CASE REPORT

A GIRL WITH TYPE 2 DIABETES MELLITUS WITH RENAL

COMPLICATION AND PULMONARY TUBERCULOSIS

By :
dr Dimas Tri Anantyo
Supervised by :
Prof. dr. M. Sidhartani, SpAK, MSc

DEPARTMENT PEDIATRICS
FACULTY OF MEDICINE DIPONEGORO UNIVERSITY
DR. KARIADI HOSPITAL SEMARANG
2016

CONTENT
CONTENT...............................................................................................................ii
CHAPTER I INTRODUCTION............................................................................31
CHAPTER II CASE REPORT..............................................................................54
CHAPTER III DISCUSSION............................................................................1110
CHAPTER IV CONCLUSION..........................................................................3332
REFERENCES...................................................................................................3433
CHAPTER I
INTRODUCTION
Diabetes mellitus (DM) is a metabolic disorder which clinically and
genetically has heterogeneous clinical manifestations including the form of the
loss of carbohydrate tolerance. DiabetesmellitusDM has a different etiology which
ultimately leads to insulin insufficiency.1 (Price, 1995 #1)Diabetes mellitusDM
can may occur slowlygradually, which makes making the patients is may not
aware of any changes such as excessive thirst drinking which became a lot,
increased frequency of urinationurinating more frequently, or andweight
lossdeclining until patients seek for treatment for and have checked his/her
glucose levels checked.2
Globally, Iin 2003 ,globally it was estimated a number of therewere an
estimated 65.000 new cases of diabetes mellitusDM in among children each year.
This amount was a considerable number, given the fact that quite a lot, and all of
these children require d treatment for the rest of theirhis life. Insulin Dependent
Diabetes Mellitus (Type-1 Diabetes MellitusDM/T1) is a metabolic disease which
became becomes a problem of pediatric endocrinologychild health in the world,
including Indonesia. This was evidenced indicated by the increase of in the
prevalence of type-1 diabetes mellitusDM in Indonesia, even thoughbut lately
prevalence

of

type-2

DMdiabetes

in

children

iswas

also

increasing.

Epidemiological studies indicate that there iswas gradual but steady increase of in

the incidence of both Type-1 DM and Type-2 DM in either both developed or and
developing countries.3
The

incidence

of

type-1

diabetes

mellitusDMwas

Type-1

DM

varyvarieswidely shows great variation either across nations orand between

population groups both within a countrybetween countries even within a country.
The highest incidence was is highest in Finland, of namely 43 per 100,000 and a
low the lowest incidence is in Japan ofis 1.5-2 per 100,000 among 10-forless than
115 year-old or youngers of age. In accordance with the incidence of type-1
diabetes mellitusDM, the prevalence of type-2 diabetes mellitusDM in among
children and adolescents is also constantly increasing also in the whole world.4
During the last past three3 decades, type-2 diabetes mellitusDM was only a
disease previously limited among in adults patients, but now the prevalence has
sharply increased its prevalence among children and adolescents. In the United
States, about 1 out ofin 3 new cases of type--2 diabetes mellitusDM was younger
less than 18 years old.5 Among children of school age in Japan, the incidence of
type-2 diabetes mellitusDM had increased from 7.2 per 100,000 cases in 19761980 to 13.9 per 100,000 cases in 1991 to 1995. The average annual incidence of
type-2 diabetes mellitusDM inAustralian among children in Australian aged aged
less younger than 16 years was 2.5 per 100,000 cases in 2001-2002.6
The data in Indonesia showed the prevalence of diabetes mellitusDM in
among children in urban areas such as Jakarta increased wasithat 65 children
cases diagnosed in 2011, up to 400% increase compared to 2009. A
coordinatedion study of pediatric endocrinology for children unit across Indonesia
in early March 2012 showed the number of people with diabetes mellitusDM
amongin children and adolescents under 20 year-old or youngers was 731
children. PDN (Pusat Diabetes dan Nutrisi / Diabetes and Nutrition Center) Dr.
Soetomo Hospital had been claimed in 2009 there were 650.000 children in
Indonesia who suffered from Diabetes MellitusDM in 2009, and most of them
were Diabetes MellitusDMtype 2 DM.6 Therefore, proper management handlingof
children and adolescents with DM is necessary in order that the prevalence of
diabetes mellitusDM in children and adolescents is not increasing. The goals of

treating a child with DM are to achieve normal growth and development with by
prevention of acute and chronic complications of DM. These goals can beare
achieved by co-ordinated care delivered by a multidisciplinary team focusing on
insulin administrations, glucose monitoring, meal planning, and screening for
complications.7
Pulmonary tuberculosis (TB) is an infectious disease that infecting the of
the lungs, which can be transmitted from person to person through the air droplet.
Diagnosis can be madeestablished based on clinical symptoms, abnormal findings
on physical examination, radiological examination of the thorax, and
bacteriological examination.8 Tuberculosis infection in diabetes mellitusDM is
more often caused by the reactivation of past focus of infection rather than recent
contact with pulmonary tuberculosisTB patients newly. For this reason,
pulmonary tuberculosisTB is described as a complication of diabetes mellitusDM
because patients with diabetes mellitusDM are more susceptible to infectious
diseasesns, have a higher risk for developing the disease.9 Number of pulmonary
tuberculosisTB patients is approximately 2.5% of all disease in which 75% of
them is , including in the productive age (15-54 years).2
Diabetes mellitusDMmay also can be found in patients treated with
urinary tract infections and pulmonary tuberculosisTB. TuberculosisTB
coinfection in and diabetes mellitusDM

are

often

found

together

is

approximately 42.1%.10 Symptoms of diabetes mellitusDM accompanied by and

pulmonary tuberculosisTB coinfection canwill overlap each other. In bBoth
diseases will simultaneously will result inmake weight loss, loss of appetite, and
general fatigue.11 The purpose of this case report is to discuss about 13 years and 8
months old girl with pulmonary tuberculosis as coinfection in DM type II .

CHAPTER II
CASE REPORT
A girl aged 13 years and 8 months had been hospitalized in Dr. Kariadi
Hospital on from 9 September tountil 18 September 2014 due to fatigue and a
productive cough with blood streak since 4 months. Patient s livesing in Kedung
Gading, Kendal.
Present Medical History
Patient arrived admitted to the emergency room Dr. Kariadi Hhospital
referredals from Soewondo Hospital, Pati with suspected type-1 Diabetes
MellitusDM.
More or lessApproximately 4 months before admission, the patientchild
had a productive cough with greenish yellow, viscous and , bloody mucus,
moderate fever (+) was not highmoderate, shortness of breath (+) sometimes,
occasionallysometimes she had a pain on the center of chest. ShePatient swaswere
taken to the health center and get had received antibiotics and cough medicine.
However, the complaint does didnt not getbecome better.
ThreeApproximately 3 months before admission the patient still had a
productive cough ingwith, greenish yellow, viscous, and bloody mucus, moderate
fever (+) was not high, shortness of breath (+), abdominal pain (+), then . pPatient
was taken to Soewondo Hhospital and injectedget subcutaneously injection and
was diagnosed with pulmonary tuberculosisTB. ShePatient got treatment for this
her pulmonary tuberculosisTB with 3 regimens.
More or less Around 2.5 months before admission (1 week after
administering starting of pulmonary tuberculosisTB medication), patient children
was complaining ed of fatigue, swelling of the face, arms and legs. Patient was
admitted taken back to Soewondo Hhospital s and obtained GDS 400 mg/dL
andand is diagnosed as diabetes, with blood glucose 400 mg/dL, and
inflammation of the kidneys. ShePatients was given antibiotics, and metformin
and, the administration of pulmonary tuberculosisTB medication was stopped.

