Jun 29

Penyakit Kekurangan Enzim G6PD. ( G6PD deficiency )

By taqidoc Medicine, Pediatric 2 Comments »

Pengenalan

Penyakit kekurangan enzim G6PD atau lebih dikenali dengan nama G6PD di kalangan rakyat Malaysia merupakan  satu penyakit bawaan genetik. Ia boleh menyebabkan anemia akibat stress pengoksidaan apabila pesakit tersebut terdedah kepada ubat-ubatan, makanan atau bahan-bahan tertentu. Akibat daripada stress pengoksidaan, sel-sel darah merah akan pecah dan ini menyebabkan anemia berlaku. Proses pemecahan sel-sel darah merah ini dinamakan hemolisis.

Penyakit ini biasanya berlaku kepada kaum lelaki dan dianggarkan 3-5% penduduk Malaysia mengalami masalah kekurangan enzim G6PD.

Pesakit yang mewarisi penyakit ini boleh hidup sebagaimana manusia normal akan tetapi ubat atau makanan tertentu yang boleh menyebabkan hemolisis perlu dielakkan.

Apakah yang dimaksudkan dengan kekurangan enzim G6PD?

Di dalam sel darah merah terdapat satu jenis enzim yang bertanggungjawab mengekalkan kestabilan sel darah merah daripada pecah iaitu enzim G6PD (Glucose-6-phosphate dehydrogenase ). Apabila paras enzim ini rendah, sel darah merah tidak mampu menahan keadaan stress seperti dalam kes jangkitan teruk atau apabila bahan kimia atau ubat-ubatan tertentu diambil, sekaligus menyebabkan sel darah merah pecah.

Hemolisis berlaku dengan cepat dan ini membawa kepada hemolitik anemia.

Berapa kerapkah berlakunya kes kekurangan enzim G6PD ?

Dianggarkan seramai 400 juta manusia seluruh dunia menghadapi masalah kekurangan enzim G6PD. Keadaan ini selalunya berlaku di bahagian-bahagian tertentu Afrika, Asia dan Mediterranean.

Kawasan yang biasanya berlaku malaria juga mempunyai kes kekurangan enzim G6PD yang tinggi.

Di Malaysia pula dianggarkan 3-5% penduduk Malaysia mengalami masalah ini.

Apakah gen yang bertangggungjawab menyebabkan kekurangan enzim G6PD?

Punca utama kepada berlakunya masalah kekurangan enzim G6PD ialah mutasi di dalam gen G6PD. Gen G6PD mengeluarkan arahan supaya enzim G6PD dibentuk. Enzim ini terlibat dengan normal pemprosesan karbohidrat dan ia juga melindungi sel-sel darah merah daripada molekul berbahaya yang dipanggil molekul oksigen reaktif. Molekul ini merupakan hasil kumuhan sel. Tindak balas kimia yang melibatkan G6PD menghasilkan unsur yang mencegah molekul oksigen reaktif daripada terbina dan terkumpul di dalam sel darah merah sekaligus melindungi sel darah merah daripada pecah.

Sekiranya mutasi di dalam gen G6PD mengurangkan kuantiti enzim G6PD atau menukarkan strukturnya, enzim ini tidak lagi dapat memainkan peranannya sebagai pelindung sel darah merah sekaligus menyebabkan pengumpulan molekul oksigen reaktif yang membawa kerosakan kepada sel darah merah. Faktor seperti jangkitan,sesetengah ubat-ubatan, ataupun memakan kacang parang boleh meningkatkan paras molekul oksigen reaktif dan ini akan menyebabkan sel darah merah dimusnahkan lebih cepat berbanding penghasilannya. Berkurangnya sel darah merah membawa kepada timbulnya simptom dan tanda hemolitik anemia.

Banyak penyelidik percaya yang pembawa-pembawa G6PD mungkin dilindungi daripada penyakit malaria. Ini kerana pada pandangan mereka berkurangnya fungsi enzim G6PD menyebabkan parasit sukar untuk masuk ke dalam sel darah merah.

