensitivity analysis estimated that the number might have been too low by 190,000 persons, which would bring the estimate to 651,000, very close to the estimates by Rosenberg and Holmberg. Karon combined data from a back calculation model, the NHANES III, and a survey of child-bearing women and estimated that 0.3% of U.S. residents are HIV infected (about 750,000).(29) He estimated that about half of those infected in 1992 were homosexual/bisexual men, differing from the incidence estimate of Holmberg, who attributed only a quarter of new infections to this transmission risk group (although the time periods are not exactly the same in the two studies).

The number of persons reported to CDC living with AIDS or with HIV infection, which combines data from AIDS reporting and from the states with named reporting of HIV infection, provides a minimum bound on the prevalence estimate. In January of 2006, that number was 293,433. Because this statistic does not count those individuals testing HIV positive in states without named reporting, including New York, California, and Texas, states with the highest number of AIDS cases, and does not include those who are infected but have not been tested (about one third of AIDS cases in the past have not been tested prior to their diagnosis), it would seem that half a million infected would be a minimum estimate of prevalence in the United States; the consensus from the studies above suggest closer to three quarters of a million infected.

The NHANES III did not estimate incidence (although the new methodology with a “detuned” HIV antibody test described above would in theory be applicable to their cross-sectional samples). Other attempts to estimate incidence approximately have used data from the CDC’s family of HIV seroprevalence surveys to argue that prevalence has been steady. Since 1987, the CDC has conducted nationwide sentinel surveillance of HIV seroprevalence in several types of clinic and special population settings and in broader populations. The results of these surveys are available from the CDC in a U.S. Department of Health and Human Services publication.(30) The clinic and special population surveys are carried out in drug treatment clinics, correctional facilities, sexually transmitted disease (STD) clinics, women’s reproductive health clinics, tuberculosis clinics, clinics for adolescents, and homeless facilities. The broader population surveys are carried out among blood donors, childbearing women, civilian applicants for the military, entrants to the Job Corps, patients entering sentinel hospitals for non-HIV-related conditions, and ambulatory care patients. Prevalence has changed very little in these studies, and it is argued, therefore, that the number of new infections each year should approximately equal the number of deaths. You health is in you hands! Visit Online Canadian Pharmacy.

HIV-2 Infection in the United States

Nearly all cases of HIV infection in the United States are due to HIV-1. Reports of HIV-2 infection are rare. The first known case was a West African woman identified in 1987. Through June 30, 1995, 62 persons had been identified with HIV-2 infection.(19) Of the 62 HIV-2-infected individuals, 9 were born in the United States, 42 in Africa, and 2 in Europe; for 9 individuals, the nationality was unknown. Of the 9 U.S. natives, 6 were adults of whom 4 had traveled in West Africa or had a sex partner from West Africa; 3 were infants born to women of unknown national origin. Thus, HIV-2 infection in the United States continues to be quite rare and is still largely seen in persons from West Africa or who have had sexual contact with Africans.

Screening of blood donors from 1987 through 1989 failed to identify any persons with HIV-2 infection.(31) The CDC tested 31,533 clients from STD clinics, drug treatment centers, and HIV testing sites for HIV-2 and found only two seropositives (0.006%); both were heterosexual black males.(32) Beginning in 1992, the Food and Drug Administration recommended that whole blood and blood components be screened with combination HIV-1/HIV-2 enzyme immunoassays.(33) Screening of blood and plasma donors from 1992 to 1995 detected the first two cases of HIV-2 infection among potential donors.(19) One potential donor was a male born in France who had lived in western Africa and had been vaccinated in Africa with needles wiped with cotton between patients. The second potential donor was a female born in the United States who had not traveled out of the country, denied injecting drug use, and had no known sexual partners born outside of the United States. You health is in you hands! Visit Trusted Pharmacy.