Patient was hospitalized for 13 days, her patients general condition had
improvedgot an improvement :. , thepatient complained had no fatigue and the
swelling had disappeared. Patient Then she was allowed to go home. Patient may
regularly visited back to the hospital to be checked have her random blood plasma
glucose measuredment levelregularly every week. and obtained Hher random
plasma blood glucose level was 146 to -200 mg/dL. Patient was referred to Dr.
Kariadi Hospital for more further diagnosis and management..
Currently, patient complained for her productive cough with, greenish
yellow, viscous mucus, without blood, abdominal pain (+), no complaint of
shortness of breath nor fatigue. Patient still has good appetite. There was no
complaint on urination nor defecation. Weight loss (-).
Past Medical History
There was no history of operatingsurgery. There was history of shortness of
breath for a long time and patient was diagnosed for pulmonary tuberculosisTB on
June 2014, had been and got treatment treated for 1 week, but then the treatmen
was stopped because of high random plasma blood glucose level (400 mg/dL).
Patient was suspected for diabetes mellitusDM because of there was history for
excessive thirst and hunger, and hungry faster, rapid thirst, frequent
micturitionurination (3-4 times at every night) since approximately 3 years ago.
Perinatal history: There was no history of disease during pregnancy. Her mother
got vitamin and Fe tablet once a day during pregnancy. The baby was born atterm
with normal delivery byon midwiferey. She was the second child with 3000 grams
birth weight and 48 cm body length. There was no history of cyanotic, icteric and
seizure during perinatal period. Patient had been breastfed only for 1 month.
Sosio-economic and family history: Father is aa nprivate employeeenterpriser,
and mother is a housewife. Family income is about two million rupiah a month.
This family lives in their own house. Patient havePatient has medical insurance
from BPJS Non PBI. They were in considerablelower middle socio economic

status. The patientss father hasd Type 2 Diabetes MellitusDM and ever suffered
diagnosed for fromtuberculosisTB (+) 5 years ago and got received 6 months of
pulmonary TB treatment. He is also a smoker.

Pedigree

Developmental history: Patient was able to: smile (2 months old), sit (8 months
old), stand up (10 months(2,5 years old), walk (13 years old). The development is
according to the age. Basic immunization was completed, she had received DPT,
Polio and Hib as booster on 18 months. Currently the patients studied in the junior
high school. Patients already hadstarted had menstruationng.
Growth history: Patients birth weight was 3000 grams and birth lenghth was 48
cm. On admission, body weight was 54 kg and height was 155 cm on percentile
25. Anthropometric score: WAZ NA, HAZ -0,57 SD, BMI/A 1.00 SD. It revealed
shows good nutrition status with, normal stature.
Physical Examination on September 9th 2014 in C1L1 pediatric ward
A 13 years and 8 months old girl, weight 54 kg and height 155 cm. General
state of the patient appearsed conscious and active. On examination of the vital
signs, pPatient's blood pressure got wass high at 130/80 mmHg (P99) whithere
7

Pp50: 106/62 mmHg, Pp90: 119/76 mmHg, P95: 123/80 mmHg, and P99: 130/80
mmHg. She had no tachycardia (heart rate: 108 times/minute), regular pulse
pressure, with content and tension was sufficient, no tachypnea with (rRespiratory
rate: 28 times/minute) nor fever (Ttemperature: 37 C).
On On ppPhysical examination from head to toe, there were no was not
foundanyfor anatomical abnormalities or acanthosis nigricansnictrigan. On the
examination of the thorax, was obtainedralesonchi in the right lung was
positiveobtained without , no wheezing sound.. On abdominal examination,
obtained flexible stomach, tenderness and painfull of epigastria (+), tenderness of
left hipochondriacal (+) were obtained. There was no enlargement of the liver and
spleen,spleen. Neither There were no abnormality of lymph nodes, genitalia, and
joints, either. Patient examination had normal reflexes and no congenital
abnormalities.
Laboratory findings
Laboratory tests were s carried out on 10 September 2014. Her hemoglobin
was 12.2 g/dL, hematocrit 37.7%, erythrocyte 5.41 million/mm3, leukcocyte
12.100/mm3, thrombocyte 555.000/mm3, MCV 69.7 fl, MCH 22.5 pg, and MCHC
32.2 g/dl. Differential count showed eosinophils 3%, basophils 0%, neutrophil
bandsstab 2%, neutrophil segment 76%, lymphocytes 12%, and monocytes 7%.
Peripheral blood smear showed mild anisocytosis, mild lightpoikkilocytsitosis,
activated lymphocytes (+), and increased platelet count increased, giant platelet
(+). PresentRandom plasma glucose level was 220 mg/dL,. impaired fasting
glucose (IFG) 189 mg/dL impaired glucose tolerance (IGT) 165 mg/dL. On
Uurinary examination was obtained proteinuri (25 mg/dL), reduction (50 mg/dL),
acetone (5 mg/dL), hematuria (erythrocytes 42.4/uL), mucus (6.89/uL), and
bacteria (260.7/uL), were observedtained.
Radiologic Findings

Chest radiography showed increased vascular marking, right apex

infiltrates. The heart was is normal. The abnormal finding his tends may lead to
active pulmonary tuberculosisTB impression.
For the diagnosis of TB in children was been shownthe scoring as
following sscores were ::
1. TB Contacts: 1
2. Tuberculin Skin Test: 3 (it was done three months before admission at
Soewondo Hospital, induration + 15 mm)
3. Weight loss: 0
4. Fever: 0
5. Cough: 1
6. Enlarged nnlllymphatic nodesnodilymphatici: 0
7. The jJoint abnormalities: 0
8. X-rays: 1
Total: 6
Diagnosis
Diabetes mellitusDM, DD/ Type 21 Diabetes MellitusDM, Type 12 Diabetes
MellitusDM; psuspect of pulmonary tuberculosisTB; hypertension stage 1; and
good nutrition, normal stature.
Therapy
Patient was given three times3x diet of rice and three times of 3x200 ml of
diabetasol milk, FFurosemide 30 mg/24 hours, RRanitidine 2x1 tablet, next
therapy was waiting for the outcome resultof tests..
Follow Up
On the 2nd day of admission: patients complained about having productive
cough, abdominal pain and nausea without vomiting. Patients appeared conscious
and less active. Vital signs were BP: 120/80 mmHg (P95), HR: 108 times/minute,
RR: 25 times/minute, regular, T: 37C, presentRandom plasma glucose level: 283

mg/dL. On examination of thorax, there was ronchi on the right lung, abdominal
examination: there was tenderness on epigastrialca, hipocondriaca sinistra, and
iliaca dexkstra. Patient got the same therapy as before.
On the 3rd day admission: patientspatientwas performed blood gas analysis
was performed and the results obtainedwas pH 7.36, pCO2 20 mmHg, HCO3 11.3
mmol / L, and BE -12.0, SO2c 72%. HbA1C 9.5%, presentrandom plasma
glucose level: 204 mg/dL, diuresis 0.82 ml/kg/hour and had pain on right
costophrenicus angle. Consultation from Division of Nephrology got suggestedthe
impression of hypertension stage I. Additional therapies yfrom them were
furosemide 40 mg/8 hours, captopril 12.5 mg/8 hours, low-salt diet. They
suggested searching assessment for the etiology of hypertension and renal
involvement by checking screening for microalbuminuria.
On the 4th day of admission: pPatient complained of fatigue and had cold
sweat. Glucose level curve (11/09): 204-239-171-232. The re-examination of
blood gas analysis showedobtained improvement with of pH 7.43, pCO2 28
mmHg, HCO3 18.6 mmol/L, and BE -4.5, SO2c 100%. From Uurinary test,it was
found microalbumin 28 mg/L, diuresis 0.46 ml/kg/hour. Patient was given
additional therapies of y that was RL infusion 2880/120/30 dpm and metformin
500 mg/8 hour.
On day 5 of admission: patient was checked for her cholesterol 265 mg/dL,
albumin 4.7 g/dL, TSHs 3.38 uIU/mL, FfT4 19.38 pmol/L. C-peptide 2.9, diuresis
0.59 ml/kg/hour. First examination for sputum was negative for acid-fast-bacilli,
but shown diplococcus positive, negative gram negative rods negative.
On the 6th day of admission: Her hemoglobin was 12.7 g/dL, hematocrit
37.4%, erythrocyte 5.6 million / mm3, leucocytesleukocyte 13,500/mm3,
thrombocyte 517.500/mm3, MCV 69.1 fl, MCH 22.7 pg, and MCHC 33.8 g/dl.
PresentRandom plasma glucose level 166 mg/dL, ureum 15 mg/dL, creatinine
0.40 mg/dL, natrium 139.1 mmol/L, potassium 3.5 mmol/L, chloride 103.1
mmol/L. Re-examination was done for hemoglobin 120.6 g/dL, hematocrit
370.24%, erythrocyte 54.1 million/mm3, leucocytesleukocyte 135.100/mm3,
thrombocyte 5313.900/mm3, MCV 74.6 fl, MCH 26.0 pg, and MCHC 34.9 g/dl.