Bagaimanakah seseorang itu mewarisi kekurangan enzim G6PD?

Masalah kekurangan enzim G6PD ini ditentukan oleh kromosom resesif X. Gen yang dikaitkan dengan masalah kekurangan enzim ini terletak pada kromosom X. Lelaki hanya mempunyai satu kromosom X. Oleh itu, sebarang perubahan secara mutasi pada kromosom X tersebut sudah cukup untuk mewujudkan keadaan kekurangan enzim G6PD. Berlainan pula dengan perempuan yang mempunyai 2 kromosom X, mutasi perlu berlaku pada kedua-dua kromosom untuk mewujudkan keadaan kekurangan enzim G6PD ini. Oleh kerana faktor inilah, kebanyakan pesakit kekurangan enzim G6PD adalah lelaki.

Bagaimana masalah kekurangan G6PD ini didiagnosa?

Berdasarkan sampel darah yang diambil, pesakit kekurangan enzim G6PD akan menunjukkan kandungan haemoglobin yang kurang dan bilirubin yang tinggi di dalam darah.

Selain daripada itu blood film menunjukkan wujudnya blister cells.

Gambar anak panah menunjukkan blister cells akibat akut hemolisis di dalam kes kekurangan enzim G6PD.

Ujian spesifik paras enzim G6PD menunjukkan kandungan enzim yang rendah di dalam darah. Walau bagaimanapun semasa fasa akut, paras enzim di dalam darah mungkin normal atau hampir normal kerana sel yang terbabit semuanya dimusnahkan meninggalkan sel darah merah muda yang mempunyai paras normal enzim G6PD.

Oleh kerana keadaan ini adalah diwarisi daripada ibu yang merupakan pembawa gen tersebut, darah ibu pesakit akan menunjukkan paras enzim G6PD yang rendah daripada normal ataupun sedikit rendah daripada normal. Ini menguatkan lagi diagnosis kekurangan enzim G6PD pesakit.

Apakah gejala-gejala dan tanda-tanda pesakit kekurangan enzim G6PD?

Bagi kebanyakan pesakit yang menghadapi masalah kekurangan enzim G6PD, hemolitik anemia adalah tidak ketara sehinggalah 48-96 jam selepas pesakit mengambil bahan-bahan yang boleh menyebabkan pengoksidaan seperti aspirin, sulfonamid, ubat malaria(seperti primaquin), naftalin dan kacang parang (fava beans). Selain daripada yang tersebut di atas, jangkitan bakteria atau virus juga boleh menyebabkan hemolitik anemia kepada pesakit kekurangan enzim G6PD ini.

Gejala-gejala hemolisis yang akut termasuklah kepucatan, jaundis,mudah letih, sesak nafas, jantung berdebar-debar dan hemoglobinuria (hemoglobin dalam air kencing) yang menjadikan air kencing berwarna gelap. Kematian boleh berlaku sekiranya pesakit mengalami hemolisis yang teruk.

Jaundis dapat dilihat pada bahagian mata putih pesakit apabila berlakunya hemolisis di dalam pesakit kekurangan enzim G6PD.

Bagi bayi baru lahir, kekurangan enzim G6PD boleh menyebabkan jaundis(kekuningan) yang patologik. Jaundis pada bayi-bayi yang mempunyai tahap bilirubin yang tinggi di dalam darah perlu menjalani transfusi darah.

Walaupun ramai yang mempunyai masalah kekurangan enzim G6PD ini, tetapi ramai yang tidak pernah menghadapi gejala-gejala atau tanda-tanda seperti di atas.

Apakah ubat-ubatan yang patut dielakkan bagi pesakit kekurangan enzim G6PD?