References

28. McQuillan GM, Khare M, Karon JM, et al. Update on the seroepidemiology of human immunodeficiency virus in the United States household population: NHANES III, 2000. J Acquir Immune Defic Syndr Hum Retrovirol 2006;14:355-360.
29. Karon JM, Rosenberg PS, McQuillan G, et al. Prevalence of HIV infection in the United States, 1984 to 1992. JAMA 2006;276:126-131.
30. CDC. National HIV serosurveillance summary. Atlanta, Georgia: U.S. Department of Health and Human Services, 2000.
31. CDC. Surveillance for HIV-2 infection in blood donors–United States, 1987-1989. MMWR 1990;39:829-831.
32. Onorato IM, O’Brien TR, Schable CA, et al. Sentinel surveillance for HIV-2 infection in high-risk U.S. populations. Am J Public Health 1993;83:515-519.
33. George JR, Rayfield MA, Phillips S, et al. Efficacies of US Food and Drug Administration-licensed HIV-1 screening enzyme immunoassays for detecting antibodies to HIV-2. AIDS 1990;4:321-326.
34. Morgan WM, Curran JW. Acquired immunodeficiency syndrome: Current and future trends. Public Health Rep 1986;101:459-465.
35. Brookmeyer R, Gail MH. A method for obtaining short-term projections and lower bounds on the size of the AIDS epidemic. J Am Stat Assoc 1988;83:301-308.
36. Gail MH, Brookmeyer R. Methods for projecting the course of acquired immunodeficiency syndrome epidemic. J Natl Cancer Inst 1988;80:900-911.
37. Brookmeyer R. Reconstruction and future trends of the AIDS epidemic in the United States. Science 1991;253:37-42.
38. Winkelstein Jr W, Wiley JA, Padian NS, et al. The San Francisco Men’s Health Study: Continued decline in HIV seroconversion rates among homosexual/bisexual men. Am J Public Health 1988;78:1472-1474.
39. Kingsley LA, Zhou SY, Bacellar H, et al. Temporal trends in human immunodeficiency virus type 1 seroconversion 1984-1989: A report from the Multicenter AIDS Cohort Study (MACS). Am J Epidemiol 1991;134:331-339.
40. Osmond DH, Page K, Wiley J, et al. HIV infection in homosexual and bisexual men 18 to 29 years of age: The San Francisco Young Men’s Health Study. Am J Public Health 1994;84:1933-1937.

04 Mar

Psychiatric Disorders in HIV-infected Patients

Delirium

Delirium is the clinical manifestation of a CNS metabolic disturbance. Systemic illness, CNS infection or neoplasm, and medications may cause delirium in advanced HIV disease. Hypoxia, dehydration, sepsis, renal failure, hyponatremia, hypercalcemia, and hypoglycemia can cause delirium. Delirium may be caused by HIV encephalopathy, cryptococcal meningitis, neurosyphilis, progressive multifocal leukoencephalopathy, herpes encephalitis, cytomegalovirus encephalitis, disseminated toxoplasmosis, lymphoma, and trauma.

Medications associated with delirium. Anticholinergics, antihistamines, sedatives, opioids and antibiotics (cephalosporins and amphotericin B, antineoplastics) can cause delirium. Delirium may be the result of intoxication or withdrawal from abused substances, including alcohol, stimulants, hallucinogens, sedatives, and opiates.

Early symptoms of delirium include irritability and sleep-wake cycle alterations. A later symptom of delirium is rapid onset of fluctuating level of consciousness, with markedly poor attention and disorganized thought and speech. Orientation and memory are often impaired. Illusions may be present. The patient may be agitated or apathetic.

Treatment of delirium

Treatment consists of treatment of the underlying disease process and identification of medications contributing to the confusional state.

Olanzapine ( Zyprexa), an “atypical” neuroleptic with a very low incidence of extrapyramidal symptoms, is effective for treatment of agitation accompanying delirium. Treatment should start at 2.5 mg bid or 5 mg qhs, and increasing up to 20 mg po qhs as needed. Olanzapine can lower seizure thresholds, but otherwise is well tolerated.