10

PresentRandom plasma glucose level was 115 mg/dL, ureum 22 mg/dL, creatinine
0.29 mg/dL, natrium 127.6 mmol/L, potassium 3.9 mmol/L, chloride 94.1
mmol/L.
On the 7th day of admission: Second test for sputum showed positive (3+)
for acid-fast bacilli, and also showed diplococcus positive, gram negative rod
bacteria (+), leuckocyte more than 25 cells/small field. Diuresis rate was 0.98
ml/kg/hour. PresentRandom plasma glucose level curve was 207-216-223-217.
On the 8th day of treatment: her hemoglobin was 13.6 g/dL, hematocrit
39.9%,

erythrocyte

6.0

million/mm3,

leucocytesleukocyte

18.100/mm3,

thrombocyte 632.500/mm3, MCV 66.8 fl, MCH 22.8 pg, and MCHC 34.1 g/dl.
Random plasma glucose level was 175 mg/dL,ureum 20 mg/dL, creatinine 0.46
mg/dL, AST 20 U/L, ALT 30 U/L. Based on cConsultation from Division of
Respirology, it was suggested to administer gave anti-TB drug FDC 3 tablets/day
(2RHZE/4RH). PresentRandom plasma glucose level curve was 217-210-228172-225.
On the 9th day of admission: aAbdominal USG shown cystitis.
PresentRandom plasma glucose level curve was 225-172-170-172.
On dated the 11th :September 18th 2014 patient was discharged with
improvement. Patient got was prescribed with Metformin 500 mg/8 hours,
Captopril 12.5 mg/8 hours, Furosemide 40 mg/12 hours, Ranitidine 1 tab/12
hours, and FDC anti-TB drug 3 tablets/day (2RHZE/4RH) for at self-administered
medicationhome.

11

CHAPTER III
DISCUSSION
The case was a 13-years13 years and 8 months -old girl with 54 kg weight,
and 155 cm height, was diagnosed with type 2 diabetes mellitusDM with renal
complication and pulmonary tuberculosisTB.
3.1.

Diabetes Mellitus

3.1.1. Definition
Diabetes mellitus (DM) is a metabolic disease characterized by absolute or
relative insulin deficiency. Absolute deficiency of insulin most commonly results
from an autoimmune destruction of insulin producing cells in the pancreas and in
general, the term tType- 1 DM (T1 DM) is used to denote childhood diabetes
associated with autoimmunity and absolute insulin deficiency. The term tType 2
DM (T2 DM) is used to denote diabetes resulting from a relative deficiency of
insulin when insulin secretion is inadequate to overcome co-existent resistance to
insulin action on carbohydrate, protein or fat metabolism; T2 DM is most
commonly associated with the prototypic insulin resistant state of obesity.7
3.1.2. Classification and Pathogenesis
Diabetes mellitus is an endocrine disorder characterized by increased
levels of blood glucose.12-14According PERKENI suggestion consensusthat as
recommended by the ADA in 1997, diabete DMmellitus can be classified by
etiology, ie:13, 14
1. Type-1 Diabetes Mellitus13, 14
Type-1 Diabetes Mellitus or known as Insulin Dependent Diabetes Mellitus
(IDDM) occurs due to damage of cells pancreas (autoimmune reactions). If
cells damage has reached 80-90%, the symptoms of diabetes DMmellitus
begin to appear. This B cell destruction occurs faster more rapidly in children
than adults. Most patientspatients with type-1 DMdiabetes mellitus have
antibodies that indicate the presence of autoimmune process, but there is small

12

part which is not because of an autoimmune process. This condition is

classified as type-1 idiopathic.

13

14

Most of cases (75%) occur before the age of 30 years, but age does is not
included in criteria for classification.14
2. Type-2 Diabetes Mellitus13, 14
Type-2 diabetes mellitus or Non-Insulin Dependent Diabetes Mellitus
(NIDDM) accounts for 90% of cases. At tThis type diabetes mellitus results
from occurs from the decreased ability of insulin that to work s in peripheral
tissues (insulin resistance) and B cell dysfunction, as a result the
consequencethe pancreas is unable to adequately produce enough insulin to
compensate for insulin resistance. Both of these cause relative insulin
deficiency.
3. Gestational Diabetes Mellitus14
Gestational Diabetes Mellitus (GDM) is a normal pregnancy that is
accompanied by an increase in of insulin resistance leads to failing toin which
pregnant women fail to maintain euglycemic conditiona circumstances. GDM
increases

the

risk

of

neonates

morbiditycomplication

of

neonates,

includingsuch as hypoglycemia, jaundice, polycythemia, and macrosomia.

This occurs because fetusbabies of GDM mothers secretes an elevated level of
larger amount of insulin whichso that stimulates the growth of infants and
leads to macrosomia. GDM frequency of prevalence is approximately 3-5%,
and the mothers are at increased risk for becoming having DM in the future.
4. Other Specific Type of Diabetes Mellitus14
This is a subclass of diabetes DM mellitusin which wherepatientssomeone is
develop experiencing hyperglycemia due to specific abnormalities (e.g
abnormal genetic abnormalitiesfunction of cells), endocrinopathy (e.g
Cushing disease, acromegaly), the use of drugs that interfere the function of
cells (e.g Dilantin), the use of drugs that interfere insulin action (e.g adrenergic), and infections and /genetic syndromes (e.g Down's syndrome,
Klinefelter's syndrome)
3.1.3. Diagnostic Criteria

14

15

The American Diabetes Associations criteria for the diagnosis of

DM were recently revised to include a new threshold for the diagnosis of
impaired glucose tolerance (IGT) and impaired fasting glucose (IFG). The
diagnosis of DM is made on the basis of one of the following criteria 7, 15:
(i)sSymptoms of hyperglycaemia including polyuria, polydipsia, weight
loss plus random plasma glucose concentration >200 mg/dl (11,1
mmol/L), f. (ii) Fasting plasma glucose (> 8-hour fasting) > 126 mg/dl (7
mmol/L), . (iii) 2 hour post prandial glucose >200 mg/dl during an oral
glucose tolerance test (OGTT),.(iv) HbA1c 6.5.
Criteria for diagnosing IGT and IFG are a 2 hour post-load plasma
glucose between 140-200 mg/dl (7.8-11.1 mmol/l)or and a fasting plasma
glucose between 100-125 mg/dl (5.6-6.9 mmol/l) respectively.15-17 The
ADA classification of DM encompasses 4 groups: tType 1, tType 2, other
specific types of diabetes, and gestational diabetes.18
For making To establish the diagnosis of type-1 diabetes
mellitusDM, it is necessary to have test result for C-peptide <0.85 ng/mL.
C-peptide is a marker of the number of functional cells pancreas is still
on its functions.19 The characteristics of type 1 and type 2 diabetes mellitus
DM can be seen on table below.
Table 1.Characteristics of type 1 and type 2 diabetes in children and adolescents7