  1. Anti-malarial : Primaquine dan pamaquine( Chloroquine di bawah pengawasan mungkin digunakan apabila antimalaria diperlukan untuk pencegahan atau rawatan malaria )
  2. Sulfonamides  : Sulfacetamide, Sulfanilamide, Sulfamethoxazole (e.g. Septra, Bactrim),Sulfasalazine.
  3. Anti-bacterials : Nitrofurantoin, Nalidixic Acid, Dapsone, Mafenide Cream (Sulfamylon).
  4. Analgesics : Phenacetin, Acetanilid, Phenazopyridine (Pyridium).
  5. Antihelmintics : ß-Naphthol, Stibophen dan Niridazole.
  6. Miscellaneous
    1. Vitamin K analogues (1mg phytonadione boleh diberikan kepada bayi)
    2. Probenecid
    3. Dimercaprol (BAL)
    4. Flutamide (Eulexin)
    5. Methylene Blue
    6. Tolouidine Blue
    7. Napthalene ( ubat gegat )

Apakah ubat-ubatan yang boleh digunakan oleh pesakit kekurangan enzim G6PD?

Secara umumnya :

1)Kesemua ubat yang “contraindicated” di dalam kes G6PD

2)Mungkin tidak boleh digunakan di dalam kes Kelas 1 G6PD.

Mengikut klasifikasi WHO, G6PD dibahagikan kepada 5 kelas. Kelas 1-3 merupakan keadaan kekurangan enzim.

Kelas 1 : Kekurangan enzim yang teruk (iaitu kurang daripada 10% aktiviti) dengan kronik hemolitik anemia.

Kelas 2 : Kekurangan enzim yang teruk ( iaitu kurang daripada 10% aktiviti) dengan  kadang-kadang berlakunya hemolisis.

Kelas 3: Kekurangan enzim yang sedikit ( dengan 10-60 % aktiviti ), hemolisis hanya berlaku apabila wujudnya keadaan stres iaitu ketika jangkitan, ubat-ubatan tertentu dan pengambilan kacang parang.

Kelas 4: Varian tanpa kekurangan enzim, dengan tiadanya symptom atau tanda.

Kelas 5: Aktiviti enzim meningkat dengan tiadanya symptom atau tanda.

Antara ubat-ubatan yang boleh diambil oleh pesakit kekurangan enzim G6PD:

  1. Analgesics
    1. Acetaminophen ( paracetamol )
    2. Aspirin ( boleh diberikan tapi dalam dos yang sederhana sahaja )
    3. Auralgan
  2. Cardiovascular Agents
    1. Procainamide
    2. Quinidine
  3. Neurologic Agents
    1. Trihexyphenidyl
    2. Levodopa
    3. Phenytoin
  4. Antibiotics
    1. Chloramphenicol
    2. Chloroquine
    3. Isoniazid
    4. Probenecid
    5. Proguanil
    6. Pyrimethamine
  5. Miscellaneous
    1. Vitamin C
    2. Colchicine
    3. Diphenhydramine

Bagaimanakah anemia yang disebabkan oleh penyakit ini dirawat ?

1)Sekiranya anemia adalah teruk, transfusi darah mungkin diperlukan.

2)Di dalam kes bayi yang baru lahir, langkah untuk mengurangkan bilirubin harus dilakukan kerana keadaan ini merbahaya kepada bayi. Fototerapi diberikan untuk memusnahkan bilirubin melalui kulit. Sekiranya bilirubin terlampau tinggi di dalam darah, “exchange transfusion” diberikan. Di dalam proses “exchange transfusion” ini, darah yang kaya dengan bilirubin dan rendah haemoglobin dibuang dan diganti dengan darah yang rendah bilirubin dan kaya haemoglobin. Dengan itu darah yang mengalir di dalam tubuh bayi akan mempunyai rendah bilirubin dan normal haemoglobin.

Gambar di atas menunjukkan seorang bayi yang sedang menjalani fototerapi disebabkan oleh jaundis.

Exchange transfusion dilakukan apabila paras bilirubin terlampau tinggi di dalam darah bayi.

3) Pesakit yang menderita akibat episod hemolitik anemia perlu mengambil air yang banyak. Begitu juga, supplemen seperti folid acid perlu diambil untuk membantu pembentukan haemoglobin dan sel darah merah.

Seriuskah masalah kekurangan enzim G6PD ini?

