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Danger Untoward Effects of Streptomycin in Anti-tuberculosis Therapy

TOOBSERVE THE UNTOWAED EFFECTS OF AMINOGLYCOSIDES(STREPTOMYCIN)IN COMBINITION THERAPY OF ANTI-TUBERCULOSIS THERAPY IN TUBERCULOSIS PATIENT’S.

Authors:Bhurgri ghulam rasool,Shamim-ur-rehman,Syeda Momina Taki Muhammad,Raj Kumar chohan.Dhri Ghulam Mustafa,Barkat sheikh.

INTRODUCTIONS:

Tuberculosis is chronic granulomatous disease of human and other mammals caused by a group of closely related obligate pathogens, the mycobacterium tuberculosis complex, comprising M. tuberculosis. The human tubercle bacillus - M. bovis - the bovine tubercle bacillus, -agricanum - a heterogeneous type found principally in effuational Africa with properties intermediate between the former two species and M-microti-a rare cause of disease involves and other small mammals but attenuated for humans. Humans are the usual, but not unique, host of M. tuberculosis. M. bovis causes disease in cattle and also in badgers, deer, and other mammals. Humans are incidental hosts, usually acquiring infection by drinking contaminated milk although infection of farm workers may occur by aerogenous route. Human may transmit M. bovis to cattle but human to human is rarely reported (PDO D awis et al, 2003).

The annual tuberculosis infection rate or annual risk of infection is the best single indicator of the status and trend of tuberculosis in both developed and developing countries. It indicates the proportion of the population that will primarily infected or reinfected in the course of one year and is usually expressed as a percentage.

The risk of tuberculosis infection in developed countries is now very low, being less than 0.5% per annum in the majority, 0.1-0 % in most and less than 0.1% in a few countries. The risk of tuberculosis in these countries is declined by about 10% per year.

In developing countries much higher rates are found. The annual risk of infection for the richest and poorest countries is shown in following table. In most industrialized countries the annual rate of infection is now below 0.1% and continues decline by 10% per annum. In Africa, the annual risk of infection may be much as 2.5% or more, and in the present context of increasing tuberculosis, notification due to HIB epidemic is increasing rather than decreasing.

Annual risk of infection

Areas

Current

Level

Annual decline

Trend (%)

Health resource

Availability

Industrialized

0.04-0.1

>10

Excellent

Middle income Latin America

West Asia

0.5-1.5

5-10

Good

Middle income East and South

Eest Asia

1.0-2.5

<5

Good

Sub-Saharan Africa

Indian Subcontinent

1.0-2.5

0-3

Poor

                                                                                                (A Gordon Leitch, 2000)

In 1990 the commission on Health Research for development stated that "the magnitude of tuberculosis problem is matched only by is relative neglect by the international community". A decade later 2000 ministers of Health and Finance from 20 countries that have 80% of world's tuberculosis cases met in Amsterdam and issued the Amsterdam Declaration". This stated that the global situation was both alarming and unacceptable" and that we commit ourselves to accelerate action against tuberculosis through expansion of coverage of population with the World Health Organization (WHO) recommended strategy to combat tuberculosis Direct observe treatment strategy (DOTS), providing for at least 70% detection of infectious cases by the year 2005" (Philip C Hopwell, 2002).

EPIDEMIOLOGY

About 8 million people developed tuberculosis in 1990 and 2.6 to 2.9 million people died of it, mostly in Asia. It is estimated that one third of world's population (1700 million) is infected with mycobacterium tuberculosis. The disease is not limited to Asia alone and its prevalence is increasing in developed countries also where it linked to acquired immunodeficiency syndrome (AIDS). According to estimate, approximately 160,000 children die from tuberculosis annually worldwide. The situation in developing countries is different where malnutrition and tuberculosis co-exist (Nizami SQ, 1998).

Developing countries in Asia have an estimated 50-100/100,000 cases of smear positive tuberculosis annually. The 1990 incidence of tuberculosis disease in Pakistan has recently been reported at 250/100,000 of which 45% are likely to be smearing positive pulmonary tuberculosis. At these rates, Karachi, a city of approximately 100,000 would have between 5000 and 11250 new cases of smear positive disease annually. Analyzed causes of deaths among adults, age 15-50 years in impoverished Karachi communities, tuberculosis, is identified as the second leading cause of adult death at an annual rate of 30/100,000 which is consistent with incidence -estimates, assuring overall case fatality ratios of 50% for untreated and 15% for treated tuberculosis (Marsh et al., 1996).