15

16

Glucose Tolerance Test4

In children, usually glucose tolerance test (GTT) usually does not
need to be performeddone to diagnose type-1 diabetes mellitus, due to the
typical distinct clinical manifestations. Indication of GTT in children is on
for the doubtful cases which iscases in which found clinical symptoms
typical for DM are found diabetes mellitus, but the examination of random
plasma glucose levels is not uncertainsure.
Assessment of glucose tolerance test results4:
1. Children suffering havefrom diabetes if:
Fasting plasma glucose 140 mg/dL (7.8 mmol/L) or
Plasma glucose levels in 1 - 2 houran hour to 2: 200 mg/dL(11.1
mmol/L)
2. Children considered to be sufferinghave from impaired glucose tolerance if:
Fasting plasma glucose levels <140 mg/dL (7.8 mmol/L) and
Plasma glucose levels in 1 - 2 houran hour to 2: 140-199 mg/dL(7.8 to 11
mmol/L)
3. Children considered as normal if:
Fasting plasma glucose levels <110 mg/dL (6.7 mmol/L) and
Plasma glucose levels in an hour 1 - 2to 2 hour: <140 mg/dL(7.8 mmol/L)
In this case:
The patient was in school-age (13 years and 8 months) who complained of
fatigue, swelling of the face, arms, and legs and obtained had random plasma
glucose concentration was 400 mg/dL. Patient also had a history of polyuria,
polydypsia, polyphagiafagia since last 3 years. There was no weight loss.
Laboratory findings:
Random plasma glucose concentration was 220 mg/dL, IFG 189 mg/dL (100-125
mg/dl), IGT 165 mg/dL (140-200 mg/dl), HbA1c 9.5%. Based on the criteria
diagnosis criteria above, patient was diagnosed with diabetes DMmellitus.
To distinguish type-1 and type-2 diabetes DMmellitus, C-peptide examination was
done performed and the result was 2.9 ng/mL, which means that the patient is
suffering from type-2 DMdiabetes mellitus (C-peptide > 0.85 ng/mL).

16

17

3.1.4. Risk Factors

Risk factors for type-2 diabetes DM mellitusinclude ing family history
(medical condition of insulin resistance), obesity, lack of physical activity, race
and ethnic.20
1. Family History
Genetic factors are associated to certain HLA patternstypes, but the HLA
system is not the only factor or the dominant factor in the pathogenesis of
ttype-1 diabetes mellitusDM. HLA system plays a role as a susceptibility gene
or susceptibility factor. It requires neededa triggering factors that usually
comes from the environment (e.g virus infections, toxins, etc.) to elicitcause
clinical symptoms of ttype-1 DM diabetes mellitusfor those in people who are
susceptiblevulnerable.
Genetic factors influence the development of type-2 DMdiabetes mellitus so
that family history is an important risk factor. The risk offor patients with a a
family history of ttype-2 DMdiabetes mellitus is 5 to 10 times higher than
patients without a family history of diabetes. In one study, 39% of those with
ttype-2 DMdiabetes mellitus have at least one parent who has the same
disease.
2. Insulin Resistance Condition
Polycystic ovary syndrome (PCOS) and acanthosis nigricans are associated
with insulin resistance, . Polycystic ovary syndrome is characterized by
hyperandrogenism and amenorrhea which is associated with chronic
anovulation. Women and young women with PCOS have a higher risk for
glucose intolerance and type-2 DMdiabetes mellitus. Acanthosis nigricans is a
skin disorder that affects the intertriginous areas of the body (eg the base of
the neck, armpits, anteicubital area), and leadsd to an increase in roughness
and thickness of the skin and hyperpigmentation. This condition is caused by
excess of insulin due to insulin resistance which and is presents in 90% of
children who have ttype-2 diabetes mellitusDM.
3. Obesity and Lack of Physical Activity

17

18

85% of patients suffering from type-2 diabetes DMmellitus are also obese.
Individuals with excessive weight and impaired glucose tolerance are more
likely to have peripheral insulin resistance and high fat deposition in visceral
organs and intramuscular.
4. Race and Ethnicity
In the United States, ttype-2 DMdiabetes mellitus is found 2 to 6 times more
common in Hispanic population compared to non-Hispanic whites. The data
from around the world show that obesity, insulin resistance, and ttype 2
diabetes mellitus DM havehas increased at the location where where the
Wwesternized lifestyles are commonly adopted. This lifestyle leads to a highcalorie diet and less of physical activity.

In this case:
Not found any aAcanthosis nigricgans and obesity were not found in this patient.
Patient already has started menstruation menstruating cycle and had s
normalenough activities. From family history, it was was known revealedthat that
her father hasd ttype-2 DMdiabetes mellitus too.
3.1.5. Management
Here is tThe management of tType 2 Diabetes Mellitus is shown as
followswing:21

18

19

Figure 1. Management of ttype 2 diabetes mellitus in children and adolescents

Diabetes care as recommended in clinical practice guidelines
requires access to appropriate medical care and medication, but the
pathophysiology and nature of the disease (with constant changes in
glucose levels) requires constant adjustments to be made by the child in
coordination with the parents, which in turn requirerequiring constant
decisions on medication, food choices, activities, etc. Diabetes selfmanagement education for every child and their family is thus necessary
to achieve appropriate managementregulation of the disease.
The first thing that must be understood by all concerned is that
diabetes cannot be cured, but quality of life can be maintained optimally
optimized with good metabolic control. The definition of good metabolic
19

20

control is commercializing maintaining plasma glucose levels within

normal limits or close to normal values, without causing hypoglycemia.
The success of therapy is assessed based on the levels of plasma glucose,
HbA1C level, and its accompanying concomitant metabolic syndromes
such as obesity, hypertension, and dyslipidemia. In addition to medical
approach to achieve ,therapeutical efficacy,

required for lifestyle

modification and overcome preventing the accompanying associated

symptoms of metabolic syndromes are required. The goal of therapy of
ttype-2 DMdiabetes mellitus as a whole is to achieve normal plasma
glucose levels, weight loss in obese patients, control of comorbid factors
such as hypertension, dyslipidemia, nephropathy, and hepatic steatosis
(fatty liver).22
1. Blood glucose monitoring
The propensity to develop chronic microvascular complications of
diabetes is strongly associated with the level of long term glycaemic
control,control. i It underscores the critical importance of maintaining blood
sugars as near normal as possible. Efforts to achieve euglycaemia requireentail
the unavoidable considerable risk of hypoglycaemia, and thus accurate,
reproducible, and easyfacile techniques to conduct home blood glucose
monitoring is key to the success of all intensive insulin management
regimens.7, 23, 24

20

21

Table 2.Target indicators of glycemic control7

2. Dietary
The term dietary now is more commonly used than diet because diet is
synonymous with efforts to lose weight so that calories should be reduced.
Weight loss needs to be done in patients with type-2 diabetes DMmellitus who
are often havesuffering from obesity, whereas in children with type-1
DMdiabetes mellitus, calorcalories are stillies still needed for growth.
ManagementArrangement of food in patients with type-1 diabetes DMmellitus
aims to achieve good metabolic control without neglecting the calories which
is required for basal metabolism, growth, puberty, as well as daily activities.
By managing these foods, it is expected that children do not become obese and
the incidence of hypoglycemia can be prevented.
The required amount number of calories per day that is required to be
calculated based on ideal body weight. Counting cCaloriescalculation requires
the information ofdata for age, sex, height, weight, and data recommended
21

22

sufficiency calories sufficiency recommendation. The recommended calorie

composition is 50-60% from carbohydrates; 10-15% comes from protein, and
30% from fat. Carbohydrates aeffect on plasma glucose levels, within 1-2
hours after having a meal with of 90% of carbohydrates iswill be glucose. The
recommended types of carbohydrates are high in fiber and have a low
glycemic index and glycemic load, such as the group of fruits, vegetables, and
cereals that will help prevent increasing of blood glucose levels.
One key of success is managing food intake and diet which is the same as
before and after the diagnosis, as well as foods that are no different from their
peers or food family. Setting the optimal meal usually consists of 3 main
meals and 3 times snacks.
3. Sports
Exercise should be the part of everyone's life, whether children,
adolescents, and adults, with or without diabetes mellitusDM. Exercise can
help you to lose weight, maintain a healthy weight, and improve selfconfidence. For diabetic patients, exercise can help to lower plasma sugar
levels, causing a feeling of healthy or well being and increase sensitivity of
insulin, thus can be reduceing the need for insulin. In sSome studies , it
explain s that exercise can increase the capacity of the heart and reduce the
incidence of long-term diabetes mellitusDMs complications.
However, for people with diabetes mellitusDM, especially for those who
are not well controlled, exercise can cause unwanted circumstances such as
hyperglycemia to diabetic ketoacidosis, more severe diabetic complications
complicationsthat have been experienced can be more severe, and
hypoglycemia. Approximately 40% incidences of hypoglycemia in patients
with diabetes mellitus DM are triggered by exercise. Therefore, diabetes
mellitus patients with DM who decide to exercise regularly, especially sports
with moderate-severe intensity is expected to consult with his/her doctors
before starting a program of exercise. They are expected to check their health