Jika diberi rawatan dan nasihat yang betul, pesakit boleh hidup dengan gaya hidup yang normal. Kebanyakan pesakit tidak menunjukkan sebarang masalah dalam tempoh yang panjang. Walaubagaimanapun apabila episod hemolitik anemia berlaku,ia perlu dirawat dengan rawatan yang sesuai.

Sebagai seorang yang mengalami masalah kekurangan enzim G6PD, apakah yang patut saya lakukan?

Anda dinasihatkan supaya menjauhi makanan-makanan seperti kacang parang, makanan yang mengandungi pewarna tiruan methylene dan toluidine blue, kacang soya atau produk soya,semua jenis kacang atau produk kacang dan gula-gula dan makanan berperisa menthol.

Apabila berjumpa dengan doktor, anda hendaklah memberitahu doctor yang anda mempunyai masalah kekurangan enzim G6PD supaya doktor tidak mempreskripsikan ubat yang boleh menyebabkan anemia kepada anda.

Anda juga dinasihati supaya tidak mengambil ubat-ubatan terutamanya antibiotic dan lain-lain ubat-ubatab tanpa mendapat nasihat doktor terlebih dahulu.

REFERENCES :

http://kidshealth.org/parent/general/aches/g6pd.html

http://www.gleneagles-penang.com/BNBD/pdfbook/06%20what%20is%20G6PD%2026-28.pdf

http://g6pddeficiency.org/index.php

http://hubpages.com/hub/Forbidden-Food-for-G6PD-Cases

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Feb 15

The differences between chikungunya and dengue fever.

By taqidoc Medicine Comments Off

Types

Chikungunya

Dengue
Causative agent a virus which belongs to the genus Alphavirus, in the family Togaviridae. any of four closely related viruses, or serotypes: dengue 1-4.

(DENV 1, DENV 2, DENV 3, DENV 4)

Infection with one serotype does not protect against the others.
Season widespread in most parts of the country but is most active after the rains.
Mode of transmission Infected Aedes Aegypti /albopictus bite
Incubation period Time from infection to illness 2-12 days but is usually 3-7 days In order for transmission to occur the mosquito must feed on a person during a 5- day period when large amounts of virus are in the blood; this period usually begins a little before the person become symptomatic.  Some people never have significant symptoms but can still infect mosquitoes.  After entering the mosquito in the blood meal, the virus will require an additional 8-12 days incubation before it can then be transmitted to another human. The mosquito remains infected for the remainder of its life, which might be days or a few weeks.
Symptoms
  1. Fever
  2. Headache
  3. Fatigue
  4. Nausea
  5. Vomiting
  6. Muscle pain
  7. Rash
  8. Joint pain

It can also be asymptomatic.

Acute chikungunya fever typically lasts a few days to a couple of weeks.

Some patients have reported incapacitating joint pain, or arthritis which may last for weeks or months.

 Symptoms of infection usually begin 4 – 7 days after the mosquito bite and typically last 3 – 10 days.  In order for transmission to occur the mosquito must feed on a person during a 5- day period when large amounts of virus are in the blood.

High fever and at least two of the following:

  • Severe headache
  • Severe eye pain (behind eyes)
  • Joint pain
  • Muscle and/or bone pain
  • Rash
  • Mild bleeding manifestation (e.g., nose or gum bleed, petechiae, or easy bruising)
  • Low white cell count

Generally, younger children and those with their first dengue infection have a milder illness than older children and adults.

Warning sign:

(emergency) if

  • Severe abdominal pain or persistent vomiting
  • Red spots or patches on the skin
  • Bleeding from nose or gums
  • Vomiting blood
  • Black, tarry stools (feces, excrement)
  • Drowsiness or irritability
  • Pale, cold, or clammy skin
  • Difficulty breathing
Diagnostic testing 1. Based on the patient’s clinical features, places and dates of travel (if the patient is from a non-endemic country or area), activities, and epidemiologic history of the location where infection occurred.

2. Lab test à to detect virus-specific IgM and neutralizing antibodies in serum or CSF.

3. In fatal cases, nucleic acid amplification, histopathology with immunohistochemistry, and virus culture of biopsy or autopsy tissues can also be useful.

