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HIV (PART 1)

AIDS was first recognized in the United States in the summer of 1981, when the U.S. Centers for Disease Control and Prevention (CDC) reported the unexplained occurrence of Pneumocystis carinii pneumonia in five previously healthy homosexual men in Los Angeles and of Kaposi's sarcoma (KS) in 26 previously healthy homosexual men in New York and Los Angeles. Within months, the disease became recognized in male and female injection drug users (IDUs) and soon thereafter in recipients of blood transfusions and in hemophiliacs. As the epidemiologic pattern of the disease unfolded, it became clear that a microbe transmissible by sexual (homosexual and heterosexual) contact and blood or blood products was the most likely etiologic agent of the epidemic.

In 1983, HIV was isolated from a patient with lymphadenopathy, and by 1984 it was demonstrated clearly to be the causative agent of AIDS. In 1985, a sensitive enzyme-linked immunosorbent assay (ELISA) was developed, which led to an appreciation of the scope of HIV infection among cohorts of individuals in the United States who admitted to practicing high-risk behavior as well as among selected populations that had been screened, such as blood donors, military recruits and active-duty military personnel, Job Corps applicants, and patients in selected sentinel hospitals. In addition, seroprevalance studies revealed the enormity of the global pandemic, particularly in developing countries.

ETIOLOGIC AGENT

The etiologic agent of AIDS is HIV, which belongs to the family of human retroviruses (Retroviridae) and the subfamily of lentiviruses. Nononcogenic lentiviruses cause disease in other animal species, including sheep, horses, goats, cattle, cats, and monkeys. The four recognized human retroviruses belong to two distinct groups: the human T lymphotropic viruses (HTLV) I and HTLV-II, which are transforming retroviruses; and the human immunodeficiency viruses, HIV-1 and HIV-2, which are cytopathic viruses. The most common cause of HIV disease throughout the world, and certainly in the United States, is HIV-1. HIV-1 comprises several subtypes with different geographic distributions. HIV-2 was first identified in 1986 in West African patients and was originally confined to West Africa. However, a number of cases that can be traced to West Africa or to sexual contacts with West Africans have been identified throughout the world. HIV-2 is more closely related phylogenetically to the simian immunodeficiency virus (SIV) found in sooty mangabeys than it is to HIV-1. In 1999, it was demonstrated that HIV-1 infection in humans was zoonotic and had originated from the Pan troglodytes troglodytes species of chimpanzees in whom the virus had co-evolved over centuries.

Proteinuria

Proteinuria is a common finding in adults in primary care practice. An algorithmic approach can be used to differentiate benign causes of proteinuria from rarer, more serious disorders. Benign causes include fever, intense activity or exercise, dehydration, emotional stress and acute illness. More serious causes include glomerulonephritis and multiple myeloma. Alkaline, dilute or concentrated urine; gross hematuria; and the presence of mucus, semen or white blood cells can cause a dipstick urinalysis to be falsely positive for protein. Of the three pathophysiologic mechanisms (glomerular, tubular and overflow) that produce proteinuria, glomerular malfunction is the most common and usually corresponds to a urinary protein excretion of more than 2 g per 24 hours. When a quantitative measurement of urinary protein is needed, most physicians prefer a 24-hour urine specimen. However, the urine protein-to-creatinine ratio performed on a random specimen has many advantages over the 24-hour collection, primarily convenience and possibly accuracy. Most patients evaluated for proteinuria have a benign cause. Patients with proteinuria greater than 2 g per day or in whom the underlying etiology remains unclear after a thorough medical evaluation should be referred to a nephrologist. (Am Fam Physician 2000;62:1333-40.)

ALCOHOL

The yearly cost of alcohol-related problems in the United States is as much as $300 billion, including accidents, health problems, lost productivity, crime, and treatment. There are more than 22,000 deaths from alcohol-related auto accidents per year, as well as almost 2 million nonfatal injuries and damage to almost 5 million vehicles. In addition, alcohol is responsible for almost 5% of missed work time, with a 25% decrease in work performance among heavy drinkers. Men and women who fulfill criteria for alcohol use disorders decrease their life span by approximately 15 years, with abuse and dependence responsible for almost 25% of premature deaths in men and 15% in women, figures that represent a three- to sixfold odds ratio of early death even among people with higher levels of education and socioeconomic functioning.

DEPRESSION

Depression Sign…

Depression (major depression) is defined as depressed mood on a daily basis for a minimum duration of 2 weeks. An episode may be characterized by sadness, indifference or apathy, or irritability and is usually associated with change in neurovegetative functions, including sleep patterns, appetite and weight, motor agitation or retardation, fatigue, impairment in concentration and decision making, feelings of shame or guilt, thoughts of death, dying or suicide. Patients with depression have a profound loss of pleasure in all enjoyable activities, exhibit early morning awakening, feel that the dysphoric mood state is qualitatively different from sadness, and often notice a diurnal variation in mood (worse in morning hours). Paradoxically, these more severe features predict a good response to antidepressant treatment.