22

23

status closelycarefully, not only for adjusting their intensity, but also for
duration of how long they can exercise with their current health state.
4. Medications
If the patient has implemented dietary program and exercise program
regularly, but the plasma glucose levels have not been are not wellyet
controlled yet, it should be added either oral hypoglycemic drugs or insulin
should be administered. Oral hypoglycemic drugs (OHO) can be found in the
form of group sulfonylurea, biguanide class and alpha glucosidase inhibitors. 25
Recently, the only oral hypoglycemic drugs which has been are approved for
use in children by the Food and Drug Administration (FDA) is only
metformin.
5. Family ResponsibilityControl
Educational, and socio-economic level and compliance trust factors are
some of the factors that should be considered in the management of patients,
especially in terms of patient education. Due to some aforementioned
problems that have been mentioned before, theThe quality of the management
of diabetes mellitus DM is highly depends ent on the results of the
consultation process between among the patient/family with and within the
team, among others, by the doctor. Good mutual, honest, open, and
determined relationship between doctor-patient will greatly help the patient
instill confidence in the doctor so as to facilitate subsequent management.
Doctors are do not only control the medication but also adjust other
management components to align so that it aligns with the growth process.
Non-interrogative interview is going to stimulate the openness of the patient,
making it easier for physicians to understand the lifestyle and aspirations of
patients. In this case the doctors would easily be assumed of their role as the
"captain" of all components to implementing that together are able to maintain
the quality of life of patients.

23

24

In this case:
Patients were given RL infusion therapy 2880/120/30 dpm,
Mmetformin 500 mg/8 hours, Ccaptopril 12.5 mg/8 hours, Ffurosemide 40
mg/8 hours, and Rranitidine 1 tab/12 hours. She had performed enoughhad
normal activities. Dietary are was given based on calculation of s, the the
patients need s 2300 kcal/24 hours and was given 3 main meals and 3
snacks. Breakfast 25% from caloric needs that is of 575 kcal, lunch 25%
calorie needs were of 575 kcal, dinner 20% caloric needs i.e.of 460 kcal,
extras 1 times evening snack with Diabetasol milk, morning and afternoon
snack (@ 230 kcal).
During admission, her random plasma glucose levelss were checked
on 06.00; 09.00; 15.00; 22.00, the results were shown in this below:
Random plasma glucose curve (11/09): 204-239-171-232
Random plasma glucose curve (14/09): 207-216-223-217
Random plasma glucose curve (9.15): 217-228-172-225
Random plasma glucose curve (16/09): 225-172-170-172

3.1.6. Complications of diabetes in children

Complications of diabetes mellitus DM are caused by changes in
microvascular

(retinopathy,

nephropathy,

and

neuropathy)

and

macrovascular. In children, macrovascular complications, it is very rare,

while complications from microvascular changes are more commoncan be
found easily. Good diabetes care prevents the development of
complications (secondary prevention). The early onset of the disease in
children putsplaces them at a higher risk to develop such complications at
an ever younger early age. Thus, iIn the USA, 40% of children and
adolescents

with

type

DMdiabetes

were

observed

to

have

microalbuminuria (MAU) after a diabetes duration of within only 18

months after being diagnosed with DM; among Pima Indians diagnosed
with diabetes DM during childhood, 22% have developedhad MAU at
diagnosis. Studies in these special populations showed that (except for
retinopathy) children have no protective or delaying factors that protect

24

25

them from complications. On average, complications occurred after a

similar duration than those in adults.26
The complications of diabetes can be very severe, leading to early
onset of cardiovascular disease,

and premature death, . Other

complications that are seriously detrimental to the health and quality of

life of people with diabetes include blindness, kidney failure and
neurological damage. Complications are not limited to medical concerns;
psychosocial complications can prevent optimal diabetes care and the
achievement of treatment goals. Diabetes care poses considerable demands
on children and their families. In addition to the normal developmental
challenges of childhood and adolescence, the additional burden of
diabetes, and especially intensive management, may could be difficult for
many children to deal with. More intensive treatment coincides with
increased psychological pressure on children with diabetes and family
members. This may add aggravate to the development of psychosocial
complications such as adjustment problems, issues with self-esteem,
depression, and particularly in adolescent girls, eating disorders. In one
study amongin adolescents and young adults who had diabetes since
childhood, about onethird needed either psychological or psychiatric
counseling after (on average) 15 yr following onset of their diabetes.27
Retinopathy was observed in 20% of those with type 1 diabetes;
MAU and hypertension were observed in 28 and 36%, respectively, of
those with type 2 diabetes. These high rates of serious complications
suggest that children as well as adults with type 2 diabetes should be
screened for complications at the time of diagnosis. The data also argue for
screening of at-risk adolescents for type 2 diabetes because early treatment
may avoid or reverse complications.28
In this case:
Patient

swas

suspected

already

had

already

experiencing

microvascular complications. First, she was suspected of having diabetic

nephropathy. This isIt was shown by in the results of the examination of
vital signs examination that was her blood pressure of 130/80 mmHg
25

26

(P99). Urinalysis resulted , urine was obtained a proteinuria (25 mg/dL),

reduction (50 mg/dL), acetone (5 mg/dL), hematuria (erythrocytes 42,
4/uL), mucus (6.89/uL), and bacteria (260.7/uL). ThenLater, she was
consulted to the Division of Nephrology. It was indicated got the idea that
patient has d hypertension stage I and give therapy was given, including.
They were Ffurosemide 40 mg/8 hours, Ccaptopril 12.5 mg/8 hours, and
low-salt diet. They suggested for exploring the etiology of hypertension
and

renal

involvement

and

they

recommended

to

test

havingmicroalbuminuria in urin.
During treatment, her diuresis was always less than normal (<1
ml/kg/hour). She complaineds for epigastric tenderness and left
hyipochkondriac atenderness. She was given RL infusion. To make
establish thea diagnosis, patient was tested for exanimatemickroalbumin,
resulted showed 28 mg/dL (High), albumin 4.7 g/dL, ureum 22 mg/dL,
creatinine 0.29 mg/dL (lLow), natrium 127.6 mmol/L, potassium 3.9
mmol/L, chloride 94.1 mmol/L. In addition, abdominal ultrasound
shownultrasound showed cystitis. In tThe presence of microalbuminuria is
an early sign of diabetes nephropathy. Diabetic nephropathy is often
associated with hypertension. This hHypertension should be treated as
microalbuminuria

with

hypertension

havemicroalbuminuria

with

hypertension has a worse prognosis compared towith those without

hypertension. Glycemic control with metformin and the use of ACE
inhibitors may prevent or slowed the progression of diabetic nephropathy.
Patient was also sought for the possibility of diabetic retinopathy
and after examination, obtainment no signs of retinopathy were obtained.
Eye examination in puberty children adolescents is performed done every
2 years (<15 years) so that complications of diabetes mellitus DM can be
detected early. Moreover, as her HbA1C level was 9.5%, which it is
necessary to repair achieve a 1% reduction in HbA1c to reduces the risk of
complications of retinopathy of approximately 20-50%.
Cholesterol was checked ksdone with the result alsoof 265 mg/dL
(high), 3.38 TSHs uIU/mL, FfT4 19,:38 pmol/L. to determine the

26

27

involvement of other metabolic. In patients with high cholesterol obtained

only and only be educated to his life style.