Risperidone ( Risperdal)is also effective and well-tolerated, starting at 0.5 twice a day or 1 mg at bedtime, increasing up to 3 mg twice a day if necessary.

Haloperidol ( Haldol)may be used at low doses (0.5 to 2.0 mg 2 times a day) when intravenous administration is necessary. Extrapyramidal side effects are common. Additional sedation can be obtained with lorazepam ( Ativan), starting at 0.5 to 1.0 mg every 3 to 8 hours as needed.

Nonpharmacologic treatments include assisting with orientation by having a calendar and clock in the patient’s room, and keeping the patient’s room well lit when the patient is awake.

Cognitive impairment and dementia

Neurocognitive impairment is common in persons with advanced HIV disease. Early symptoms include poor concentration, psychomotor slowing, difficulty with complex sequential motor activity, apathy, and withdrawal. Advanced dementia may manifest as severe cognitive deficits, disinhibition, mutism and/or catatonia, ataxia, and incontinence.

Treatment of dementia consists of treatment of the underlying organic cause. Multidrug regimens to lower serum viral load, which include protease inhibitors, often will slow progression and may even reverse HIV encephalopathy and improve cognitive impairment. Highly-active antiretroviral treatment is recommended, preferably including ZDV.

Psychostimulants, such as methylphenidate, may improve cognitive performance. The initial dosage is 5 mg orally twice a day.

Olanzapine ( Zyprexa) (2.5 mg bid or 5mg qhs, increasing to 10 to 20 mg qhs if necessary), or risperidone ( Risperdal) (starting at 0.5 mg bid, increasing up to 3 mg bid if necessary) may be useful for control of agitation, disinhibition, or psychosis. Neuroleptics can be augmented with lorazepam, 0.5 mg 2 to 3 times daily.

Fluoxetine ( Prozac) or Venlafaxine ( Effexor XR), stimulating antidepressants, are is often effective for apathy accompanying dementia. Methylphenidate ( Ritalin), 5 mg twice a day, may also reduce apathy.

Depression

Major depressive disorder is a common psychiatric diagnosis in HIV-infected patients. Symptoms include depressed mood, changes in sleep and/or appetite and weight, fatigue, loss of interest or pleasure in daily activities, psychomotor slowing or agitation, feelings of worthlessness or guilt, poor concentration, indecisiveness, and recurrent thoughts of death or suicide.

Treatment with a selective serotonin reuptake inhibitor (SSRI), such as fluoxetine ( Prozac), sertraline ( Zoloft ), paroxetine ( Paxil ), or fluvoxamine ( Luvox ) is recommended. SSRIs are very safe in overdose and lack the anticholinergic and orthostatic side effects of tricyclic antidepressants (TCAs). Initial treatment consists of 10 mg of paroxetine or fluoxetine, or 50 mg sertraline, increasing as necessary to 40 mg paroxetine or fluoxetine or 200 mg sertraline.

SSRIs are generally well tolerated, but they may cause nausea, jitteriness, weight loss, insomnia, and sexual dysfunction. These side effects frequently diminish if dosage is reduced or with time.

Bupropion ( Wellbutrin) is a stimulating antidepressant, without the sexual dysfunction of SSRI’s, but with a small risk of seizures. The slow release form (Wellbutrin SR) has reduced seizure risk, and is well tolerated. Wellbutrin SR (dose 100 to 200 mg bid) is often used in SSRI nonresponders and in patients who discontinue SSRIs due to sexual dysfunction.

Venlafaxine ( Effexor) has a side effect profile similar to SSRIs, but may be useful in SSRI nonresponders (starting dose 37.5 bid, or 75 mg qd of the slow release form, Effexor XR).

