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TUBERCULOSIS
Tubercle bacilli may invade one or more (or even all) of the organs of the
genitourinari tract and cause a chronic granulomatous infection that shows the
same characteristics as tuberculosis in other organs.
It develops during many years after the first clinical displays of tuberculosis.
The urogenital tuberculosis exists mainly in age 20—40 years, rarely — at children
and seniors. It occupies the first place among the unpulmonary forms of
tuberculosis.
TUBERCULOSIS OF BUDS AND THE URINARY WAYS
Ethiology. The specific exciter — mycobacteria of tuberculosis (by the Koch
stick) predetermines a process, which reaches the genitourinary organs by the
hematogenous route from the lungs. The primary site is often not symptomatic or
apparent.
The kidney and possibly the prostate are the primary sites of tuberculous
infection in the genitourinary tract. All other genitourinary organs become
involved either by ascent (prostate to bladder) or descent (kidney to bladder,
prostate to epididymis). The testis may become involved by direct extension from
epididymal
infection.
Pathogeny. Basic by diffusion of tubercular infection there is hematogenical. At
first kidney are struck, and from there the infection on the blood vessels gets in the
kidney bowl, ureter, urinary bladder. Infection takes place in the period of primary
or second generalisation tubercular process from the basic cell in lights, lymphatic
nodes, bones, and muscles. Although the tubercular cells develop in both kidneys,
the process makes progress in 70 % cases - only in one. Only after the
unfavourable conditions to the clinical displays of tuberculosis of one kidney the
defect symptoms join and second, which was until now considered healthy. That it
is the principal reason of transformation of milliary tuberculosis of crust matter of
bud in the destructive defeat of cerebral matter.
Мicobacteria strike cortex and medulla matters of kidney. The tubercular cells,
which are localized in the crust matter, heal over relatively quickly, and they are
disposed in the cerebral matter, most frequent cavity disintegrates.
Acute and chronic forms of tuberculosis of the urogenital system.
Acute (milliary) form is displayed of general tubercular process and it hasn’t
an independent clinical motion. An attention of urologists is concentrated on the
chronic form of tuberculosis of the urogenital system.
Pathomorphology. At a acute form of tuberculosis of kidney in the crust matter
the typical lymphoidal or epitheliodal cellular humps, that have characteristic giant
cages, similar to the Pirogov-Lanhgance cages arise up. At the chronic form of
tuberculosis of buds humps are disposed at first in the crust and cerebral matter,
mainly in area of kidney papillae and pyramids. Gradually they take shelter by
ulcers, are added disintegration and form the cavities, which unite with the kidney
bowl, by bowl or are isolated.
Petrification of those cells or substitution of them by the fibrous fabric can take
place in some cases, in other ones — form plural cavities, which often unite
between it. Round cavities the inflammatory changes arise up and the humps
appear, that testifies to combination of different stages of motion of tubercular
process. These changes can be completed by full destruction of bud with
development of pyonephrose. Gradually the tubercular process engulfs a fibre, and
then Fatty capsule of kidney, that results in development of sclerosic or festering
paranephritis.
In case of diffusion of tubercular infection on the urinary bladder in the
submucose basis the specific elements of productive inflammatory process appear.
The process begins at first near the opening of ureter. The tubercular humps appear
on the mucus shell. In the case of their confluence between itself and necrotisation
the ulcers and then scars appear at that place.
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The defeat of all layers of wall of urinary bladder and substitution of her by the
sclerozed fabric can result in the wrinkling a urinary bladder (microcystis).
Immunity
Immunity in tuberculosis is the result of a complex series of reactions which are
not yet completely understood and which do not give the same high degree of
protection which follows, say, diphtheria immunization. In a primary infection the
bacilli are ingested by macrophages, processed to produce antigens which are
presented to specific receptors on T-lymphocytes in association with HLA DR
(human leucocyte antigen D related) glycoprotein on the macrophage surface. The
need for the correct HL antigen may explain why individuals appear to vary in
their resistance to tuberculosis. The presentation of the antigen to the helper T-cell
also requires the production of interleukin 1 by the macrophage. The activated Tcell produces interleukin 2 and a number of lymphokines, which mediated the
following reactions:
1. Stimulation of B-cells to produce antibody;
2. Induce delayed type hypersensitivity;
3. Activate cytotoxic cells;
4. Cause inhibition of macrophage motility.
An excess of mycobacterium antigens may stimulate suppressor T-cells.