PATHOGENESIS:

INDEX CASE WITH INFECTOUS TUBERCULOSIS

Cough and generate droplet nuclei, which are inhaled by a contact

Primary

Onset of CMI response

Bacillimia                                      Apical Implant

                            Sterilization of the primary complex

Immunosuppressive event

Multiple of tubercle bacilli

Restoration of CMI

Cessation of necrosis

        Infectous tuberculosis

Figure: Schematic representation of the basic events in the pathogenesis of tuberculosis.

CMI: Cell mediated immune.

(VB Balasurbramanian et al., 1994).

DIAGNOSIS OF TUBERCULOSIS

The different diagnostic methods are as follows:

1.                History and clinical features.

2.                2Blood CP and ESR.

3.                Chest radiography.

4.                Sputum for AFB (Acid Fast Bacilli). (Sputum is stand with Zeihl Neilson (ZN) stain.

5.                Culture on Lowenstein Jensen medium.

6.                Bronchoscopy if no sputum is available.

7.                Biopsy with histological examination.

(Saurders, 1998).

DRUG TREATMENT OF TUBERCULOSIS

Tuberculosis is among the top ten cause of global mortality and affects low-income countries in particular. The treatment of smear positive tuberculosis using World Health Organization (WHO) directly observed treatment, short course, Direct observe treatment strategy (DOTS) has far highest impact while BC immunization reduces childhood tuberculosis mortality (Martien W Borgdorff et al. 2002).

Drugs used in the treatment of tuberculosis can be divided into two major categories. First line after combined the greatest level of efficacy with unacceptable degree of toxicity. These include isoniazid, rifampin, ethambutol, streptomycin and pyrazinamide. Excellent results for patients with non drug resistant tuberculosis can be treated with 6 month course of treatment, for the first 2 months, isoniazid, rifampin and pyrazinamide are given, followed by isoniazid and rifampin for remaining 4 months (William A Petri Jr, 2001).

STREPTOMYCIN

Streptomycin is tuberculocidal, but less effective than isoniazid or rifampin, acts only on extracellular bacilli (because of poor penetration into cells). Thus, host defense mechanisms are needed to eradicate the disease. It penetrates tubercular cavities, but doesnot cross to the cerebrospinal fluid (CSF), and has poor action in acidic medium. Resistance developed rapidly when streptomycin was used alone in tuberculosis most patients had a relapse (Tripathi, 2003).

Streptomycin is bactericidal for tubercle bacillus in vitro. Concentration as low as 0.4 mg/ml may inhibit the growth. vast majority of strains of mycobacterium tuberculosis are sensitive to 10mg/ml (William A Petri Jr, 2001).

 It crosses the placenta and fetal serum levels are half of those in maternal blood, the drug is excreted almost entirely by glomerular filtration and dosage must be modified in renal failure to avoid toxicity (A Gordan Leitch, 2000).

Untoward effects include rash and fever, auditory and vestibular function of eighth cranial nerve is affected (William A Petri Jr, 2001).

Popularity of streptomycin in treatment of tuberculosis had declined due to need for intramuscularly injections and lower margins of safety because ototoxicity and nephrotoxicity especially in the elderly and those with impaired renal function.

Streptomycin is ototoxic and nephrotoxic. Vertigo and hearing loss are most common side effects and may be permanent. Toxicity is dose related and risk is increased in the elderly. As with all aminoglycosides the dose must be adjusted according to renal function. Toxicity can be reduced by limited therapy to no more than 6 months (Henry FC, 2001).

Minor adverse effects are pain, rash, swelling and pus formations at injection site, numbness around the mouth and tingling soon after the injection.

Major adverse effects are cutaneous hypersensitivity, vestibular and auditory nerve damage to the patient and in a pregnant woman, also in fetus, renal damage (A Harries, 2003).