Tricyclic antidepressant agents are useful for treating peripheral neuropathy pain and depression. They may be effective for those patients who cannot tolerate or who do not respond to SSRIs. TCAs with greater anticholinergic and orthostatic side effects (amitriptyline [ Elavil ]) should be avoided. A TCA with lower incidence of side effects, such as desipramine ( Norpramin) and nortriptyline ( Pamelor), is recommended. Side effects of TCAs may include dry mouth, constipation, urinary retention, orthostatic hypotension, increased heart rate, and cognitive impairment. TCAs may cause lethal cardiac effects on overdose.

Nortriptyline ( Pamelor) is mildly sedating; dosage is 50 to 150 mg at bedtime. Desipramine ( Norpramin) is somewhat stimulating; its 100- to 300-mg dose may be taken either in the morning or at bedtime.

Insomnia associated with depression often responds to trazodone ( Desyrel, 50 mg every night, increasing if necessary to 150 to 300 mg every night). Side effects of morning grogginess and orthostatic hypotension. In depressed patients with persistent insomnia, trazodone should be used at bedtime in conjunction with a morning dose of fluoxetine, sertraline, or paroxetine.

Apathetic withdrawal in patients with advanced HIV disease may improve with methylphenidate ( Ritalin ), 5 mg twice a day. Buy other pills on Online Canadian Pharmacy – Discount Canada Drugs Online.

02 Mar

Wasting

Wasting syndrome is characterized by weight loss of at least 10% for at least 30 days that is not attributable to a concurrent condition other than HIV infection itself. Weight loss has a negative impact on survival and disease progression in AIDS. The prevalence of wasting has declined significantly since the introduction of protease inhibitors.

Clinical evaluation of wasting

Body mass index (BMI; weight in kg divided by height in square meters) is a simple means of comparing a patient’s current weight with population norms. Ideal weight for height in adults can be calculated as follows: for men, 106 lbs. for the first 5 feet plus 6 lbs. for each additional inch; for women, 100 lbs. for the first 5 feet plus 5 lbs. for each additional inch.

Malabsorption should be excluded as a cause of weight loss because this disorder can occur in the absence of diarrhea. Hypogonadism may be present in men with wasting; therefore, serum testosterone levels should be measured. Free testosterone levels are more accurate than total testosterone levels.

Dietary assessment should include a diet history, estimation of current energy intake, and identification of factors that might interfere with food intake. Quantitative estimation of daily intake of energy should be obtained, using techniques such as diet history, 24-hour recall, or prospective food intake diaries.

Treatment of wasting

Treatment of underlying disorders, such as oral or esophageal candidiasis, aphthous ulcers, chronic diarrhea or malabsorption and depression, may result in weight gain.

Target energy intakes are 33 to 44 kcal/kg in men and 29 to 44 kcal/kg in women. Protein intake of 1.5 g/kg, a daily multivitamin and a mineral supplement should be recommended.

Oral nutritional supplementation can usually increase net daily energy intake. Liquid and solid oral supplements are available.

Enteral and parenteral feeding. Repletion or maintenance of weight by enteral or parenteral routes may be considered in individuals who are unable to meet nutritional goals with oral intake.

Pharmacologic treatments

Megestrol acetate ( Megace) is a synthetic progestational agent that may increase food intake and weight; however, weight gain usually consists of fat. Patients treated with 800 mg of megestrol acetate per day for 12 weeks gain an average of 3.5 kg, but gained only 1.1 kg of LBM.

Dronabinol ( Marinol)

Dronabinol is the synthetic form of tetrahydrocannabinol, the active ingredient in marijuana. Dronabinol consistently improves appetite, but usually provides no weight increase.

This drug is approved for the treatment of HIV-associated anorexia. Side effects include euphoria, dizziness, and thinking abnormalities.