Factors That Can Make Someone Depression

The incidence of depression increases with age; the disorder is approximately twice as prevalent in women as in men, regardless of age. These gender differences were previously believed to reflect sociocultural factors, but recent longitudinal twin studies indicate that the liability to major depression in adult women is largely genetic in origin, and that the effect of environmental factors is transitory and does not affect lifetime prevalence. The relationship between psychological stress, negative life events, and the onset of depressive episodes is complex. Negative life events can precipitate and contribute to depression, but recent data indicate that genetic factors influence the sensitivity of individuals to these stressful events. In most cases, both biologic and psychosocial factors are involved in the precipitation and unfolding of depressive episodes. The most potent stressors appear to involve death of a relative, assault, or severe marital or relationship problems.

Some Agent That Can Induce Depression

• Antihypertensive drugs (b-adrenergic blockers, calcium channel blockers)
• Anticholesterolemic agents
• Antiarrhythmic agents
• Glucocorticoids
• Antimicrobials
• Systemic analgesics
• Antiparkinsonian medications
• Anticonvulsants

Diseases which associate with depression

• Cardiac diseases about 20 and 30% manifest a depressive disorder.
• Cancer, depend on tumor site, severity of illness, and type of medical or surgical intervention. There is an overall mean prevalence of 25%.
• Neurologic disorders (cerebrovascular disorders, Parkinson's disease, multiple sclerosis, traumatic brain injury, left-hemisphere strokes)
• Diabetes mellitus
• Hypothyroidism

Learn More About Depression Mechanism

The neurobiology of unipolar depression is poorly understood. Although evidence for genetic transmission is not as strong as in bipolar disorder, monozygotic twins have a higher concordance rate (46%) than dizygotic siblings (20%), with little evidence for any effect of a shared family environment. Parallels between the affective, motor, and cognitive dysfunctions seen in unipolar depression and those observed in diseases of the basal ganglia have suggested that neural networks involving prefrontal cortex and the basal ganglia may be involved. This hypothesis is supported by positron emission tomography (PET) studies of brain glucose metabolism that show a decrease in metabolic rate in the caudate nuclei and frontal lobes in depressed patients that returns to normal with recovery. Single-photon emission computed tomography (SPECT) studies show comparable changes in blood flow. Magnetic resonance imaging (MRI) findings in some patients include an increased frequency of subcortical white matter lesions. However, because these findings are more prevalent in patients with late onset of depressive illness, their significance remains unproven. A number of studies document increased ventricle-to-brain ratios in some patients with recurrent depression, but whether this finding is state-dependent or represents true cerebral atrophy is controversial.

Postmortem examination of brains of suicide victims suggest altered noradrenergic activity, including increased binding to a1-, a2-, and b-adrenergic receptors in the cerebral cortex and a decreased total number and density of noradrenergic neurons in the locus coeruleus. Involvement of the serotonin system is suggested by findings of reduced plasma tryptophan levels, a decreased cerebrospinal fluid level of 5-hydroxyindolacetic acid (the principal metabolite of serotonin in brain), and decreased platelet serotonergic transporter binding. An increase in brain serotonin receptors in suicide victims is also reported. Depletion of blood tryptophan, the amino acid precursor of serotonin, rapidly reverses the antidepressant benefit in depressed patients who have been successfully treated. However, a decrement in mood after tryptophan reduction is considerably less robust in untreated patients, indicating that, if presynaptic serotonergic dysfunction occurs in depression, it likely plays a contributing rather than a causal role.

Neuroendocrine abnormalities that reflect the neurovegetative signs and symptoms of depression include (1) increased cortisol and corticotropin-releasing hormone (CRH) secretion, (2) an increase in adrenal size, (3) a decreased inhibitory response of glucocorticoids to dexamethasone, and (4) a blunted response of thyroid-stimulating hormone (TSH) level to infusion of thyroid-releasing hormone (TRH). Antidepressant treatment leads to normalization of these pituitary-adrenal abnormalities.

Diurnal variations in symptom severity and alterations in circadian rhythmicity of a number of neurochemical and neurohumoral factors suggest that biologic differences may be secondary to a primary defect in regulation of biologic rhythms. Patients with major depression show consistent findings of a decrease in rapid eye movement (REM) sleep onset (REM latency), an increase in REM density, and, in some subjects, a decrease in stage IV delta slow-wave sleep.
Although antidepressant drugs result in a blockade of neurotransmitter uptake within hours, their therapeutic effects typically emerge over several weeks, implicating neuroadaptive changes in second messenger systems and transcription factors as possible mechanisms of action.

Depression Treatment

Treatment planning requires coordination of short-term symptom remission with longer term maintenance strategies designed to prevent recurrence. The most effective intervention for achieving remission and preventing relapse is medication, but combined treatment, incorporating psychotherapy to help the patient cope with decreased self-esteem and demoralization, improves outcome.
It is essential to counsel patients about depression and the medications they are receiving. An educational approach is best, describing what is known about the depressive syndrome and how the medications may help. Advice about stress reduction, side effects, and expected length of treatment and cautions that alcohol may exacerbate depressive symptoms and impede drug response are helpful. Patients should be given time to describe their experience and the impact it has had on them, their family, and their outlook. Occasional empathic silence may be as helpful for the treatment alliance as verbal reassurance.