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HPV na Prática Clínica

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.Infertilidade
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HPV na Prática Clínica

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Recognizing the Clinical Presentation
The urinary tract, adjacent to the bacteria-rich lower gastrointestinal tract, produces and stores urine. The periurethral area is typically colonized with gut and other flora, some capable of causing UTI.[2] While the process of urination flushes bacteria from the urethral orifice, periurethral pathogens on occasion enter the urethra and ascend, reaching the bladder and resulting in UTI; this is the most common route for UTI acquisition. On rare occasion, hematogenous UTI can occur when a pathogen is delivered to the urinary tract via the bloodstream from a distant source of infection, such as the lungs in a patient with pneumonia.[3]
Urinary tract infections can involve mucosal tissue (cystitis) or soft tissue (pyelonephritis, prostatitis). Anatomically, the infection can be limited to the lower urinary tract (cystitis involving the bladder and urethra) or the upper tract (pyelonephritis). Complicated UTI can occur in either the upper or lower urinary tract but is accompanied by an underlying condition that increases the risk for failing therapy, such as obstruction, urologic dysfunction, or resistant pathogens. Most UTIs occur via an ascending route.[4]
UTI is typically diagnosed by clinical presentation and a limited number of physical exam findings. In the otherwise healthy woman, history of the present illness usually reveals a complaint of dysuria, often reported as an internal discomfort, with urinary frequency and urgency but without fever or constitutional symptoms. Although suprapubic tenderness and pain are often considered part of the clinical presentation, they are only found in about 20% of women with an uncomplicated UTI. Back pain, fever, nausea, and vomiting are more often associated with pyelonephritis, and rarely with cystitis; many with pyelonephritis will also report lower UTI symptoms. While vaginal infection and irritation can cause dysuria, most women who have dysuria without vaginal discharge have a UTI, not vaginitis.[5]
In urethritis, the inflammation and infection is limited to the urethra only, or urethra and vagina in women; its etiology is usually a sexually transmitted pathogen such as Chlamydia trachomatis, Ureaplasma urealyticum, Neisseria gonorrhoeae, or Trichomonas vaginalis.[6] Found in men and women, complaints include discomfort during voiding, but there are usually no symptoms of postvoid suprapubic pain or urinary frequency.
Hemorrhagic cystitis is characterized by large quantities of visible blood in the urine. Its etiology can be bacterial or adenovirus types 1-47 infection or as a result of radiation, cancer chemotherapy, or select immunosuppressive medication. Clinical presentation usually depends on its origin; with all causes, irritative voiding symptoms are typically reported. When infectious in origin, signs and symptoms of infection may also be encountered. Adenovirus is a common cause and is self-limiting in nature. Hemorrhagic cystitis is often confused with glomerulonephritis, but hypertension and abnormal renal function are absent in the former. When radiation-induced, symptoms may develop months after cessation of treatment.[7,8]
Acute pyelonephritis is an infection of the renal parenchyma and renal pelvis, caused by an ascending cystitis; most episodes are uncomplicated and not accompanied by risk of treatment failure such as obstruction, urologic dysfunction, or a multidrug-resistant uropathogen.[4] Irritative voiding symptoms similar to cystitis are usually reported, along with fever and flank pain, often with vomiting. Clinical findings usually include an acutely ill appearance, costovertebral tenderness, and pyuria. Table 1 outlines the clinical findings in women with dysuria and pyuria.
Table 1. Clinical Findings in Women With Dysuria and Pyuria[3,9]