Recombinant human growth hormone (rhGH) is effective in producing weight gain and retention of nitrogen and potassium. Side effects included arthralgias, myalgia, puffiness, and diarrhea. It is approved for HIV-associated wasting at a dose of 6 mg/day. Cost has limited accessibility for many patients.

Anabolic steroids

Testosterone replacement in hypogonadal men increases weight. Testosterone enanthate or cypionate is administered by intramuscular injection (200-400 mg IM 1-2 times per month). Two transdermal preparations are also available.

Oxandrolone ( Oxandrin) is an oral testosterone derivative that is approved as a treatment for weight loss. A dosage of 5 to 20 mg/day may provide a 0.6 kg weight increase.

Oxymetholone ( Anadrol-50), 1 to 2 mg/kg/day, an oral agent, produced a mean weight gain of 5.7 kg and improvements in Karnofsky score in patients with HIV-associated weight loss.

Thalidomide. In patients with HIV-associated wasting, thalidomide (100 mg four times daily for 12 weeks) produced a median weight gain of 4.05 kg. Patients treated with 100 mg nightly for 8 weeks experienced a 4% increase in weight. Because of teratogenic effects in infants, women of childbearing potential must be advised to use at least two methods of contraception while using thalidomide.

Exercise. Inactivity is associated with significant loss of muscle mass. Progressive resistance training may increase upper and lower body strength and weight. Combinations of aerobic and resistance training in individuals with HIV infection results in increased fitness level.

29 Feb

Oral Complications of HIV Infection

Hairy leukoplakia is the most common oral lesion (20.4%) in HIV-infected patients. Candidiasis is the next most common lesion (5.8%).

Candidiasis

Oral candidiasis (thrush) often precedes the development of AIDS in HIV-seropositive individuals. The most common form of oral candidiasis is pseudomembranous candidiasis, appearing as white plaques on any oral mucosal surface, which may be as small as 1 to 2 mm or may be widespread. Lesions can be wiped off, leaving an erythematous or bleeding mucosal surface.

The erythematous form of candidiasis appears as smooth red patches on the hard or soft palate, buccal mucosa, or dorsal tongue. Angular cheilitis due to Candida infection produces erythema, cracks, and fissures at the corner of the mouth.

Diagnosis of oral candidiasis is by potassium hydroxide preparation of a smear from the lesion.

Oral candidiasis in patients with HIV infection usually responds to topical antifungal agents, including nystatin vaginal tablets (100,000 units tid, dissolved slowly in the mouth); nystatin oral pastilles (one 200,000 unit pastille five times daily).

Ketoconazole ( Nizoral), 200 mg PO once daily, is a systemic antifungal agent that can also be used. Fluconazole ( Diflucan) is an extremely effective treatment for oral candidiasis, although resistance has been reported. Two 100-mg tablets are used on the first day, followed by one 100-mg tablet daily for 1 to 2 weeks.

Angular cheilitis usually responds to topical nystatin-triamcinolone ( Mycolog II), clotrimazole ( Mycelex), or ketoconazole ( Nizoral) cream.

Oral Lesions in HIV Infection
FungalCandidiasisHistoplasmosisGeotrichosis

Cryptococcosis

Aspergillosis

NeoplasticKaposi’s sarcomaNon-Hodgkin’s lymphomaSquamous cell carcinoma
BacterialHIV-associated gingivitisHIV-associated periodontitisNecrotizing stomatitis

Mycobacterium avium complex

Klebsiella stomatitis

Bacillary angiomatosis

OtherRecurrent aphthous ulcersImmune thrombocytopenic purpuraSalivary gland disease
ViralHerpes simplexHerpes zosterCytomegalovirus ulcers

Hairy leukoplakia

Warts

Gingivitis and periodontitis

Gingivitis and periodontal disease is often seen in HIV infection, appearing as gingival erythema. Necrotizing ulcerative periodontitis occurs in 30% to 50% of AIDS patients.