Apart from hypersensitivity reactions such as fever and rash, Streptomycin also potentiate neuromuscular blocking agents used during anesthesia and should be avoided in-patient with myasthenia gravis (T Frieden and M Espinal, 2003).

Significantly rare adverse effects of aminoglycosides include fever, rash, neuromuscular blockade, hypokalemia and hypomagnesaemia (Edward D Chan et al.,2004).

MATERIAL AND METHODS

This study was carried out in the department of Pharmacology and Therapeutics, Free T.B Clinical of Muhammad Medical College Mirpurkhas SINDH, Pakistan, under kink supervision of Dr,. SHAMIM-UR-REHMAN, Head of Department from January 2005 to June 2005.

The 100 newly diagnosed patients of pulmonary tuberculosis, enrolled is this study after taking informed and written consent.

The patients were selected as diagnosed cases of pulmonary tuberculosis from medical chest OPD and chest ward of Muhammad medical college mirpurkhas. Out of these 97 patients were associated through out the study period. Out of remaining three have not come for follow up.

                           

All patients, in this study, were selected according to following criteria:

 INCLUSION CRITERIA

• Diagnosed cases of pulmonary tuberculosis.
• Age between 20 to 70 years.
• Sex either male or female.

EXCLUSION CRITERIA

• Patients suffering from liver disease.
• Patients suffering from cardiac disease.
• Patients suffering from renal disease.
• Patients suffering from diabetes mellitus.
• Patients suffering from other respiratory disease.
• Patients suffering from HIV infections.
• Pregnant or nursing women.
• Patients with previous multiple drug resistance.

The study period extended up to 24 weeks and 12 follow up visits of patients were taken. The required information such as name, age, sex, occupation, address, details of follow up visits and laboratory investigations etc, of each patients were recorded on proforma especially designed for this study.

The selected patients were divided according to untoward effects of drugs during study period.

Group A:         In this group those patients were included who manifested the nephrotoxicity in different age group and gender.

Group B:         In this group those patients were included who manifested the ototoxicity in different age group and gender.

MATERIALS:

Streptomycin -- 15 mg/kg - maximum 1 gm

D/syringes

Ophthalmoscope

Rhinoscope

DETERMINATION OF CREATININE

• Take a 5 cc disposable syringe.
• Take a cotton spirit swab.
• Clean the arm with spirit swab.
• Prick the needle incubital vein.
• Take 3-5 ml of blood.
• Put the blood sample into plain tube.
• Wait for clotting the sample for ½ to 1 hour.
• The sample was centrifuged and collected the serum.

PRINCIPLE

            Protein free filtrate (pH below 2) in treated with alkaline picrate solution (Jaffe’s reaction ) to yield red colour of creatinine picrate. This colour is due to tautomer of creatinine picrate and is dependent on formation of a salt and ketoenol changed creatinine molecule. The red yellow colour thus formed is compared photometrically to a series of standards prepared from pure solution of creatinine.

Reagents

Sodium tungstate 5%:   Dilute 1:1 10% Sodium tungstate.

Sulfuric acid:                 2/3N

Picric acid:0.04 M        (9.16g/l) It may be dried between filter paper or an allowance of 10-12% made for the added water.

Sodium hydroxide:        0.75N

Stock standard:            (1mg/ml) dissolve 1 g of pure creatinine in 0.1 N hydrochloric acid and make up to one litre with the acid. The solution is stable indefinitely.

Working standard:        (0.2 mg/ml): Dilute 2 ml stock standard to 1dl.

PROCEDURE:

A)    For plasma/serum creatinine:

Protein precipitation / sample preparation:

·        2 ml plasma + 2 ml distilled water + 2 ml sodium tungstate. Mix and let stand for 5 minutes, and the centrifuge.

·        To the 3 ml of above protein free filtrate add 1 ml picric acid, heat in biling water bath for about 45 minutes.

·        Make up to volume 4 ml with distilled water after heating. Add 1 ml NaOH. Let stand for 15 minutes and read with standards.