Pulmonary TuberculosisTB29

3.2.

3.2.1. Pathogenesis
After inhalation, the droplet nucleus is carried down to the bronchial tree
and implanteds in a respiratory bronchioles or alveolus. Whether inhaled tubercle
bacillus causes or not an inhaled tubercle bacillus establishes an pulmonary TB
infection in the lung or not, depends on both the bacterial virulence and the
inherent microbicidal ability of the alveolar macrophage that ingests it.30, 31 If the
bacillus is able to survive initial defenses, it can multiply within the alveolar
macrophage. The tubercle bacillus grows slowly, dividing approximately every 25
to 32 hours within the macrophage. Mycobacterium tuberculosis has no known
endotoxins or exotoxins; therefore, there is no immediate host response to
infection. The organisms grow for 2 to 12 weeks, until they reach 103 to 104 in
number, which is sufficient to elicit a cellular immune responses (19, 20) that can
be detected by a reaction to the tuberculin skin test.32, 33
Before the development of cellular immunity, tubercle bacilli spread via
the lymphatics to the hilar lymph nodes and thence through the bloodstream to
more distant sites. Certain organs and tissues are notably resistant to subsequent
multiplicationof these bacilli. The bBone marrow, liver, and spleen are almost
always seeded with mycobacteria, but uncontrolled multiplication of the bacteria
in these sites is exceptional. OrganismsBacteria deposited in the upper lung zones,
kidneys, bones, and brain may find environments that favor their growth, and
numerous considerable bacterial bacterial cell divisions may occur before specific
cellular immunity develops and limits multiplication.
In

Among

peoplepersons

with

intact

cell-mediated

immunity,

collectionsgroups of activated T cells and macrophages form granulomas that

limit multiplication and spreading of the bacteriaorganism. Antibodies against M.
tuberculosisTB are formed but do not appear to be protective.34 The organisms
tend to be localized in the centerof the granuloma, which is often necrotic. For
27

28

themajority of individuals with normal immune function, proliferationof M.

tuberculosisTBis arrested once cell-mediated immunitydevelops, even though
small numbers of viable bacilli mayremain within the granuloma. Although a
primary complexcan sometimes can be seen on chest radiograph, the majority
ofpulmonary

tuberculosisTB

infections

are

clinically

and

radiographicallyinapparent.31Most commonly, a positive tuberculin skin test result

is the only indication that infection with M. tuberculosisTB has had occuredtaken
place. Individuals with latent tuberculosisTB infection but not active disease are
not infectious and thus cannot transmit the organism. It is estimated that
approximately10% of individuals who acquired tuberculosisTB infection and are
were not given preventive therapy will develop active tuberculosisTB.
3.2.2. Criteria Diagnostic Criteria
The dDiagnosis of TB in children heavily relies on careful and thorough
assessment of all the evidence derived from a careful history, clinical examination
and relevant investigations, e.g. TST, chest X-ray (CXR) and sputum smear
microscopy.
1. Careful history (including history of TB contact and symptoms consistent
with TB)
a. Contact
Close contact is defined as living in the same household as or in a frequent
contact with a source case (e.g. the childs caregiver) with sputum smearpositive pulmonary TB. Source cases that are sputum smear-negative but
culture-positive are also infectious, but to a much lesser degree.
b. Symptoms
In most cases, children with symptomatic TB develop chronic symptoms.
The most common symptomsest are:
Chronic cough
A persistentn unremitting cough that is not that has not been
improveding and has been present for more than 21 days.
Fever
28

29

Body temperature of >38 C for 14 days, after common causes

such as malaria or pneumonia have been excluded.
Weight loss or failure to thrive
In addition to asking about weight loss or failure to thrive, it is
necessary to look at the child's growth chart.
2. Clinical examination (including growth assessment)
There are no specific features on clinical examination that can
confirm that the presenting illness is due to pulmonary TB. Some signs,
although uncommon, are highly suggestive of extrapulmonary TB (i.e. TB
inof organs other than the lungs). Documented weight loss or failure to
gain weight, especially after being treated in a nutritional rehabilitation
programme, is a good indicator of chronic disease in children, of which
TB may might be the cause.
3. Tuberculin skin test
A positive TST occurs when a person is infected with M.
tuberculosisTB, but does not necessarily indicate disease. However, the
TST can also be used as an adjunct in diagnosing TB in children with signs
and symptoms of TB and when used in conjunction with other diagnostic
tests. There are anumber numerous of TSTs available, but the TST using
the Mantoux method is the recommended test. A TST should be regarded
as positive as follows:
in high-risk children (includinges HIV-infected children and severely
malnourished children, i.e. those with clinical evidence of marasmus or
kwashiorkor): >5 mm diameter of induration;
in all other children (whether they have received a bacilleCalmetteGurin
(BCG) vaccination or not): >10 mm diameter of induration.
There It can be either false-positive as well as or false-negative
TSTs. Sometimes it is useful to repeat the TST in children once their
nutritional status has improved or their severe illness (including TB) has

29

30

resolved, as they may be initially TST negative, but positive after 23

months on treatment. A negative TST never rules out adiagnosis of TB in a
child.
4. Bacteriological confirmation whenever possible
It is always advisable to confirm diagnosis of TB in a child using
wheneverwhatever specimens and laboratory facilities are available.
Appropriate specimens from the suspected sites of involvement should be
obtained for microscopy and, whenre facilities and resources are available,
for culture (and also histopathological examination). Appropriate clinical
samples include sputum, gastric aspirates and certain other material (e.g.
lymph node biopsy or any other material tissues that is biopsiedbiopsy). In
addition to increasing the yield of confirmed TB cases, mycobacterial
culture is the only way to differentiate M. tuberculosisTB from other
nontuberculous mycobacteria. Bacteriological confirmation is especially
important for children who have:
suspected drug-resistant TB
HIV infection
complicated or severe cases of disease
an uncertain diagnosis.

5. Investigations relevant for suspected pulmonary TB

Chest radiography is useful in the diagnosis of TB in children. In
the majority of cases, children with pulmonary TB have CXR changes
suggestive of TB. The most commonest picture is that of persistent
opacification in the lung together with enlarged hilar or subcarinal lymph
glands. A miliary pattern of opacification in HIV-uninfected children is
highly suggestive of TB. Patients with persistent opacification which
isdoes not improved after a course of antibiotics should be investigated for
TB.

30

31

Adolescent patients with TB have CXR changes abnormalities

similar to adult patients with large pleural effusions and apical infiltrates
with cavity formation being the most common forms of presentation.
Adolescents may also develop primary disease with hilar adenopathy and
collapse lesions visible on CXR. Good-quality CXRs are essential for
proper evaluation. CXRs should preferably be read by aradiologist or a
health-care worker trained in their reading. A practical guide for
interpreting CXRs has been developed.
6. HIV testing
In areas with a high prevalence of HIV infection in the general
population, where TB and HIV infections are likely to coexist, HIV
counselling and testing is are indicated for all TB patients as part of their
routine management. In areas with lower HIV prevalence, HIV
counselling and testing is are indicated for TB patients with symptoms
and/or signs of HIV-related conditions, and in TB patients having a history
suggestive of high risk of HIV exposure.
Standard case definitions of TB in children35
The diagnosis of TB refers to the recognition of an active case, i.e.
a patient with symptomatic disease (due to M. tuberculosisTB infection).
Beyond the diagnosis of TB disease, the type of TB case should also be
defined to enable appropriate treatment to be given and the outcome of
treatment to be evaluated. The case definition is determined by the: (i) site
of disease, (ii) result of any bacteriological tests, (iii) severity of TB
disease, and (iv) history of previous anti-TB treatment.
Pulmonary TB, sputum smear-positive
The criteria are:
two or more initial sputum smear examinations positive for acid-fast
bacilli; or

31

32

one sputum smear examination positive for acid-fast bacilli plus CXR
abnormalities consistent with active pulmonary TB, as determined by a
clinician; or
one sputum smear examination positive for acid-fast bacilli plus sputum
culture positive for M.tuberculosisTB.
Pulmonary TB, sputum smear-negative
Case of pulmonary TB that does not meet the above definition for smear-positive
pulmonary TB. Such cases condition include cases without smear results, which
should be exceptional uncommon in adults but relatively more frequent in
children. In keeping with good clinical and public health practice, diagnostic
criteria for sputum smear-negative pulmonary TB should include:
at least three sputum specimens negative for acid-fast bacilli; and
radiological abnormalities consistent with active pulmonary TB; and
no response to a course of broad-spectrum antibiotics; and
decision by a clinician to treat with a full course of anti-TB chemotherapy.