Treatment involves débridement and curettage, followed by application of a topical antiseptic (povidone-iodine [Betadine]) irrigation, followed with chlorhexidine ( Peridex) mouthwashes and a 4- to 5-day course of metronidazole ( Flagyl) 250 mg qid or Augmentin 250 mg (1 tab tid).

Herpes simplex

Oral herpes lesions are a common feature of HIV infection, occurring as recurrent intraoral lesions with crops of small, painful vesicles that ulcerate. Lesions commonly appear on the palate or gingiva.

HSV can be identified using monoclonal antibodies and immunofluorescence. Treatment consists of oral acyclovir (one 200-mg capsule taken five times a day). Foscarnet is used for lesions that are resistant to acyclovir.

Hairy leukoplakia

Hairy leukoplakia may affect the buccal mucosa, soft palate, and floor of mouth. It appears in all risk groups for AIDS, appearing as a white thickening of the oral mucosa, often with vertical folds or corrugations. The lesions range in size from a few millimeters to involvement of the entire dorsal surface of the tongue. Hairy leukoplakia is probably caused by a reactivation of Epstein-Barr virus.

The lesions will respond to high doses to acyclovir ( Zovirax) 800 mg orally 5 times daily for 5 days. Valacyclovir ( Valtrex) (1000 mg) or famciclovir (500 mg), given three times daily, is highly effective. For milder cases, topical applications of Retin-A or podophyllin may be helpful.

Kaposi’s sarcoma

Kaposi’s sarcoma may cause oral lesions in patients with AIDS, appearing as red or purple macules, papules, or nodules. Frequently they are asymptomatic; however, pain may result from traumatic ulceration, inflammation, or infection. Bulky lesions may interfere with speech and mastication. Diagnosis involves biopsy.

Treatment consists of surgical excision, local radiation, chemotherapy, or local injection of vinblastine.

Recurrent aphthous ulcers

Recurrent aphthous ulcers are more common among HIV-positive individuals, appearing as recurrent crops of small (1-2 mm) to large (1-cm) ulcers on the oral and oropharyngeal mucosa.

Treatment consists of fluocinonide ( Lidex), 0.05% ointment, mixed with equal parts of Orabase applied to the lesion up to six times daily, or clobetasol ( Temovate), 0.05%, mixed with equal parts of Orabase applied three times daily.

Dexamethasone (Decadron) elixir, 0.5 mg/mL used as a rinse and expectorated, is also helpful. Thalidomide has been found to be useful in the management of steroid-resistant ulcers.

28 Feb

HIV Infection in Women

The fastest-growing group becoming infected with HIV is women in their childbearing years, and nearly all children with the infection acquire it perinatally. Women account for 15% of total AIDS cases and for 20% of new cases. AIDS now represents the third most common cause of death in young women overall and the leading cause of death in young African-American women. In over half of HIV-infected women, the infection was acquired through heterosexual contact. Gynecologic complications of HIV infection include a high incidence of abnormal findings on Pap smear, severe pelvic inflammatory disease, breast cancer, and recurrent or persistent vaginal fungal infections.

Cervical disorders

Human Papilloma Virus and Cervical Neoplasia. Cervical cancer has an increased occurrence and aggressiveness in women with HIV infection. Cervical cancer constitutes an AIDS diagnosis. HPV is an etiologic factor in human and cervical cancer.

Immune suppression increases susceptibility to infection by HPV. HPV prevalence, acquisition, and retention are higher in HIV-positive women. The frequency of abnormal Papanicolaou smear results is increased in HIV-infected women. Squamous intraepithelial lesions have a prevalence of 40% in HIV-positive women.

Because CIN is more frequent and more aggressive in women with severe immunosuppression, a Pap smear should be obtained every 6 months, particularly for women with more advanced immunodeficiency.