At the primary infection macrophages ingest the tubercle bacillus, but they are
unable to kill the bacilli which may multiply within it. The cells retain their
motility and, at this stage can, carry the bacilli to other parts of the body. When
delayed hypersensitivity develops 3-6 weeks after infection, the macrophages
acquire the ability to kill the tubercle bacillus, although this is not entirely
successful. They and helper T-cells now accumulate around focus of infection. The
lymphokines inhibit the motility of the macrophages and induce them to become
epitheloid cells or Langhans giant cells. The typical tuberce now forms with
epitheloid cells surrounded by lymphocytes and fibrous tissue at the periphery. The
tubercle may heal at this stage or at any further stage or it can enlarge and perhaps
undergo central necrosis of a special type called caseous necrosis. This caseum can
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liquefy and discharge into a renal tubule, lymphatic or blood vessel liberating large
numbers of tubercle bacilli which spread the infection locally or to other organs.
Healing is associated with much fibrosis and calcium salts are laid down in this
caseum.
It is only after delayed hypersensitivity develops that tissue damage occurs.
Neither the tubercle bacillus, extracts of neither it nor culture filtrates can be
shown to possess toxic properties for the uninfected animal or human being.
Hypersensitivity is demonstrated by the intradermal injection of Old Tuberculin or
Purified Protein Derivative (Mantoux Test). This test may be of use in diagnosis if
it is known that the patient has previously been skin test negative and has not had
BCG vaccination. There is an association between a moderate degree of
hypersensitivity and resistance to tuberculosis, but a high degree has usually
disadvantageous. Some protection can be given to a healthy animal by the injection
of lymphocytes from a tuberculous animal but the transfer of serum gives no
protection. Tuberculous antibodies can be assayed in the serum of tuberculous
patients by a variety of methods but their significance is unclear. Corticosteroids
cause a lymphopenia and thus abolish delayed hypersensitivity. For this reason the
administration of corticosteroids and cytotoxic drugs is sometimes associated with
the reactivation of tuberculosis. Infections with M. Tuberculosis, M. bovis or
atypical mycobacteria are common in patients suffering from AIDS in which
helper T-cells are reduced.
Classification.
In practice they make a use of the сlinical-roentgenologic
classification of tuberculosis of buds offered by М. О. Lopatkin with coll. (1977):
I stage — nondestructive (infiltrate) tuberculosis of kidney;
II — initial destruction (papillitis or small, by diameter about 1 cm, single
cavity);
III —marked destruction (caverns or policavernosial tuberculosis one of
kidney segments);
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IV — total or subtotal destruction (policavernose tuberculosis of two
segments, tubercular pyonephrose, calcification kidney).
The one criterion (degree of destruction of kidney fabric) is fixed on basis of
this classification. They distinguish three forms of tuberculosis: tuberculoinfiltrative, ulcerous and scar.
Clinical picture.
For
kidney
urinary
tract
T.B
main
features
are.
On the early stages of disease, when in parenchyma the first tubercular humps
appear, sometimes-general weakness, indisposition, rapid fatigue, reduction of
body weight, lose of appetite, dull pain in the lumbar region, subfebril temperature
of body exists. In the case of the process sharpening, penetration of tubercular cell
in the kidney bowl the chill can appear. The temperature curve gains a gectic
character, sharp or dull pain appears in the lumbar region, and disurical discords
exist. The kidney pain exists at the corking by ureter rawsimilar (caseosic) the
masses. On the late stages of process, especially in case of bilateral defeat, all signs
of
chronic
insufficiency
of
kidney
appear.
