Letter to Professor Gubler (The Father of Wild Viral Infection Theory)

Dear Professor Gubler

I think it's time for you to leave your wild virology theory as the basic of DHF. While virology theory cannot answer why DHF mostly attacking South East Asia and West Pacific people not the American even though the American live in South East Asia and in West Pacific which filled with plenty of Aedes Aegeypti mosquito. I have watched it happened directly when I was working in Caltex company in Riau, Indonesia in 1998 and on that year there was an endemic attack in Indonesia. Or wild virulogy theory couldn't answer why a man can getting the light or not serious clinical symptoms although he got infection by the wild dengue virus or so did the opposite. A wild virulogy theory are extremly rare in the later age especially after 60 years old. And the wild virulogy virus couldn't told us why DHF clinical symptoms that happened in the well nutrition patient is more serious (endanger) rather than patient with worst nutrition. Moreover in my resarch patients that given corticosteroit imunosupressif dose with the strongest corcticosteroit (methyl prednisolon) got a not serious clinical symptom more than patient without corticosteroid.
Click www.dhf-revolution.blogspot.com afankelijkheid cirebon, in that blog I have said that the basic of pathophysiology and pathogenesis DHF is hipersensitivity type III reaction (because it has been clearly proven antigen antibody complex in all over human body system), with variation there is an autoimune reaction that has discovered platelet antibody in some patient. So, sensitivity each individual has take part more than wild virulogy virus in pathogenesis DHF. We must pay more attention to viral dengue for it's ability to change it's genetic strucure so dengue virus when in the first time is not sensitive to individual and after that it will be sensitive. Or with some reason the sensitivity of individual was change and then he will be vulnurable to viral dengue. Maybe this is the reason why the American, European and the Australian that is in the first time is not sensitive became sensitive. Moreover until now there is a lot of cases on the American and Australian that got DHF without having dengue infection repeatedly (IgM positive). I believe this is the reason which is causing the epidemic in Cuba or India or maybe in the bigger part of the world in the future (World DHF Attack).
At last Professor Gubler have you researching about long term thrombositopenia (ITP) maybe in whole life of the patient which is happened in some patient with the history of Dengue Hemorrhagic Fever (IgM or IgG positive) ? And nowdays the trend of ITP is increasing in Indonesia I think if we give methylpretnisolon high dose on the first attack in Dengue Hemorrhagic Fever the accident of ITP is decrease or never happened for the patient after DHF disease.

I'm waiting your answer in my blog Mr. Gubler

Letter to Father of Secondary Heterologus Infection Theory

Honorable Professor Halstead

What is your opinion if I said to you genetic or increasing human leucocyte antigen have identical with individual sensitivity or not in viral dengue. In patients which have sensitivity to viral dengue the clinical symptoms become more serious or severe even though the viral is not wild. In the other hand, even the viral is wild but the individual is not sensitive clinical symptom to the patient wiil be light or not severe. I have prove that in my research (click dhf-revolution.blogspot.com afankelijkheid cirebon). I have said about the basic of pathophysiology and pathogenesis of DHF is hipersensitivity type III (it has been clearly proven antigen antibody complex in most of human body system) with variation there is an autoimune reaction with discovered platelet antibody in some patient. High dose (immunosupresif dose) with the strongest corticosteroid (methyl pretnisolon) to DHF patient whose fever less than 5 days gave the satisfying result.

I'm waiting for your comment in my blog. Thank you very much.

RINGKASAN PENELITIAN PERAN SUMSUM TULANG DAN ANTIBODI TROMBOSIT PADA PENDERITA DBD DEWASA DENGAN TROMBOSITOPENIA

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Table 2. Hasil Pemeriksaan Sumsum Tulang



Table 3. Hasil Pemeriksaan Darah Tepi



Table 4. Hasil Pemeriksaan Fisik, Antibodi Trombosid, D-Dimer, isolasi virus dan pemberian steroid




Tabel 5. Lama Trombositopenia pada kelompok demam / sakit 2-4 hari dan kelompok demam/sakit 5-d 7 hari.



LT = Lama Trombositopenia, AbTr = Antibodi Trombosit, str = Steroid

LT of 27 patients

1. Rata-rata
2. AbTr (+), Str (+)
3. AbTr (-), Str (-)
4. Abtr (-), Str (+)
5. AbTr (+), Str (-)

2-4 day fever group

6. Rata-rata
7. AbTr (+), Str (+)
8. Abtr (-), Str (-)
9. Abtr (-), Str (+)
10. Abtr (+), Str (-)

5-7 day fever group

11. Rata-rata
12. AbTr (+), Str (+)
13. Abtr (-), Str (-)
14. Abtr (-), Str (+)
15. Abtr (+), Str (-)


IV. KESIMPULAN
1. Proses perifer adalah penyebab utama trombositopenia pada semua fase DBD.
2. Urutan kekuatan pengaruh DBD <5 hari antibody trombosit, DIC tak terkompensasi perdarahan, penekanan sumsum tulang.
3. Urutan kekuatan pengaruh DBD ≥5 hari adalah aktivitas RES, DIC tak terkompensasi, antibody trombosit.
4. Steroid dosis imunosupresif pada DBD <5 hari, mempercepat normalnya trombosit.
5. Steroid dosis imunosupresif pada DBD ≥5 hari hanya mencegah penurunan tajam dari jumlah trombosit.
6. Reaksi hipersensitivitas tipe III perlu dipertimbangkan sebagai dasar patofisiologi DBD.

KETERANGAN : Hasil itu semua didapatkan dengan analisa statistic yaitu Regresi multiple,uji Kai kuadrat, Risiko relatif berdasarkan Spss, WR 6.0