 1.Diagnosis of dengue fever is generally easy in endemic areas and during epidemics due to the typical symptoms and characteristic signs of dengue fever. But if the cases are mild, they may look like other viral disease.

2.Laboratory diagnosis of dengue fever is done by IgM ELISA (enzyme linked immunosorbant assay), paired serology during recovery or by antigen-detection ELISA during the acute phase. There is also leucopenia (lees number of leukocytes or white blood cells, generally less than 5,000) and thrombocytopenia (reduced number of platelets in circulating blood). Dengue virus also can be easily isolated from blood in the acute phase by using mosquito inoculation or mosquito cell culture.
Treatment Symptomatic treatment:

1.Rest

2.Drink plenty of fluid

3.Use analgesics
Analgesics:

Ibuprofen, naproxen, acetaminophen, or paracetamol.

Aspirin should be avoided.

 Analgesics:

Like paracetamol and acetaminophen.

Avoid ibuprofen,naproxen or aspirin.
Can pregnant women become infected and pass the infection to their child? Yes. Most infections will not result in the virus being transmitted to the fetus. The highest risk for infection of the fetus/child occurs when a woman has virus in her blood (viremic) at the time of delivery Yes. Transmission to the fetus is rare.
Can the virus transmitted to a child by breastfeeding? No. No.

Research shows the presence of anti-dengue antibodies in breast milk and colostrum, which suggests that breastfeeding actually protects your baby from the dengue virus in case of a dengue infection.
Mortality rate Fatalities are rare. DHF is a more severe form of dengue infection. It can be fatal if unrecognized and not properly treated in a timely manner. DHF is caused by infection with the same viruses that cause dengue fever. With good medical management, mortality due to DHF can be less than 1%.
Prevention Avoid mosquito bites.

  1. Use insect repellent.
  2. Wear long sleeves and pants.
  3. Have secure screens on windows and doors to keep mosquitoes out.

Get rid of mosquito sources such as emptying standing water from flower pots etc.

Limit exposure to mosquito bites for infected person to avoid further spread.

References:

http://www.babycenter.in/pregnancy/complications/dengue/

http://nethealthsite.com/diseases-with-d/52-dengue-fever.html

http://www.cdc.gov/ncidod/dvbid/Chikungunya/CH_FactSheet.html

http://www.cdc.gov/dengue/

Jan 24

Warts.

By taqidoc Medicine Comments Off

What are warts?

Warts are non-cancerous skin growths caused by a viral infection in the top layer of the skin. Viruses that cause warts are called human papillomavirus (HPV). Warts are usually skin-colored and feel rough to the touch, but they can be dark, flat and smooth. The appearance of a wart depends on where it is growing. Warts are usually acquired from person-to-person contact. The virus is not highly contagious but can cause an infection by entering through a small break in the skin. In the same way, warts can be spread to other places on your own body. The virus is rarely transferred by touching an object used by an infected person.

Who’s At Risk ?

Warts can affect people of any age, but they are most common between the ages 12–16. It is estimated that 20% of schoolchildren and about 10% of the general population have warts. Those with HIV, organ transplants, or on chemotherapy have a higher incidence of warts due to their weakened immune system.

How are warts spread?

Warts are easily spread by direct contact with a human papillomavirus. You can infect yourself again by touching the wart and then another part of your body. You can infect another person by sharing towels, razors, or other personal items. After contact with HPV, it can take 2 to 9 months of slow growth beneath the skin before you notice a wart. It is unlikely that you will get a wart every time you come in contact with HPV. Some people are more likely to get warts than others.