COLOUR DEVELOPMENT

Materials

Standards S1 to S6

Total creatinine

Blank

Wouking standard

0.5 50 3.0 ml

-

-

Distilled water

Up to 3 ml

-

3.0 ml

Protein-free       filtrate

-

3.0 ml

-

Picric acid

1.0 ml to each tube

Sodium hydroxide

1.0 ml to each tube

Let stand for 15 minutes and then read at 520 nm against blank.

CALCULATION

                                        OD of test                                                                          100

Creatinine (mg/dl)  =     ___________              X         Amount of Std           X     _________

                                        OD of Std                                                                   Sample used

Creatinine = (Total creatinine – preformed creatinine) 1.16

(Where 1.16 is the ratio of the molecular weight of creatinine to creatine).

DETERMINATION OF BLOOD UREA NITROGEN (BUN)

PRINCIPLE

            Diacety1 monoxime is hydrolyzed in acidic medium to diacety1, which reacts with urea in the presence of ferric ions, to form a condensed coloured molecule. The colour is intensified and stabilized by thiosemicarbazide.The intensity of red colour comples formed is proportion to the quantity of urea present in the sample.

Urea                             = urea nitrogen 2.14

Urea nitrogen                = Urea 0.4665

REAGENTS

Oxime solution Dissolve 1 gm diacety1 monoxime (also called 2,3 butanedione monoxime), 0.2 gm thioemicarbazide and 9 gm naCI in water and dilute to 1L.

Acid solution                Cautiously add 60 ml concentrated sulfurc acid and 10 ml 85% orthophosphoric acid to 800 ml distilled water. Add 0.1 gm FeCI3 and dilute to 1I.

Standard stock solution: (1mg/ml) 100 mg of urea in 100 ml of distilled water.

Standard working (0.01 mg/ml) Dilute 1 ml of stock standard

Solution:                       solution up to 100 ml distilled water.

PROCEDURE

To 0.1 ml serum/plasma add 9.9 ml distilled water.

COLOUR DEVELOPMENT

Materials

Standards S1 to S6

Total creatinine

Blank

Working standard

0.1 to 1.0 ml

-

-

Distilled water

Up to 2 ml

1.5 ml

2.0 ml

Protein-free    filtrate (PFF)

-

0.5 ml

-

Add to each tube 2 ml of mixed colour reagent and w ml of mixed acid reagent. Heat for 20 minutes in boiling water. Cool and dread at 540 nm (colours are stable for several minutes.

CALCULATION

                                       OD of test                                                                            100

Urea nitrogen (mg/dl)=  ___________      X     Amount of Std        X     _________

                                        OD of Std                                                                   Sample used

All the patients examined for optic neuritis before anti-tuberculosis treatment

Method

Ocular examination

Visual acuity

Pupil reaction

Fundus examination by Keeler direct ophthalmoscope

Colour vision

Befor antituberculosis therapy

Visual acuity                 6/6

- Normal                      6/6

Pupil reaction

Round – regular – reactive

Fundus

Optic disc pale

Visible margins

Cup / disc ratio 0:3

Normal vascular pattern

Macula looks normal

Colour vision:   no red /green defect.

EXAMINATION OF EAR

            Ototoxicity as an acverse effect of streptomycin

First we ruled out the, wax, foreing body, or any other ear disease.

            Then we cheked the position of tympanic membrane, any kind of perforation of iy. Then we checked the function of middle ear and inner ear. Then we do the test for hearing and balance

1.      Whisper Test:

It was done in ENT OPD room (silent), the distance of patient and doctor was about 1 meter and talked slowly and gradually increased voice frequency.

2.      Tunning Fork test

a.       Renies test: We see in this test the ear conduction is better than bone conduction.

b.      Weber’s test: In this test, we characterized the disease of ear, and function of proni conduction.

c.       ABC (Air Bone Conduction test): We rule out the waning proth doctor, and patients.

d.      PTA (Pure tone Audionetery): By this method we watch air conduction, bone conduction .

Cochlear function tests are infact tests of hearing and include:

a)      voice tests.

b)      Tuning fork tests.

c)      Audiometery.

Voice tests are the tests which we do with the gelp of our voice. Depending on the type of voice which we use they are called the whisper voice test , conversation voice test, and loud voice test, Normal distances from which the various voices should be couuectly heard by the patient are as follows:

Whisper                       =          20 feet

Conversation                =          40 feet 

Loud                            =          100 feet

Thesedistances gowever, apply to tests done in a sound proof room and not in the noisy background of the out patient department .

