CDK 178

328

| JULI - AGUSTUS 2010

ENGLISH

SUMMARY

Blood Peroxydase

and Catalase Enzyme

Activity in Down

Syndrome in South

Kalimantan

Roselina Panghiyangani

, Fujiati

Eko Suhartono

, Marisa Vasa

, Najwa

Wulandari

Dept of Biology,

Dept. of Biochemistry,

Basic Program in Medicine,

Faculty of Medicine, Lambung Mangkurat

University, Banjarmasin, Indonesia

Down syndrome is a genetic abnor-

mality caused by abnormal autosomal

chromosome 21. Oxidative stress is

increased in Down syndrome patients.

The stress can be measured through

peroxydase and catalase activity. Per-

oxydase and catalase was the antioxi-

dant enzymes that catalyzed hydrogen

peroxide to water and oxygen.

This research was analytical observa-

tional research with cross sectional ap-

proach to measure blood peroxydase

and catalase activities in 30 Down

syndrome patients and 30 non Down

syndrome patients. Samples were

obtained by purposive sampling. Per-

oxydase activities were measured by

Kanehira and Shibata method. Cata-

lase activities were measured by the

fi rst order of reaction velocity constant

parameter.

Result showed that mean peroxidase

activity in Down syndrome patients

was 0,335/minute and peroxidase ac-

tivity in non Down syndrome patients

was 0,162/minute. The mean catalase

activity in Down syndrome patients

was 47,478/minute and catalase activ-

ity in non Down syndrome patients

was 29,480/minute. Data was analyzed

by unpaired t test with = 0,05; showed

that peroxydase and catalase activities

were signifi cantly different between

Down syndrome patients group and

non Down syndrome patients group.

Conclusion: peroxydase and cata-

lase activities in Down syndrome was

higher than in non Down syndrome

patients.

Keywords: Down syndrome, peroxy-

dase, catalase, oxidative stress

CDK 2010; 37(5): 339-44

Central Pontine

Myelinolysis : Diagnosis

and Managemant

Michael Setiawan

Dept. of Neurology Pluit Hospital, Puri

Indah Hospital, Siloam Hospital Kebon Jeruk,

Jakarta, Indonesia

Central pontine myelinolysis (CPM)

was described by Adams and col-

leagues in 1959 as a disease affecting

alcoholics and the malnourished. The

concept was extended in 1962 with

the recognition that lesions can oc-

cur outside the pons, so-called extra-

pontine myelinolysis (EPM). When the

pathologic process involves pontine

and extrapontine sites, the term os-

motic demyelination syndrome (ODS)

is used. In 1982 a link between these

disorders and the rapid correction of

sodium in hyponatraemic patients was

substantially established. The clinical

presentation of CPM is highly variable,

usually depressed level of conscious-

ness, quadriparesis and pseudobul-

bar symptoms such as dysarthria and

dysphagia. Less often, CPM manifests

with ataxia, movement disorders, or

behavioral symptoms. Diagnosis of

CPM is based on clinical suspicion and

confi rmed by magnetic resonance im-

aging (MRI). Recommended treatment

is supportive only. Reports of treat-

ments including Thyrotropin-releasing

hormone (TRH), methylprednisolone,

intravenous immunoglobulins (IVIg),

and plasmapheresis. Recognizing

patient at risk, preventing rapid cor-

rection of hyponatremia, prompt diag-

nosis, and managing associated com-

plications will decrease morbidity and

mortality.

CDK 2010; 37(5): 350-54

Muscular Dystrophy

with Cardiomyopathy

case report

Juliani Dewi, Tinny Endang Hernowati

Clinical Pathology Dept., Faculty of Medicine,

Brawijaya University / Dr. Saiful Anwar

Malang General Hospital, East Java,

Indonesia

Introduction:

Duchenne Muscular

Dystrophy is the most common type of

muscular dystrophy. The incidence is

30 per 100.000 newborn male. CK level

increased in 50 - 75 % cases and is very

useful for disease evaluation ; CKMB

level increased in 10 % cases, LDH level

increased in 10 % cases, and transami-

nase level increased in 15 % cases.

Case: A 22 year-old male with Duch-

enne-type muscular dystrophy com-

plicated by cardiomyopathy. CPK level

was 2508 U/L, CKMB level was 50 U/L,

LDH level was 568 U/L, SGOT level was

109 mU/L, dan SGPT level was 72 mU/L.

Muscular biopsy revealed progressive

muscular dystrophy pattern. Thorax

photo revealed cardiomegaly, EKG pat-

tern revealed sinus tachycardia with left

and right ventricle hypertrophy.

Conclusion: A case of chronic pro-

gressive muscular dystrophy with car-

diomyopathy.

Suggestion: Genetic examination

with Western Blot muscle biopsy, mus-

cular immunocytochemistry stained

with dystrophyn antibody, and DNA

mutation peripheral blood leucocyte

analysis.

Keywords : Muscular dystrophy, CK,

cardiomyopathy

CDK 2010; 37(5): 361-64

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