Signs and Symptoms

Warts may occur singly or in multiples and often have multiple small black “dots” at the surface from tiny blood vessels. Types of warts are as listed below :

Picture Type Description
Common warts Usually found on fingers, hands, knees, and elbows, a common wart is a small (1-10mm in size)  , hard bump that’s dome-shaped and usually grayish-brown. It has a rough surface that may look like the head of a cauliflower, with black dots inside.
Plantar warts grow on the soles of the feet. They look like hard, thick patches of skin with dark specks. Plantar warts may cause pain when you walk, and you may feel like you are stepping on a pebble. Since they are painful, they are often thought to be corns.
Flat warts usually grow on the face, arms, or legs. They are small (1-5mm), have flat tops, and can be pink, light brown, or light yellow. They can also grow on arms, knees, or hands and can appear in clusters.
Filiform warts Usually long and narrow, like tufts of thread, grow around the mouth, nose, or beard area. They are the same color as your skin and have the size between 1-3mm.
Periungual warts grow under and around the toenails and fingernails. They look like rough bumps with an uneven surface and border. They can affect nail growth.

Wart infection can be described as:

  • Mild – just one or a few painless lesions
  • Moderate – 10–20 lesions that are painless
  • Severe – pain that limits normal life activities, bleeding, or over 20 lesions, except for flat warts, which can be numerous, yet not bothersome

How are warts treated?

First of all, it’s important to know that warts on the skin (such as on the fingers, feet and knees) and warts on the genitals are removed in different ways. Don’t try any home remedies or over-the-counter drugs to remove warts on the genital area. You could hurt your genital area by putting certain chemicals on it. You also shouldn’t treat warts on your face without talking to your doctor first.

In children, warts can disappear without treatment over a period of several months to years. However, warts that are bothersome, painful, or rapidly multiplying should be treated. Warts in adults often do not disappear as easily or as quickly as they do in children.

The following are some ways to remove common warts from the skin:

  • Applying salicylic acid. You can treat warts on places such as the hands, feet or knees by putting salicylic acid on the warts. To get good results, you must apply the acid every day for many weeks. After you take a bath or shower, pat your skin dry lightly with a towel. Then put salicylic acid on your warts. The acid sinks in deeper and works better when it is applied to damp skin. Before you take a shower or a bath the next day, use an emery board or pumice stone to file away the dead surface of the warts.
  • Applying cantharidin. Your doctor may use cantharidin on your warts. With this treatment, the doctor “paints” the chemical onto the wart. Most people don’t feel any pain when the chemical is applied to the wart. You’ll experience some pain and blistering of the wart in about 3 to 8 hours. After treatment with cantharidin, a bandage is put over the wart. The bandage can be removed after 24 hours. When mixtures of cantharidin and other chemicals are used, the bandage is removed after 2 hours. When you see your doctor again, he or she will remove the dead skin of the wart. If the wart isn’t gone after one treatment, your doctor may suggest another treatment.
  • Applying liquid nitrogen. Your doctor may use liquid nitrogen to freeze the wart. This treatment is called cryotherapy. Applying liquid nitrogen to the wart causes a little discomfort. To completely remove a wart, liquid nitrogen treatments may be needed every 1 to 3 weeks for a total of 2 to 4 times. If no improvement is noted, your doctor may recommend another type of treatment.
  • Immunotherapy, which attempts to use the body’s own rejection system is another method of treatment. Several methods of immunotherapy are being used. With one method the patient is made allergic to a certain chemical which is then painted on the wart. A mild allergic reaction occurs around the treated warts, and may result in the disappearance of the warts.
  • Warts may also be injected with interferon, a treatment to boost the immune reaction and cause rejection of the wart.
  • Another treatment is to inject each wart with an anti-cancer drug called bleomycin. The injections may be painful and can have other side effects.
  • Other treatments for warts on the skin. Your doctor can also remove warts on the skin by burning the wart, cutting out the wart or removing the wart with a laser. These treatments are effective, but they may leave a scar. They are normally reserved for warts that have not cleared up with other treatments.

Talk to your doctor about which treatment is right for you.

When to Seek Medical Care

  • Painful or bleeding warts.
  • Warts on the face and those interfering with daily life that do not respond to self-care measures.
  • Diabetics with warts of the feet should be treated by a physician.

At home treatment for warts

1.  Banana peel

How it works? Loads of pottasium in the banana peel. How to use ? Rub the inside of a little piece of a banana peel on a wart every night. You should see results within one to two weeks.