32

33

Figure 2. Diagram for diagnosing TB in children

33

34

In this case:
Patient had close contact (her father) with a person suspected of pulmonary TB
person(her father), but there was no documentation whether father had smearpositive or smear-negative sputum. She had a chronic productive cough and
history for bloody cough (approximately 4 months), no be found history of fever
or weight loss in this child. For clinical manifestationpresentation, there was no
specific sign on this child. Patient got had tuberculin skin test in Soewondo
Hhospital with 15 mm induration, Pati and been diagnosed as positive for being
infected of M. tuberculosisTB. To confirm the diagnosis, patient hadwas tested for
bacteriological confirmation and chest X-Ray.
Laboratorium findings:
On The first examination for sputum was negative for acid-fast-bacilli, but shown
showed positive for diplococcus positive and negative for, gram negative rods
negative. Sputum and the second test for sputum showed positive (3+) for acidfast bacilli, and also showed diplococcus positive for diplococcus and, gram
negative rod bacteria. (+), leukcocyte was more than 25 cells/small field.
Radiologic finding:
Chest radiography showed tends to showedprompted an active pulmonary
tuberculosisTB impressionfinding.
This patient hadwas been shown scoringscored for TB as follows:
a. TB Contacts: 1
b. Tuberculin Skin Test: 3
c. Weight loss: 0
d. Fever: 0
e. Cough: 1
f. Enlarged nnll: 0
g. The joint abnormalities: 0
h. X-rays: 1
Total: 6

34

35

3.2.3. Management
Anti-TB treatment is divided into two phases: an intensive phase and a
continuation phase. The purpose of the intensive phase is to rapidly eliminate the
majority of organisms and to prevent the emergence of drug resistance. This phase
uses a greater number of drugs than the continuation phase. The purpose of the
continuation phase is to eradicate the dormant organisms. Fewer drugs are
generally used in this phase because the risk of acquiring drug resistance is low, as
most of the organisms have already been eliminated. In either phase, treatment
can be given daily or three times weekly. Table 3 shows the first-line (or essential)
anti-TB drugs and their recommended doses.
Table 4. Recommended doses of first-line anti-TB drugs for adults and
childrena

a
b

Source: Treatment of tuberculosis: guidelines for national programmes.36

The recommended daily dose of ethambutol is higher in children (20 mg/kg)

than in adults (15 mg/kg), because the pharmacokinetics are different (peak serum
ethambutol concentrations are lower in children than in adults receiving the same
mg/kg dose). Although ethambutol was frequently omitted from treatment
regimens for children in the past, due in part to concerns about the difficulty of
monitoring for toxicity (particularly for optic neuritis) in young children, a
literature review indicates that it is safe in children at a dose of 20 mg/kg (range
1525 mg/kg) daily.37

35

36

Streptomycin should be avoided when possible in children

because the injections are painful and irreversible auditory nerve damage
may occur. The use of streptomycin in children is mainly reserved for the
first 2 months of treatment of TB meningitis.
The recommended treatment regimens for each TB diagnostic
category (see Table 5.) are generally the same for children as for adults.36
Table 6. Recommended treatment regimens for children in each TB
diagnostic category

In this case:
Patient was defined as new pulmonary TB, sputum smear-positive. Patient would
get be managedundergoing a six months treatment with 2RHZ/4RH regiments.
Patient got received FDC anti-TB drugs which be drunk to be given 3 tablets
every each day. The complication of TB with DM type II are The complications of
pulmonary TB in DM Type II children can be very severe, leading to early onset
of cardiovascular disease, blindness, kidney failure and neurological damage.
36

37

Patient was suspected already had microvascular complications. She was

suspected of having diabetic nephropathy. It was shown by the results of the vital
signs examination that her blood pressure of 130/80 mmHg (P99). Urinalysis
resulted proteinuria (25 mg/dL), reduction (50 mg/dL), acetone (5 mg/dL),
hematuria (erythrocytes 42, 4/uL), mucus (6.89/uL), and bacteria (260.7/uL).
Managing the side effects of medication is important in helping people to
complete their TB treatment. This is crucial to minimize the impact of TB on a
persons health and to stop them spreading the illness. Patient should be tested for
liver and kidney function before starting treatment and also evaluated every two
months, careful monitoring throughout treatment will be needed.

37

CHAPTER IV
SUMMARYCONCLUSION
A 13-years and 8 months old girl had been diagnosed with type-2 diabetes
mellitus with renal complication and pulmonary tuberculosisTB based on
anamnesis, physical examination, and several additional diagnostic teststest. After
treated, she were was clinically improved and discharged on 11th 8th day.
Type-2 diabetes mellitus is does not only happen affecton adults, but also
can happen onamong children. Early diagnosis and adequate therapy for the
illness and its complication may give a better prognosis to. This the patient. It is
hoped that this patient had a better prognosis.will have a better prognosis if doctor
can give good treatment for the illness and its complication.
Pulmonary tuberculosisTB in children is difficult to be diagnosed. It
Aneeds careful assessment and several additional examinations are required
assessment to make sureconfirm the diagnosis. This patient was newly diagnosed
as a new positively pulmonary tuberculosisTB with sputum-smear positive and
she had received a lengthy tuberculosisTB got a long medication regimen for 6
months duration. The compliance for this medication is strongly extremely needed
to make provideresult a well favorable prognosis. In this patient the compliance of
TB is enshowed by chronic productive cough and history for bloody cough
(approximately 4 months). For clinical presentation, there was no specific sign on
this child. Patient had tuberculin skin test in Soewondo Hospital with 15 mm
induration, Pati and been diagnosed as positive for being infected of M. TB.
The complications of pulmonary TB in DM Type II children can be very
severe, leading to early onset of cardiovascular disease, blindness, kidney failure
and neurological damage. Complications are not limited to medical concerns;
psychosocial complications can prevent optimal diabetes care and the
achievement of treatment goals. Those complication should be closely monitored
and referral to the nearest hospital is necessary.

38

39

40

REFERENCES

1.

Prober CG. Respiratory Pathophysiology And Regulation. In: Behrman RE,

Kliegman

RM,

Jenson

HB,

editors.

Nelson

Textbook

of

Pediatrics.16thed.Philadelphia: WB Saunders Company;2016.p.761-65.

Price A, Wilson L. Patofisiologi. Buku 2. 4 ed. Jakarta: Penerbit Buku Kedokteran
EGC; 1995. p. 1117-9.
2.

Pasipanodya J. Tuberculosis and other mycobacterial diseases. In ET

Bope, eds. Conn's Current Therapy. Philadelphia: Saunders. 2011:295301.

Noer, dkk. Ilmu Penyakit Anak Jilid I. Edisi Ketiga ed. Jakarta: Penerbit FK
3.

UI; 1999.
Aanstoot H-J, Anderson BJ, Daneman D, Danne T, Donaghue K, Kaufman
F, et al. The Global Burden of Youth Diabetes: Perspectives and Potential A

4.

Charter Paper. Pediatric Diabetes. 2007;8.

UKK Endokrinologi Anak dan Remaja. Konsensus Nasional Pengelolaan
Diabetes Mellitus Tipe 1. Jakarta: Badan Penerbit Ikatan Dokter Anak

5.