            For accurate results of voice tests, one has to observe the following rules:

• Ear being tested should face the doctor.
• Patient should be blind folded.
• Opposite ear should be plugged.
• Use only forced expiration speedh i.e., words spoken during the expiration following a deep inspiration.
• Use only phonetically balanced worlds (P.B. words), e.g., ninety nine, fifty five etc.
• Start from the maximum normal audibility range and then gradually come nearer to the patient.

The main merit of the voice tests is that they are simple to perform and do not repiure any specialized equipment.But they are not very accurate and only give a rough idea as to whether the patient is deaf or not.

Tuning fork tests tell us about the type of hearing loss, i.e., conductive or perceptive, and include RINNE’s tests, ABC or SCHWABACH’s test, and WEBER’s test, In addition, GELLE’s test also merits description. Lidke any other instrument we must know the correct use of tuning fork which is as follows:

Always hold it by its stem.

Always hit it gently against one of tour bony points, either elbow or knee cap.

While putting it over the external meatus, make sure that the acoustic axis of the fork coincides with the long axis of the external auditory canal.

Whenever tou put it over the mastoid, you must block the gearing across the skull bones by making the opposite ear, either with Barany’s nioise box or with a piece of paper.

Rinne’s test: Rinne’s test is the test of conductive defness. It compares the air conduction of the ear with its bone conduction. Normally, the air conduction is twice more than the bone conduction (Rinne’s positive). In nerve deafness, the air conduction is more than the bone conduction but both are reduced (Rinne’s reduced positive).In conductive deafness, the bone conduction is more than the air conduction (Rinne’s negative).

Absoluter bore conduction test: A,B,C test or schwabach’s test is the test of nerve deafness. It compares the bone conduction of the patient with that of the doctor . Normally, the two are equal. Same is the case in conductive deafness. In nerve deafness, the patient’s bone conduction is reduced and is less than the doctor’s bone conduction. Weber’s test: Weber’s test is the test of lateralization. In conductive deafness, it is lateralized to the more diseased ear. We take a tuning fork, hit it gently against one of our bony points, place it over the middle of patient’s forehead, and ask him as to where does he hear it best, Normally, he either hears it best in the middle of the forehead or equally well in the two ears. In conductive deafness, he hears it better in the more diseased ear. In nerve deafness, he hears it better in the more normal ear.

Gelle’s test: Gelle’s test is the test of stapedial mobility. A vibrating tuning fork is placed over the patient’s mastoid and he is asked to note the intensity. The air pressure in the esternal auditory canal is then increased either by pressing the tragus or withy the help of siegle’s speculum and he is aked to note the intensiye once again. Afailure to hear the fork better means that the stapes is fixed.

Audiometery is testing the hearing with an electrical instrument called the audiometer and plotting the result on a graph paper called the audiogram. It is of three types, namely.

a)      Pure tone audiometery.

b)      Speech audiometery.

c)      Bekesy’s audiometery.

d)      Impedance audiometery.

Pure tone audiometery is the one which we commonly do in our departments. It uses the pure tones as the sound stimuli and finds the threshold of hearing for the various audible frequencies. In the audiogram, the sound intensities are marked on the vertical lines and the sound frequencies, ranging from 250 c.p.s. to 8000 c.p.s. are marked on the horizontal lines.

Caloric tests

Caloric tests are tests of vestibular function, using hot and cold water for stimulation.

Instruments

a)      Water can.

b)      Kidney tray.

c)      Centigrade thermometer.

d)      Stop watch.

Materials

a)      Water at 44*C

b)      Water at 30*C.

Canal stimulated

Lateral semicircular canal.

To make it vertical we put a pillow under the head and thus fles the neck by 30*C.

Method

Run water into the ear for 40 seconds.

Notice the after nystagmus, its direction, and its amplitude. The time duration is couted right from the moment we start running water into the ear.

N.B.

First we complete the test with water at 44*C and then we do it with water at 30*C.