For tuberculosis of kidneys of change in blood also are unspecific. Frequently they
mark a moderate lecocytosis with shift to left and by the insignificant reduction of
quantity of granulocyte leukocytes. Leukopenia and hypohromic anaemia can
exist. The ESR (erythrocyte sedimentation rate) changes answer a process activity.
If changes of blood are not specific for tuberculosis of urinary systems, the
appearance of pyuria, microhaematuria, proteinuria is signfull for a doctor. In a
sick on the bud tuberculosis the urine reaction is acid. For the exposure in its
sediment of pathological elements they apply a provocative test — hypodermic
enter 15—20
tuberculin. The leukocyte- and erithrocyturia increases at
tuberculosis.
The tuberculosis of ureters results in the increase of retention of urine in kidney,
worsening the same a motion of tubercular process. The specific narrowing of
ureters causes the development of ureterohydronefrosis, pyonephrosis. The attacks
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of kidney pain exist at ureters obturation. As far as death of kidney parenchyma the
pain diminishes, and the kidney becomes “mute”.
The objective displays of tuberculosis of urinary bladder at first are wretched.
There is a frequent, painfully, imperative urination that is accompanied with the
terminal hematuria which is impossible to consider an early sign. The same is up to
the changes of mucous membrane, which expose during the cystoscopy.
Diagnosis.
The most reliable and objective sign of tuberculosis of urinary organs is an
exposure in sediment of urine the mycobacteria tuberculosis. For this purpose they
apply bacterioscopical, bacteriological, biological methods of research, a frequent
sowing of urine and other.
For the exposure of morphological and functional changes in kidney they use the
roentgenologic methods of research.
In the initial stages of disease the pathological changes on excretory urograms
can’t be find if there are the same violations, how at unspecific pyelonefritis or
necrotic papillitis — eaten uneven contours in area of small bowls. As far as
progress of process on excretory urograms expose single or plural cavities, which
have uneven edges.
At the productive stage of kidney tuberculosis on urograms it is possible to
expose a defect of the filling, compression or amputation of bowl. The expansions
often exist and even obliteration kidney bowl. In the case of diffusion of tubercular
process on ureter pulls, even narrowing and expansion of it without the visible
peristaltic waves are marked. After wards the plural narrowing of ureters appears.
If the excretorial urography through the considerable decline of kidney function
doesn’t give a clear image, the retrograde pyelography is recommended. In case of
a sharp decline of kidney function the conducting of antegrade pyelography is
expedient. On the high-quality pictures it’s successfully to expose the same
changes, as well as at the ascending pyelography.
The kidney angiography is applied rarely, so far as in the early stages of disease
on angiogramms it is impossible to expose the specific characteristics concerning
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the tuberculosis changes. Its value grows in that case, when a resection of kidney is
planned. From data of arteriogramms they determine location of cavity and arterial
kidney vessels.
The cystoscopy is the most informative method of diagnostics of tuberculosis of
urinary bladder. In the early stages of tuberculosis of urinary bladder the mucous
membrane can be normal. On background pink mucous membrane expose small
areas of hyperemia and hemorrhages. Near the opening of the ureters staggered
kidney it is possible to expose a shallow primrose or grey-yellow tubercular humps
with the reddish rim on periphery. The opening ureterus is pulled in, deformed; it
has the shape of crater. Thus a function of its locking vehicle, that results in the
origin of bladder-ureteral reflux is violated. To the extent of process progress the
humps can be, the surface of mucous membrane above them takes shelter by
ulcers. The characteristic changes of the opening of the ureterus staggered kidney
exist – swollen mucous membrane.
It is possible to expose the considerable changes by cystography. The
diminished, deformed urinary bladder is exposed considerably at the neglected
processes on cystograms. Its contours are eaten. They often establish bladderureteral reflux in bud, that is staggered less. The ureter tuberculosis exists very
rarely.
Diagnose is based on data of bacteriological research of urine, excretions from
urinary tract. The narrowing of ureter exposes on ureterograms.