Selecting Laboratory Tests
Laboratory testing has traditionally been used to support the diagnosis of UTI. Urine sampling for diagnostic testing is obtained through midstream voiding. A midstream urine sample can be used for dipstick, microscopic urinalysis, and urine culture. Urine dipstick testing is commonly done in the office setting when UTI is suspected because it is simple and convenient and yields immediate results.
Leukocyte esterase, nitrates, protein, and blood are the important features in evaluating for UTI. The presence of leukocyte esterase on a urine dipstick is equivalent to >/= 4 white blood cells per high-power field (WBC/hpf). Nearly all (>/= 96%) patients with UTI have pyuria equivalent to > 10 WBC/hpf.[5] Some uropathogens are capable of reducing dietary nitrates in the urine to nitrite; this is an indirect test for bacteriuria. When coupled with a leukocyte esterase response, the likely offending organism is a Gram-negative pathogen (Escherichia coli, Proteus spp., Klebsiella pneumoniae).
The nitrite test may be falsely negative in UTI with a low colony count, or in recently voided or dilute urine. In addition, this test does not detect organisms unable to reduce nitrate to nitrite, such as enterococci, staphylococci, or adenovirus.[10] Small amounts of protein and red blood cells may also be positive on dipstick in cases of UTI. Table 2 highlights common urinalysis dipstick findings in UTI. However, in one study of healthy young adult women with dysuria for less than 1 week without vaginal discharge, signs of pyelonephritis, or predisposing conditions, empiric therapy guided by clinical presentation alone was the most cost-effective strategy; culture and treat-later strategies were significantly more expensive, and use of the dipstick alone was the most expensive approach.[11] Further prospective clinical trials will be helpful in establishing the most cost-effective and clinically effective strategy, including patient-directed therapy.
Table 2. Common Urinalysis Dipstick Findings in Urinary Tract Infection[12,13]

Microscopic urinalysis can be used to confirm UTI but requires additional equipment and considerable technical skill if done in the office, or delay in time if performed in a laboratory. When coupled with classic symptoms, a finding of 2-5 WBCs or >/= 15 bacteria per hpf in a centrifuged urine sediment is consistent with UTI.[10] The presence of many epithelial cells usually indicates a contaminated specimen.
Urine culture is important when diagnosis is not clear or UTI is recurrent. The presence of more than one organism may indicate a contaminated urine specimen and collection and testing should be repeated. The presence of >/= 105 CFU/mL of bacteria is the traditional diagnostic indicator for UTI. However, in the presence of dysuria and other symptoms for UTI, 102 CFU/mL confirms the diagnosis.
Approximately 10% to 20% of women with acute uncomplicated pyelonephritis will have blood cultures positive for the offending pathogen. However, this is not predictive of a poorer outcome or need for protracted length of treatment in the otherwise healthy woman. While typically obtained when a patient pyelonephritis needs to be hospitalized, obtaining blood cultures will likely be of benefit only when there is evidence of complicated infection, multidrug-resistant pathogen or treatment failure.[4]