In hot water test, the nystagmus is directed towards the ipsilateral side.In cold water test, the nystagmus is directed towards the opposite side.

Contra-indications

Acute suppurative otitis media.

Chornic suppurative otitis media.

Perforated ear drum.

Labyrinthitis.During the attack of Meniere’s disease, vestivular neuronitis etc.

Results

Normal value.

Normally, the ensuing nystagmus lasts 120-180 second.

Plotting.

Major abnormalities:

Meniere’s disease, canal paresis.

Dead labyrinth, no response.

In order to poick the nystagmus better, direct observation of the eyes has been replaced by electronystagmography, which depends on detecting the difference in electrical potential between the cornea and retina and gives us an automatically recorded graph, called the electronystagmograph.

RESULTS AMD OBSERVATIONS:

Table 1 and figure 1 shows nephrotoxicity as an adverse effect. Streptocomycin was main drug to manifest the nephrotoxicity in combined therapy during treatment of pulmonary tuberculosis in combined therapy during treatment of pulmonary tuberculosis patients. Out 97 patients, there were 3 reactions documented in this table.

Table 2 and figure 2 shows nephrotoxicity in gender after taking the anti tuberculosis drugs. Two males and one female was affected during the study.

            Table 3 and figure 3 shows the nephrotoxicity in different age group. In the age group 30-39 1, 40-49 1, and 50-59 1 reaction was documented in this study.

Table 22 and figure 22 show the ototoxicity after taking anti tuberculosis drugs. There were 2 reactions recorded in this study.

TABLE 1

DRUGS AND NEPHROTOXICITY

Drugs

Yes

No

Total

Combined therapy*

3

94

97

Streptomycin

3 (3.1%)**

94

97

Pyrazinamide

-

-

-

Rifampin

-

-

-

Ethambutal

-

-

-

Isoniazid

-

-

-

*Occurance of nepgrotoxicity is tested by excluding combined therapy.

**Percentage in calculated out of 97 patients.

TABLE 2

DRUGS AND NEPHROTOXICITY IN GENDER

Drugs

Male

Female

Total

Combined therapy*

2

1

3

Streptomycin

2 (2.1%)**

1 (1.03%)

3

Pyrazinamide

-

-

-

Rifampin

-

-

-

Ethambutal

-

-

-

Isoniazid

-

-

-

*Occurance of nephrotoxicity is tested by excluding combined therapy.

**Percentage is calculated out of 97 patients.

TABLE 3

DRUGS AND NEPHROTOXICITY ACCORDING TO AGE

Drugs

20-29

30-39

40-49

50-59

60-69

Total

Combined therapy*

0

1

1

1

3

Streptomycin

0

1 (1.03%)**

1 (1.03%)

1 (1.03%)

3

Pyrazinamide

Rifampin

Ethambutal

Isoniazid

*Occurance of nephrotoxicity is tested by excluding combined therapy.

**Percentage is calculated out of 97 patients.

TABLE 4

DRUGS AND OTOTOXICITY AS AN ADVERSE EFFECT

Drugs

Yes

No

Total

Combined therapy*

2

95

97

Streptomycin

2 (2.1%)**

95

97

Pyrazinamide

-

-

-

Rifampin

-

-

-

Ethambutal

-

-

-

Isoniazid

-

-

-

*Occurance of ototoxicity is tested by excluding combined therapy.

**Percentage is calculated out of 97 patients.

TABLE 1

Frequency of Nephrotoxicity

In Anti tuberculosis Drugs

FIGURE 2

Nephrotoxicity according to gender in Anti tuberculosis Drugs

FIGURE 3

Nephrotoxicity according to Age Groups in

Anti tuberculosis Drugs

FUGURE 4

Frequency of Ototoxicity in

Anti tuberculosis Drugs

Table 5 and figure 5 shows the ototoxicity in different gender. There was one reaction in male and female resplectively after taking anti tuberculous therapy.

Table 6 and figure 6 shows the ototoxicity in different age group. The age group between 20-29 and 40-49 were manifested ototoxicity in this study after taking anti tuberculous drugs.