Tubercular defeat of urinary bladder, that is accompanied by the swelling up of
mucous membrane, after motion reminds a tumor of urinary bladder, and
tubercular ulcer — simple ulcer of urinary bladder (intersticial cystitis). In case of
diagnosis in such case establishment takes into consideration the results of
bacteriological research, and in the case of doubt they recommend an endovesical
biopsy.
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Differential
Chronic nonspecific cystitis or pyelonephritis may mimic tuberculosis
perfectly, especially since 15-20% of cases of tuberculosis are secondarily
invaded by pyogenic organisms.
If nonspecific infections do not respond to adequate therapy, a search for
tubercle bacilli should be made. Painless epididymitis points to tuberculosis.
Cystoscopic demonstration of tuberculosis and ulceration of the bladder wall
means tuberculosis. Urograms are usually definitive.
Acute or chronic nonspecific epididymitis may be confused with
tuberculosis, since the onset of tuberculosis is occasionally quite painfull. It
is rare to have palpatory changes in the seminal vesicles with nonspecific
epididymitis, but these are almost
routine findings in tuberculosis of the
epididymis.
The presence of tubercle bacilli on a culture of the urine is diagnostic.
On occacion, only the pathologist can make the diagnosis by microscopic
study of the surgically removed epididymis.
Amicrobic cystitis usually has an acute onset and is often proceeded by a
urethral discharge. “Sterile” pyuria is found, but tubercle bacilli are absent.
Cystoscopy may reveal ulcerations, but there are acute and superfical.
Although urograms show mild hydroureter and even hydronephrosis, there is
no ulceration of the calices as seen in renal tuberculosis.
Interstitial cystitis is typically characterized by frequency, nocturia, and
suprapubic pain with vesical filling. The urine is usually free of pus. Tubercl
bacilli are absent.
Multiple small renal stones or nephrocalcinosis seen by x-ray.
May suggest the type of calcification seen in the tuberculous kidney. In
renal tuberculosis, the calcium is in the parenchyma, although secondary
stones are occasionally seen.
Necrotizing papilitis, which may involve all of the calices of one or
both kidneys or, rarely, a solitary calyx, shows caliceal lesions (including
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calcifications) that simulate those of tuberculosis. Careful bacteriologic studies
will fail to demonstrate tubercle bacilli.
Medullary sponge kidneys may show small calcifications just distal to
the calices. The calices, however, are sharp, and no other stigmas of
tuberculosis can be demonstrated.
Urinary bilharziasis is a grate mimic of tuberculosis. Both present with
symptoms of cystitis and often hematuria. Vesical contraction, seen in both
diseases, may lead to extreme frequency. Schistosomiasis must be suspected
in endemic areas; the typical ova are found in the urine; cystoscopic and
urographic findings are definitive in differential diagnosis.
Complication
A. Renal Tuberculosis. Perinephric abscess may cause an enlarging mass
in the flank. A plain film of the abdomen will show obliteration of the renal
and psoas shadows. Sonograms and CT scans may be more helpful . Renal stones
may develop if secondery nonspecific infection is present . Uremia is the end stage
if both kidneys are involved .
B. Ureteral Tuberculosis : Scarring with strcture formation is one of the typical
lesions of tuberculosis and most commonly affects the juxtavesical portion of the
ureter . This may cause progressive hydronephrosis . Complete ureteral obstruction
may cause complete non-function of the kidney.
C. Vesical Tuberculosis: When severely damaged , the bladder wall becomes
fibrosed and contracted. Stenosis of the ureteres or reflux occurs, causing
hydronephrotic atrophy.
D. Genital Tuberculosis: The ducts of the involved epididymis become
occluded. If this is bilateral, sterility results. Abscess of the epididymis may
rupture into the testis, through
the scrotal wall, or both, in which case the
spermatogenic tubules may slough out.
Treatment
The main principles in the treatment of tuberculosis are that:
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1. No antituberculous drug is to be given alone;
2. Treatment should be continued for 4 months or longer if necessary;
3. The doctor should be able to convince the patient of the necessary to take the
prescribe drugs regularly.