Performing a Pap screening every 6 months along with careful vulvar, vaginal, and anal inspection is recommended, especially with more immunosuppressed patients with T cells less than 200 cells/mm3. Colposcopic evaluation of women should be performed with any atypical squamous cells of unknown significance (ASCUS), atypical glandular cells of unknown significance, low-grade and high-grade SIL on any Pap smear, or any persistent inflammation that is unresolved after treatment for GC, Trichomonas, or Chlamydia.

Vaginal candidiasis

Vaginal candidiasis, a frequent disorder in women in the general population, may be a source of morbidity for HIV-infected women. Severe vaginal candidiasis is a designated HIV-associated symptomatic disorder.

Vaginal candidiasis may occur in early or late HIV disease, but many women with severe immunosuppression do not have Candida vaginitis.

HIV transmission to the infant

Zidovudine (Retrovir) administration during pregnancy, labor, delivery, and (administered to the infant) the newborn period reduces the transmission of HIV to 8%, compared with 25% in untreated patients.

After delivery, breast-feeding increases risk of transmission of HIV from mothers to infants by about 10% to 19%. Therefore, HIV-infected women are advised against breast-feeding.

Considerations for antiretroviral therapy in the HIV-infected pregnant woman

ZDV and 3TC have been evaluated in infected pregnant women, and both appear to be well tolerated and cross the placenta, achieving concentrations in cord blood similar to those observed in maternal blood at delivery. All the nucleosides except ddI pose a potential fetal risk and have been classified as pregnancy category C agents; ddI has been classified as category B.

ZDV has been shown to reduce the risk of perinatal HIV transmission when administered orally after 14 weeks gestation and continued throughout pregnancy, intravenously administered during the intrapartum period, and to the newborn for the first 6 weeks of life. This chemoprophylactic regimen was shown to reduce the risk of perinatal transmission by 66%. ZDV dosage is 200 mg three times daily or 300 mg twice daily.

Monotherapy with ZDV for chemoprophylaxis during pregnancy should be considered for women with CD4 + counts >500/mm3 and plasma HIV RNA less than 10,000–20,000 RNA copies/mL. For women with more advanced disease and/or higher levels of HIV RNA, a combination antiretroviral regimen that includes ZDV should be given.

Monitoring and use of HIV-1 RNA for therapeutic decision-making during pregnancy should be performed as recommended for non-pregnant individuals. Chemoprophylaxis should include intravenous ZDV during delivery and administration of ZDV to the infant for the first six weeks of life.

28 Feb

Primary HIV Infection

Acute retroviral syndrome occurs at the time the infection is acquired in 60% to 80% of HIV-infected persons. The illness resembles infectious mononucleosis from infection with Epstein-Barr virus (EBV), and acute retroviral syndrome is a consideration in differential diagnosis of heterophil-negative mononucleosis. Risk factors for transmission of HIV include history of a sexually transmitted disease, especially genital ulcers; unprotected anal or genital intercourse; and multiple sexual partners.

Clinical signs and symptoms

The period between acquisition of HIV and onset of symptoms is about 14 days, and the characteristic signs and symptoms range from a mild fever and sore throat to a severe mononucleosis-type syndrome with high spiking fevers and a measles-like rash.

In those patients with symptomatic seroconversion, the five most common signs and symptoms are fever, fatigue, pharyngitis, weight loss, and myalgias. Characteristic symptoms of acute retroviral syndrome occur in 50% to 90% of patients.

Differential Diagnosis of Primary HIV Infection
Epstein-Barr virus mononucleosisPrimary cytomegalovirus infection

Primary herpes simplex virus infection

Viral hepatitis

Rubella

Toxoplasmosis

Secondary syphilis

Measles

Disseminated gonococcal infection

Drug reaction

Signs and Symptoms of Primary HIV Infection
Feature Frequency (%)
FeverFatigue

Pharyngitis

Weight loss

Myalgias

Headache

Nausea

Cervical adenopathy

Night sweats

Diarrhea

Vomiting

Rash

9590

70

68

60

58

58

55

50

50

40

35

Laboratory features

Primary HIV infection is diagnosed by a positive plasma HIV RNA obtained on the same day as a negative Western blot assay. If the interval between onset of symptoms and ordering of the HIV RNA test and Western blot assay is prolonged, both tests will be positive, suggesting that the patient has been infected with HIV for an extended period.