Indonesia; 2009.
Springer SC, Silverstein J, Copeland K, Moore KR, Prazar GE, Raymer T, et
al. Management of Type 2 Diabetes Mellitus in Children and Adolescents.

6.

Pediatrics. American Academy of Pediatrics. 2013:648-62.

Erhardt E, Molnar D. Is Type 2 Diabetes Mellitus A Significant Problem in

7.

European Adolescents? Scandinavian Journal of Nutrition. 2004;48:155-60.

Dejkhamron P, Menon RK, Sperling MA. Childhood diabetes mellitus:

8.
9.

Recent advances & future prospects. Indian J Med Res 125. 2007:231-50.
Chan Y. Diagnosis Tuberkulosis. Majalah Kedokteran Andalas. 2005:28-36.
Rao PV. Active TuberculosisTB Should Be Treated With Insulin. JEET
TaDS, editor. Hyderabad, India: Nizam's Institute of Medical Sciences;

10.

2005.
Misnadiarly. Penelitian Survey Penyakit Penyerta pada Penderita TB Paru/
Mycobacteriosis Paru Secara Retrospektif.

Research Report from

JKPKBPPK Center for Research and Development of Disease Control.

Jakarta: NIHRD. Badan LitbangKesehatan; 2001.

40

41

11.

American Thoracic Society, Centers for Disease Control and Prevention,

Infectious Diseases Society of America (2003). Treatment of tuberculosis.
American Journal of Respiratory and Critical Care Medicine, 167(4): 603662.

Guptan A, Shah A. TuberculosisTB& Diabetes Mellitus: An Appraisal. Indian

12.

Journal of TuberculosisTB. 2000.

Dods RF. Diabetes Mellitus. In: Clinical Chemistry: Theory A, Corellation,,
Kaplan L, Pesce A, editors. Third ed. USA: Mosby Inc; 1996. p. 613-40.

13.

13.

World

Health

Organization

(2011).

Guidelines

for

the

programmatic management of drug-resistant tuberculosis: 2011 update.

European Respiratory Journal, 38(3): 516-528.
Foster DW. Diabetes Mellitus. In: Harrisons Principles of Internal Medicine,
Fauci, Braunwald, Isselbacher, et al, editors. USA: McGraw-Hill
14.

Companies; 1998. p. 623-75.

Sack DB. Carbohydrates. In: Tietz Fundamentals of Clinical Chemistry,
Burtis C, Ashwood E, editors. 5th ed. USA: W.B Saunders Company;

15.

2001. p. 427--61.
American Diabetes Association. Diagnosis and classification of diabetes

16.

mellitus. Diabetes Care. 2006;29(1):S43-8.

Report of the Expert Committee on the Diagnosis and Classification of

17.

diabetes mellitus. Diabetes Care. 1997(20):1183-97.

Genuth S, Alberti KG, Bennett P, Buse J, Defronzo R, Kahn R, et al. Followup report on the diagnosis of diabetes mellitus. Diabetes Care.

18.

2003(26):3160-7.
International Diabetes Federation. Global IDF/ISPAD Guideline For
Diabetes in Childhood and Adolescents.

Definition, Epidemiology, and

Classification. Belgium: ISPAD; 2011. p. 8-15.

19.

Medelln G, Cortez E, Milan S, Magana A. Clinical Pharmacokinetics of

Rifampin in Patients with Tuberculosis and Type 2 Diabetes Mellitus:
Association with Biochemical and Immunological Param. Antimicrobial
Agents And Chemotherapy. 2015:7707-14

Rustama DS, dkk. Diabetes Mellitus. ISPAD Clinical Practice Consensus

Guidelines 2009. 2010.

41

42

20.

WHO. Obesity: Preventing and managing the Global Epidemic. Geneva:

21.

WHO technical Report Series; 2000.

International Diabetes Federation. Global IDF/ISPAD Guideline For
Diabetes in Childhood and Adolescents. Type 2 diabetes. Belgium: ISPAD;

22.

2011. p. 21-30.
Diani A, Pulungan AB. Tatalaksana Metformin Diabetes Mellitus Tipe 2
pada Anak Dibandingkan dengan Obat Anti Diabetes Oral yang Lain. Sari

23.

Pediatri. 2010(11):295-400.
Klonoff DC. A review of continuous glucose monitoring technology.

24.

Diabetes Technol Ther. 2005(7):770-5.

Sieg A, Guy RH, Delgado-Charro MB. Noninvasive and minimally invasive
methods for transdermal glucose monitoring. Diabetes Technol Ther.

25.
26.

2005(7):174-97.
Waspadji S. Pedoman Diet Diabetes Mellitus. Jakarta: FKUI; 2002.
Pavkov ME, Bennett PH, Knowler WC, Krakoff J, Sievers ML, Nelson RG.
Effect of youth-onset type 2 diabetes mellitus on incidence of end-stage
renal disease and mortality in young and middle-aged Pima Indians. JAMA.

27.

2006;296:421-6.
Bryden KS, Peveler RC, Stein A, Neil A, Mayou RA, Dunger DB. Clinical
and psychological course of diabetes from adolescence to young adulthood:

28.

a longitudinal cohort study. Diabetes Care. 2001;24:1536-40.

Yokohama H, Okudaira M, Otani T, et al. Higher incidence of diabetic
nephropathy in type 2 than in type 1 diabetes in early-onset diabetes in

29.

Japan. Kidney Int. 2000;58:302-11.

WHO. Guidance for national tuberculosisTB programmes on the
management of tuberculosisTB in children. Geneva: World Health
Organization; 2006.p.. p. 361.

30.

30.

Centers for Disease Control and Prevention (2005). Guidelines TB

test for diagnosing latent Mycobacterium tuberculosis infection. MMWR,

31.

54(RR-15): 49-55.
Edwards D, Kirkpatrick CH. The immunology of mycobacterial diseases.
Am Rev Respir Dis. 1986;134:1062-71.

42

43

31.

Matthew B, Alimuddin Z. The development, evaluation and performance

of molecular diagnostics for detection of Mycobacterium tuberculosis.

32.

Expert Review of Molecular Diagnostics. 2016:1-16

Danneberg AM. Immune mechanisms in the pathogenesis of pulmonary
tuberculosisTB. Rev Infect Dis. 1989;11:S369-78.

32.

Senedu B, Solomon A. Yimer, Gunnar A. Bjune. Tuberculosis Case

Notification and Treatment Outcomes in West Gojjam Zone, Northwest
Ethiopia: A Five-Year Retrospective Study. Journal of Tuberculosis
Research. 2016:23-33

33.

Smith D, Wiengeshaus E. What animal models can teach us about the

pathogenesis of tuberculosisTB in humans. Rev Infect Dis. 1989;11:S38593.

33.

Robert L. Tuberculosis as a three-act play: A new paradigm for the

pathogenesis of pulmonary tuberculosis. Tuberculosis.2016:8-17

Dannenberg AM. Pathogenesis of pulmonary tuberculosisTB: hostparasite

interactions, cell-mediated immunity, and delayed type hypersensitivity. In:
TuberculosisTB BPi, editor. New York1992.
34.

34.

Sifrash M. Socioeconomic Factors Associated with Knowledge on

Tuberculosis among Adults in Ethiopia. Tuberculosis Research and

Treatment. 2016:1-11
Reggiardo Z, Middlebrook G. Failure of passive serum transfer of immunity
against aerogenic tuberculosisTB in guinea pigs. Proc Soc Exp Biol Med.
35.

1974;145:173-5.
Gie R. Diagnostic atlas of intrathoracic tuberculosisTB in children: a guide
for

low

income

countries.

Paris:

International

Union

Against

36.

TuberculosisTB and Lung Disease; 2003.

WHO. Treatment of tuberculosisTB: guidelines for national programmes.

37.

3rd ed. Geneva: World Health Organization; 2003.

WHO. Ethambutol efficacy and toxicity. Literature

review

and

recommendations for daily and intermittent dosage in children. Geneva:

World Health Organization; 2006. p. 365.

43