The standard drugs for the treatment of tuberculosis are now isoniazide,
rifampicin, pyrazinamide and ethambutol given in daily doses (Table). Treatment
is started with the first three drugs and maintained until the sensitivity results are
known. In light of this information, treatment is continued with two drugs to
which the organism is sensitive, isoniazid and rifampicin will be prefered. If the
organism is resistant to two or more of the standard drugs then streptomycin and
ethambutol may replace them. Multiple resistance is now rare in the developed
world and it should not be necessary to fall back on any of the other drugs formerly
in use. This system is well tried and can be expected to give excellent results in the
majority of cases. The course of treatment should last 4 months or longer
according to the severity of the disease.
Gow and Barbosa (1984) consisting of 2 months` daily treatment with
rifampicin, isoniazid and pyrazinamide followed by isoniazide and rifampicin three
times a week for 2 months recommend a short course of treatment. The American
Thoracic Society (1980) have reviewed the results of trials of short-course and
intermittent treatment of pulmonary tuberculosis and recommended a minimum
duration of 9 months` treatment with isoniazid and rifampicin for uncomplicated
pulmonary tuberculosis. However, they excluded nonpulmonary tuberculosis from
short-course treatment.
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Table
DOSAGE TABLE FOR STANDARD TREATMENT
Streptomycin
Isoniazide
1 g daily
200-300 mg daily
i. m.
oral
Rifampicin
600 mg daily
oral
Ethambutol
25 mg/kg daily for 2 months
oral
15 mg/kg daily thereafter
Pyrazinamide
1,5-2 g daily
oral
The British Thoracic Association (1980) reported a 7% relapse rate after 6
months` treatment of pulmonary tuberculosis with daily isoniazid and rifampicin
plus an initial supplement of ethambutol or streptomycin for 2 months. The followup lasted from 3 to 4 years. The current use of three bactericidal drugs may explain
the success of the short course given by Gow and Barbosa. At the same time it
should be noted that surgery still plays an important part in their regime. If the
urologist has little experience in the chemotherapy of tuberculosis the advice of a
chest physician should be sought.
If tuberculosis is treated with a single drug, the organism quickly develops
resistance to it. For example, after 3 months` treatment with isoniazid alone,
resistance to it was found in 62 % of the patients still producing a positive culture.
If the organism is resistant to one of a pair of drugs used in treatment, resistance
will develop to the second drug as if it were being given alone.
The reason for starting treatment with three drugs is the possibility of primary
resistance. In Scotland in 1985 the incidence of primary resistance to isoniazid and
pyrazinamide single or together was 7 % of newly diagnosed cases. One patient
was resistant to ethambutol and one was multiresistant.
Isoniazid is a highly effective bactericidal drug, which can promote the healing
of recent lesions by resolution without fibrosis. In standard doses it is almost nontoxic. Rifampicin is also bactericidal and very active. In normal daily dosage
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toxicity is low, but if pretreatment liver function tests are abnormal it should not be
used. During treatment with rifampicin the liver function tests may become
abnormal, but if there is no clinical evidence of liver damage, treatment can be
continued as the test usually reverts to normal. When rifampicin is used in
intermittent treatment the dose may be raised to 1200 mg twice weekly. In this
situation toxic reactions are more frequent and may be serious enough to stop
treatment. The principal side effects with this dosage are the `flu` syndrome and
thrombocytopenia often associated with the development of antibodies to
rifampicin. The major toxic effect of ethambutol is retrobulbar neuritis whose early
signs are blurred vision and defective color vision. This can be minimized by not
exceeding a daily dose of 25 mg/kg for the first 8 weeks and then reducing to 15
mg/kg.
Tests of visual function should precede treatment, which should be
stopped immediately the patient complains of any visual disturbance and a full
ophthalmological examination is carried out. In view of the difficulty of testing
visual activity in young children, ethambutol should not be prescribed for them.