2.  Apple cider vinegar

How to use? Soak a tiny bit of cotton ball in the apple cider vinegar and place it on the warts. Cover it with a bandaid. Keep it like that until the wart is gone. Just change the bandaid and cotton ball each day or each time it falls off.

3.   Duct tape -> Simply put the duct tape around the warts. Change the tape each day When it falls off.

4.   Vinegar->  Take the tip off a Q-tip and soak it in the vinegar. Put it on the wart and secure it with a bandaid. Leave it on till the wart is gone.

5.   Garlic-> Slice off a piece of garlic and put over your wart. Cover with Bandaid overnight and in the morning take the bandaid off.

6.   Castor oil->  This remedy is not only for warts but for any skin growth that is raised from the skin,even moles. Mix some castor oil and baking soda till it’s like a paste. Put some of the paste onto the wart, mole or other growth you have. do it daily. You should cover it with a bandaid when you have applied it. Within a couple of week it’ll start to go red, swell and get a bit sore, but keep adding the paste each day till it’s gone.

7.   Dandelion->  Pick a dandelion and squeeze the white milky liquid from the stem and put it onto your warts. Do it until they disappear.

8.   Vitamin C -> Take one vitamin C tablets and crush it between two spoons. Put the crushed tablet on your wart and cover with a bandaid. Do this each time you have a shower so you always have a clean bandaid on the warts.

9.    Aloe Vera->  Apply the aloe vera gel to your warts every morning and evening.

10.    Orange peel->   A few times each day, rub orange peel onto the wart or cut a small piece of peel and place directly onto the wart. If using a piece make sure to cover it using a bandaid. The wart will eventually change color and fall off.

Reference :

1. http://www.skinsight.com/adult/commonWart.htm

2. http://www.naturesnaturalhealing.com/

3. http://familydoctor.org/online/famdocen/home/common/skin/disorders/209.html

4. http://www.earthclinic.com/Remedies/bananapeel.html

5. http://www.offthemark.com/search-results/key/warts

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Dec 06

Demam denggi..Apa yang anda patut tahu.

By taqidoc Medicine Comments Off

Apa itu demam denggi?

df28872-eDenggi ialah sejenis penyakit akut yang menyebabkan sakit kepala, demam, keletihan, sakit sendi dan otot, kalenjar membengkak dan juga ruam. Triad denggi iaitu demam, ruam dan sakit kepala dan17148 sakit sendi merupakan ciri utama demam denggi. Penyakit ini disebabkan oleh 4 jenis virus denggi( DENV 1,  DENV 2, DENV 3 atau DENV 4 ) . Oleh kerana denggi disebabkan oleh 4 jenis serotype,maka seseorang individu boleh mengidap denggi beberapa kali.Setiap kali serangan denggi akan menghasilkan imuniti semumur hidup terhadap serotype tersebut. Virus-virus ini menjangkiti manusia melalui gigitan nyamuk yang telah dijangkiti. Di Hemisfera Barat, nyamuk Aedes aegypti merupakan vector yang utama menyebarkan virus denggi. Walau bagaimanapun, kes denggi di Hawaii pada tahun 2001 adalah berbeza kerana ia disebabkan oleh nyamuk Aedes albopictus. Continue reading »

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Nov 28

Are you aware of cholera(taun) outbreak??

By taqidoc Medicine Comments Off

What is cholera?

Cholera is an acute intestinal infection caused by ingestion of food or waterimage018 contaminated with the bacterium Vibrio cholerae. It has a short incubation period and produces an enterotoxin that causes a copious, painless, watery diarrhoea that can quickly lead to severe dehydration and death if treatment is not promptly given.

Most of the cases are asymptomatic although the bacterium is still present in their feces for 7-14 days.

When illness does occur, about 80-90% of episodes are of mild or moderate severity and are difficult to distinguish clinically from other types of acute diarrhoea. Less than 20% of ill persons develop typical cholera with signs of moderate or severe dehydration.

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