TABLE 5

DRUGS AND OTOTOXICITY AS AN ADVERSE EFFECT IN GENDER

Drugs

Male

Female

Total

Combined therapy*

1

1

2

Streptomycin

1 (1.03%)**

1 (1.03%)

2

Pyrazinamide

-

-

-

Rifampin

-

-

-

Ethambutal

-

-

-

Isoniazid

-

-

-

*Occurrence of ototoxicity is tested by excluding combined therapy.

**Percentage calculated out of 97 patients.

TABLE 6

DRUGS AND OTOTOXICITY ACCORDING TO AGE

Drugs

20-29

30-39

40-49

50-59

60-69

Total

Combined therapy*

1

0

1

0

0

2

Streptomycin

1 (1.03%)**

0

1 (1.03%)

0

0

2

Pyrazinamide

Rifampin

Ethambutal

Isoniazid

*Occurance of ototoxicity is tested by excluding combined therapy.

**Percentage is calculated out of 97 patients.

FIGURE 5

Ototoxicity according to gender

In Anti tuberculosis Drugs

FIGURE 6

Ototoxicity according to age Groups in

Anti tuberculosis Drugs

DISCUSSION:

Streptomycin (1 g per day) – it was started with other drugs. After 3-7 weeks of medication, 3 patients complaint of oliguria and 2 patients presented during follow up with hearing deficit. These reactions proved clinically and laboratory investigations.

Nephrotoxicity was recorded in these patients two in male and 1 in female. According to age group 1 in 30-39, 2 40-49 and 1 50-59 side effects were documented in this study. Drug was stopped for 3 weeks and found that blood urea nitrogen and creatinine levels were decreased, therefore this drug was permanently stopped and the remaining four drugs were continued.

The proximal renal tubule cells may accumulate aminoglycoside, accounting for nephrotoxicity associated with aminoglycosides. The mechanism of renal toxicity is hypothesized to by the inhibition of intracellular phospholipase in the proximal tubule.

The renal insufficiency is typically characterized by the nonoligouric decrease in glomerular filtrate rate occurring after at least taking a week therapy. Baseline and periodic surveillance of analysis blood urea nitrogen levels, creatinine values is indicated (Edward et al., 2004).

Streptomycin is nephrotoxic and should used with caution in patients with renal impairment. If reaction is trouble some which is an infrequent occurrence, the dose may be reduced (NCG,2002).

Ototoxicity – there were 2 reactions recorded in this study. According to gender, 1reaction was in male and 1 in female was documented in this study. Side effects of streptomycin were recorded. One in age group 20-29 and one in 40-49. The drug was astopped and patients were advised to consult in Ear Nose and Throat OPD. Remaining other drugs were continued.

Interestingly, the damage may be fairly isolated to either the choclear or vestibular component, or rarely both. The mechanism for the cochlear toxicity is unclear, although the target site is considered to the outer hair cells of the organ of corti.

Aminoglycoside induced cochlear dysfunction is generally considered to be irreversible. Infury to the hair cells of the ampullar cristae by aminoglycosides is the mechanism of the vestibular toxicity. Sign and symptoms of vestibular toxicity include nausea, vomiting, vertigo and nystagmus (Edward et al., 2004).

It proved that like other anti-biotic streptomycin must be careful to continue in combination therapy of Anti-Tuberculosis Therapy.

Tuberculosis is a granulomatous disease, caused by mycobacterium tuberculosis. As world Health Organization estimates more than 300,000 new cases of tuberculosis develop in Pakistan every year. Cure of infectious cases of tuberculosis is the key to effective control of the disease. Treatment of tuberculosis patients reduces suffering and, if adequately, prevents death from tuberculosis. The first tine of drugs used in the treatment of tuberculosis consists of isoniazid, pyrazinamide, rifampin, streptomycin, and ethambutol. The major side effects are those giving rise to serious health hazards, and require discontinuation of the drug and referral to chest physician. Minor side effects

Cause relatively little discomfort; they often respond to symptomatic or simple treatment but occasionally persist for the duration of drug treatment. Chemotherapy should be stopped or temporarily interrupted only of severe drug intolerance toxicity occurs. In fact tuberculosis drugs are relatively toxic and mild side effects are not uncommon but most do not warrant drug withdrawal.

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