Impaired renal function is a contraindication at any age. A full recovery from
visual toxicity can be expected if the ethambutol is stopped immediately. In the
past, pyrazinamide has been regarded as too hepatotoxic for routine use, but now a
single daily dose of 1-5 g before breakfast has been found to be effective and free
from side effects. It is a bactericidal drug effective at the acid pH to be found
inside cells. M. bovis is naturally resistant to pyrazinamide.
Rifampicin may stimulate the drug metabolizing enzyme system of the liver.
As a result of this the serum concentrations of the following drugs may be reduced
when given along with rifampicin – cardiac glycosides, oral contraceptives,
anticoagulants, oral antidiabetics, corticosteroids and narcotics and analgesics.
Women treated with rifampicin and wishing to avoid pregnancy should use a
method other than an oral contraceptive.
Sensitization rashes occur with all the antituberculous drugs.
Once the
offending drug has been identified it is simpler nowadays to switch to an
alternative drug. If this is not possible, the patient may be desensitized by giving a
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small dose and gradually increasing it. Alternatively, treatment can be continued
with normal dosage under cover of corticosteroids, but it is absolutely essential that
the organism be known to be sensitive to the drugs in use if disastrous
consequences are to be avoided.
If ureteral obstruction is discovered at the time of diagnosis or later, oral
Prednisolone 20 mg daily should be started. This must be monitored weekly in
case of surgical intervention is required.
In the average case of renal tuberculosis sufficient healthy nephrones are
present to maintain renal function within normal limits, but if there is over 50,
renal function may be poor because of disease other than tuberculosis, so it is
advisable to have renal function tests performed on these patients before starting
treatment and if they are found abnormal then the drug levels should be monitored.
If streptomycin has to be given to an elderly patient, the dose should not exceed 075 g per day so as to avoid ototoxicity.
In-patient treatment is no longer necessary, but whether a short course as given
by Gow and Barbosa (1984) or daily dosage for 9-12 months is used, close
supervision is necessary because the need for surgical intervention can appear
rapidly. Follow-up for an uncomplicated case need no longer than 1 year, but
should
be
for
several
years
if
calcification
is
present.
A medical treatment of patient with tuberculosis of the urinary system is based
on the general principles of antituberculouse therapy and includes the measures of
both conservative and surgical nature. The volume of medical treatment relies on
stage of pathological process.
A conservative medical treatment is to be complex: specific chemotherapy,
good feeding, climate- that vitaminetherapy, resort, medical treatment. They
usually apply simultaneously three specific antituberculouse drugs of different
mechanism of action. To drugs of I line-belongs streptomycin, sodium of
paraaminosalicylatis, isoniazid (tubasin) and its derivatives (phtivasid, metasid,
salusid, larusan, inga-17І). To drugs II line-belong aetionamid, cycloserine,
tyoacetason, aetoxid, pirasinamid, and florimycin sulfate.
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The primary course of continuous medical treatment by the antituberculous
preparations proceeds not less than year. Out that it is carried under surveillance of
urologist-phtisiatrist. The antirecidive courses by duration the 1,5— 2 months are
conducted during the 3—4 years in the spring-autumn periods. For the medical
treatment they use one of the derivatives tubasidum in combination with aetoxidum
or to sodium of paraaminosalicylatis.
In children with limited destruction of kidney (III stage) during the 10 months
they conduct therapy by drugs I line, where upon they appoints drugs II line. On
the whole antibacterial medical treatment at this pathology there are to proceed 2
years. They conduct the antirecidive therapy by courses for the 2—3 months
during the 3 years. They use the combinations of sodium of paraaminosalicylatis,
tubasidum and preparations II line.
Application of rifampicin, ethambutol considerably promotes the efficiency of
therapy of a sick on tuberculosis.
In case of united defeat of kidney by the tubercular process and pyelonephritis
they conduct the medical treatment taking into consideration the second microflora
of urine, its sensitiveness to the antibiotics.
In period of medical treatment it is necessary to appoint group vitamins,
enzymes and biogenic drugs (lidase, aloe, vitreous body).
In the case of tubercular defeat of urinary bladder the antituberculosic drugs
are appointed together with instillation cods-liver oil, solutions of tybonum, to
sodium of paraaminosalicylatis. The medical treatment proceeds 12-18 months.