What Factors Determine the Risk of UTI?
Certain factors protect against or increase the risk for UTI. Male sex is recognized as a potent protective factor, in part due to the longer urethral length compared with women. In addition, certain women with a closer proximity of the urethral orifice to the anus appear to be at increased UTI risk.[14] In addition, the scrotum provides a physical barrier between the glans and the perianal region, a potential source of uropathogens. Unlike the periurethral area in women, the male periurethral area does not support bacterial growth. Zinc-rich prostatic secretions are antibacterial, further discouraging pathogen growth.[15] In women, the intestinal tract or periurethral area becomes colonized with uropathogens. Once colonization occurs, the organisms may remain in place, whether or not these cause a urinary tract infection.
In either sex, efficient bladder emptying helps prevent urine stagnation and minimizes UTI risk. Factors that can alter efficient bladder emptying, such as cystocele, rectocele, and benign prostatic hyperplasia (BPH) increase UTI risk. In addition, robust fucosyltransferase activity discourages bacterial adherence; the presence of relatively few bacterial adhesion receptor sites in the bladder and urethra acts similarly. Women with these receptors who do not have mucosal secretion of the fucosyltransferase enzyme to help block bacterial adherence are more likely to have colonization of E coli and other coliforms from the rectum and less likely to have lactobacilli in the periurethral area, resulting in frequent episodes of cystitis. The uroepithelial receptors can also be found in the upper urinary tract, increasing the risk of pyelonephritis.[6] Women who are nonsecretors of ABH blood group antigens show enhanced adherence of uropathogenic E coli to uroepithelial cells compared with women who are secretors; this becomes a major UTI risk factor when coupled with spermicide use or frequent vaginal sexual intercourse.[16]
The woman who is exposed to the spermicide nonoxynol-9, either through vaginal use or with a male partner who uses condoms with this spermicide, is at increased risk of UTI. The proposed mechanism of this risk is due to the spermicide's antibacterial effect, reducing lactobacilli, a normal component of the periurethral flora. Lactobacilli produce hydrogen peroxide and lactic acid, providing the periurethral area and vagina with a pH that inhibits bacterial growth and blocks potential sites of attachment, as well as being toxic to uropathogens.[17] Recent studies also propose that spermicides containing the antibacterial detergent benzethonium chloride, often used as a preservative, may contribute to this problem. Although often recommended, voiding at regular intervals, wiping patterns, and postcoital voiding have not been proven to provide uncomplicated UTI protection[14,18]; hot tubs, pantyhose, douching, and obesity have not been demonstrated to increase UTI risk.[14]
In postmenopausal women, estrogen deficiency leads to a marked reduction in lactobacilli colonization in the vaginal-perineal areas; topical estrogen use results in reestablishment of the normal protective flora and a reduction of UTI risk.[17] Recent antimicrobial use potentially increases UTI risk by the same mechanism.[14] The replenishment of urogenital microflora with probiotics or exogenous application of protective, "friendly" bacteria, via vaginal douche or capsule or taken orally in capsules, drinks, or yogurt, is gaining popularity for genitourinary tract infections.[19]
In children and elders, constipation has been noted to contribute to bladder instability and may encourage UTI.[20] Elders often have a number of risk factors for UTI, including alterations in urinary tract structure such as uterine prolapse, cystocele, rectocele, and BPH, and limited functional status impairing mobility, hygiene, and toileting.[20]

UTI in Special Populations
Most uncomplicated UTIs occur in women of reproductive age who otherwise do not have chronic health problems or voiding disorders; assessment is often straightforward and treatment is effective. However, certain populations, including elders, pregnant women, and people with clinical conditions such as asymptomatic bacteriuria, bear special mention.

Asymptomatic Bacteriuria
Asymptomatic bacteriuria, in which urine culture reveals a significant growth of a pathogen (> 105 bacteria/mL)[20] but the patient has no symptoms of UTI, can be found at equal rates in pregnant and nonpregnant women during the reproductive years. Incidence increases with age. Asymptomatic bacteriuria is noted in approximately 20% to 25% of community-dwelling women age 65 and older and in around 10% of community-dwelling men age 65 and older. In the nonpregnant woman of reproductive age or the well elder, asymptomatic bacteriuria poises no health threat and should only be treated if bladder instrumentation or surgery is planned. In fact, treatment may result in the development of resistant organisms. A course of an appropriate antimicrobial is indicated if bladder instrumentation is planned.[10,21]
The incidence of asymptomatic bacteriuria among elders residing in long-term-care facilities increases to 20% to 50% for those without an indwelling urinary catheter, but virtually all with an indwelling catheter have bacteriuria. Risk factors for bacteriuria in the elderly include altered elimination (fecal impaction and the use of medications that encourage constipation and urinary retention such as anticholinergic drugs), anatomic variations in the urinary tract (cystocele, BPH), hygienic issues (fecal soiling, poor perineal hygiene), neurologic impairment affecting mobility and bladder emptying, and postmenopausal hormonal changes. In the person with an indwelling urinary catheter and evidence of sepsis, bacteriuria should be treated.[18] Cunha proposes the following formulas to assist with the differentiation between UTI and bacteriuria: pyuria alone = inflammation; bacteriuria without pyuria = colonization; pyuria + bacteriuria + nitrites = infection.[22]