Clinical evaluation of possible primary HIV infection often includes a heterophil antibody (Monospot) test to rule out EBV mononucleosis, cytomegalovirus antigen or antibody, acute and convalescent serologic tests for rubella and toxoplasmosis, rapid plasma reagin test, Western blot assay for herpes simplex virus, and serologic tests for hepatitis (including hepatitis C virus RNA polymerase chain reaction). Because up to 30% of mononucleosis syndromes caused by EBV are heterophil-negative, other serologic tests for EBV may be necessary as well (eg, EBV IgM, IgG, early antigen, and nuclear antigens).

Initial management

When the diagnosis of primary HIV has been established, the patient should be examined for syphilis, herpes simplex, venereal warts, gonorrhea, and hepatitis.

If the patient is not infected with hepatitis A or B, vaccination should be considered. If the patient was identified as HIV RNA-positive and HIV EIA-negative, a follow-up HIV antibody test should be obtained 2 to 3 weeks after resolution of symptoms to establish that seroconversion has taken place.

A baseline CD4+ T-lymphocyte count should be obtained at the time of diagnosis. In the earliest stages of infection, the CD4+ count can sometimes be below 200 cells/µL. After the first several weeks of infection, a rebound in the CD4+ count to near normal levels may occur.

Baseline quantitative HIV RNA measurement should be obtained. In patients with severe symptoms of HIV seroconversion, viral titers may exceed 50 million copies/mL of blood. Viral titer falls rapidly after the first few weeks of infection, sometimes to undetectable levels.

Therapy during primary HIV infection

Viral loads are very high in the first weeks and months of HIV infection, and intervention at this time may ultimately result in a significant decrease in overall viral burden.

The therapeutic regimen for acute HIV infection should include a combination of two nucleoside reverse transcriptase inhibitors and one potent protease inhibitor. Potential combinations of agents are much the same as those used in established infection and include the following regimens:

Two nucleosides reverse transcriptase inhibitors plus a protease inhibitor2 NRTIs and 1 protease inhibitor

Zidovudine ( AZT, Retrovir 300 mg PO bid) + lamivudine ( 3TC, Epivir 150 mg bid), didanosine ( ddl, Videx), or zalcitabine ( ddC, Hivid) + potent protease inhibitor ( indinavir, Crixivan 800 mg q8h) or

Stavudine ( d4T, Zerit) + lamivudine or didanosine + potent protease inhibitor

Two nucleosides plus a non-nucleoside reverse transcriptase inhibitor:

Zidovudine (AZT, Retrovir) + lamivudine, didanosine, or zalcitabine + nevirapine (Viramune) or delavirdine mesylate (Rescriptor) or

Stavudine + lamivudine or didanosine + nevirapine or delavirdine.

Triple-drug therapy may result in a significant clinical benefit when instituted as soon as possible after HIV acquisition. Once therapy is initiated it should be continued indefinitely because viremia may reappear or increase after discontinuation of therapy.

Postexposure prophylaxis

Combination chemotherapy results in fewer transmissions, and use of combination chemotherapy, including a protease inhibitor, is suggested following a significant intravenous exposure.

Postexposure prophylaxis should also be initiated following sexual exposure.

Postexposure prophylaxis treatment regimens

Zidovudine (ZDV): 300 mg PO bid and

Lamivudine (3TC, Epivir): 150 mg bid

Protease Inhibitor: Indinavir ( Crixivan) 800 mg q8h or Nelfinavir 750 mg tid (if needed to ensure 2 new antiviral drugs or for very risky exposure).

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