The duration of the conservative medical treatment concerning tuberculosis of
kidney and urinary tract depends on the disease stage, but in any case it is to be
protracted and continuous. The patients are under the supervision in the
antituberculosic clinic. For the control after efficiency of the medical treatments
they conduct regularly the ambulatory and hospital inspection (analyses of urine
and blood, bacteriological research of urine with determination of sensitiveness of
micobacterias tuberculosis to drugs), if it’s necessary they conduct the
roentgenologic
and
radionuclide
research
of
the
urinary
organs.
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The organsafe operations execute at the limited destructive tuberculosis (cavity of
largenesses or policavernose process in one of kidney segments) of one or both
kidney with normal their total function, and also at the destructive tuberculosis of
one bud in combination with tuberculosis of ureterus and at tuberculosis of urinary
tract (in the case of a necessity renewal urine arcade).
If the destructive tuberculosis of kidney has a limited nature, shown
cavernotomy, cavernectomy, and resection of kidney. Cavernectomy and
cavernotomy aren’t now practically applied. In case of the single narrowing of
ureterus on the small distance they execute the resection of this area and they
impose anastomosis after type end to end, at strictures of pyeloureteral segment —
resection with imposition of anastomosis after the Anderson-Haync method or
Coachman. In the case of strictures pelvic part of ureters necessary direct or
indirect ureterocystoneostomy. At plural strictures ureters they execute an
operation of substitution by its a thin bowel on mesenterium, that is the intestinal
plastic of ureterus. After operation a patient have to get antituberculosic drugs for a
year.
In the case of the wrinkling of the urinary bladder (microcystis) they execute
the intestinal plastic. Thanks to this interference a capacity of urinary bladder is
multiplied and the urine outflow gets better from the upper urinary tract. An
additional reservoir is usually created from the ileum (ileocystoplastic) bowel or
sygmocystoplastic. In the postoperative period-protracted (close 3— 6 months)
specific chemotherapy in the conditions of permanent establishment is necessary.
About the full convalescence they testify absence of changes with the complement
of urine during 5 years after the completion of medical treatment and positive
dynamics of immunological and roentgenoradiological indexes.
Prognosis
The prognosis depends upon severity & prolongation of the disease and the
organs involved, but the overall control rate is 98 % at 5 years. The urine must be
investigated bacteriologically every 6 months during treatment and then every year
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for 10 years (Wechsler and Lattimer, 1975). Relapse will indicate the need for
reinstitution of treatment. Nephrectomy is rarely necessary. In the healing process,
ureteral stenosis or vesical contraction may develop. Appropriate surgical
intervention may be necessary.
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1. Donald R. Smith, M.D. General Urology, 11-th edition, 1984.
2. O.F.Vozianov, O.V.Lyulko. Urology.- Kyiv: Vischa shkola, 1993.
3. Urology edited by N.A.Lopatkin, Moscow, 1982.
4. Scientific Foundations of Urology. Third Edition 1990. Edited by Geoffrey
D. Chisholm and William R. Fair, MD. Heinemann Medical Books, Oxford.
5. Urinary Tract Infection and Inflamation / Jackson E. Fowler, JR. MD. Year
Book Medical Publishers, Chicago 1989.
6. Bloom Barry R., Small Peter M. The Evolving Relation between Humans
and Mycobacterium tuberculosis //The New England Journal of Medicine.- 1998.V.338, N10.-P. 677-678.
7. Fisher C., Kallerhoff M. Weidner W., Ringert R. H. Citrobacter
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surveillance for Antituberculosis-Drug Resistance, 1994-1997 //The New England
Journal of Medicine.- 1998.- V. 338, N 23.- P. 1641-1649.
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Tuberculosis // The New England Journal of Medicine. - 1988. - V. 338, N 23. - P.
1689-1690.
10. Treatment of tuberculosis. - Guidelines for national programs. - Geneva.
Word Health Organization publication, 1994. - 46 p.
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