Symptomatic UTI in the Elderly
The healthy elder with an uncomplicated lower UTI, regardless of gender, is likely to have a classic presentation including urinary frequency, urgency, and suprapubic discomfort; new-onset urinary incontinence may also be reported. The frail elder with multiple health problems and complicated UTI may have an atypical or subtle presentation of infection, including change in appetite, delirium, and agitation. An elder with urinary incontinence and UTI may experience an increase in the number of episodes of urine loss.[20,22]

UTI and Asymptomatic Bacteriuria During Pregnancy
Pregnancy-related anatomic changes in the urinary tract, such as pressure on the bladder from enlarging uterus and increase in the size of the ureters, contribute to urinary reflux. UTI in the pregnant woman is a significant risk factor for low-birthweight infants and prematurity.
Asymptomatic bacteriuria occurs in 5% to 9% of both nonpregnant and pregnant women. If left untreated in pregnancy, progression to symptomatic UTI including acute cystitis and pyelonephritis occurs in 15% to 45%, or 4-fold higher than in nonpregnant women. This is due largely to the lower interleukin-6 levels and serum antibody responses to E coli antigens that occur during pregnancy, resulting in less robust immune response.
Since asymptomatic bacteriuria, usually caused by aerobic Gram-negative bacilli or Staphylococcus haemolyticus, can lead to UTI, a urine culture should be obtained from all women early in pregnancy, even in the absence of UTI symptoms.[10] Approximately 20% to 40% of women with bacteriuria will develop UTI during the course of the pregnancy; only 1% to 2% of those with a negative urine culture develop UTI. Bacteriuria should be treated with a 3- to 7-day course of antimicrobials, which reduces the risk of symptomatic UTI by 80% to 90%.[10,21]
Therapeutic options for the treatment of asymptomatic bacteriuria and symptomatic UTI during pregnancy are guided by pathogen susceptibility, and preferred antimicrobials include those with US Food and Drug Administration (FDA) pregnancy risk category B. Table 3 identifies FDA pregnancy risk and Hale's lactation risk categories for commonly prescribed antimicrobials in UTI. Antimicrobials in pregnancy risk category B include the beta-lactams (amoxicillin, cephalexin, cefpodoxime, cefixime, and amoxicillin/clavulanate) and nitrofurantoin. Nitrofurantoin has the advantage of sparing disruption of normal vaginal flora and consistent efficacy against E coli and Staphylococcus saprophyticus. Nitrofurantoin should be avoided after the 36th week of gestation due to the potential (though unlikely) risk for hemolysis if the fetus is G6PD-deficient and in infections caused by Proteus mirabilis. Beta-lactam use usually fails to eradicate the offending pathogen from the periurethral and perivaginal area, increasing the risk of reinfection.
Table 3. FDA Pregnancy Risk and Hale's Lactation Risk Categories for Commonly Prescribed Antimicrobials in Urinary Tract Infection

The fluoroquinolones and TMP-SMX are FDA pregnancy risk category C; TMP-SMX is also associated with a higher risk of treatment failure due to resistant pathogens.[6] Women with symptomatic UTI during pregnancy should be treated for 7 days, and asymptomatic bacteruria is usually treated for 3 days. Once UTI is documented, monthly screening urine cultures should be obtained for the duration of the pregnancy. Daily antimicrobial prophylaxis with an appropriate agent should be considered with evidence of 2 days of a symptomatic UTI or persistent, unresolved bacteruria, in spite of effective antimicrobial therapy. Urologic evaluation should also be considered to rule out structural abnormality.[10,21]

UTI in Men
UTI is often thought to be rare in men, but it is the most common cause of male dysuria. It typically occurs during the first 3 months of life or after age 50 years. Potential obstruction to urine flow may be caused by the foreskin in early life and by the prostate in mid and later life.[24] The male presenting with fever, dysuria, and back pain should be evaluated for acute bacterial prostatitis or pyelonephritis; a urology referral should be considered with any male UTI. Table 4 reviews the clinical findings in men with dysuria and pyuria.[25] Asymptomatic bacteriuria in the older man should not be treated unless bladder instrumentation, surgery, or prostatic massage is planned.[21]
Table 4. Clinical Findings in Men with Dysuria and Pyuria[25]

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