Penatalaksanaan menurut Wijanarko, (2021) secara umum yaitu : 1.

Pertahankan
kebersihan yang baik termasuk mandi setiap hari, perawatan kulit yang cermat, dan
pemangkasan kuku. 2. Pengobatan topikal dapat menggunakan bedak untuk mencegah
pecahnya vesikel terlalu dini, dapat ditambahkan zat anti gatal (menthol, kamper). 3.
Antibiotik topikal dapat digunakan jika ada infeksi sekunder. 4. Pengobatan sistemik
berupa antivirus analog nukleosida (guanosin analog), yaitu asiklovir dan pensiklovir.
Valasiklovir (ester valin dari asiklovir) dan famsiklovir (prodrug pensiclovir) diserap
lebih baik dan dalam tingkat darah yang lebih tinggi, sehingga lebih disukai dalam
pengobatan varisela daripada asiklovir. Pemberian terapi dalam waktu 24 jam dari onset
mengurangi waktu pengerasan kulit, keparahan penyakit, durasi gejala dan demam. Dosis
yang dapat diberikan pada remaja (≥ 40 kg) dan orang dewasa adalah valasiklovir 1 g per
oral (PO) setiap 8 jam selama 7 hari, atau famsiklovir 500 mg po setiap 8 jam selama 7
hari, atau asiklovir 800 mg po 5 kali/ hari. selama 7 hari. 5. Lini kedua adalah foscarnet
(analog dari pirofosfat) terutama untuk kasus VVZ yang tahan nukleosida. Baris ketiga
adalah cidofovir. Pada kasus dengan 14 komplikasi pneumonia, asiklovir (dalam 36 jam
rawat inap) dapat diberikan 10- 15 mg/kgBB secara intravena (iv) setiap 8 jam selama 7-
10 hari serta bantuan pernapasan. Komplikasi lain seperti ensefalitis, meningoensefalitis,
mielitis, dan komplikasi okular juga diobati dengan asiklovir IV. 6. Sedangkan terapi
simtomatik dapat berupa analgesik antipiretik dan antihistamin (dengan efek sedatif atau
sedatif) untuk pruritus. Antibiotik oral dapat diberikan jika ada infeksi sekunder.(Devi et
al., 2022)

Wijanarko, M. S. P. (2021). Varisela pada Dewasa, Kehamilan, dan Kondisi 71

Imunokompromais. Jurnal Kedokteran Meditek, 27(1), 81–87.
https://doi.org/10.36452/jkdoktmeditek.v27i1.1938
 (Kasus, 2016)

Devi, M., Ismunandar, H., & Wintoko, R. (2022). Exsa Hadibrata, Anisa Nuraisa Djausal|
Penegakan Diagnosis dan Penatalaksanaan. Herpes Zoster Medula |, 12(April), 40.
Kasus, L. (2016). Varisela hemoragik pada anak dengan idiophatic thrombocytopenic purpura.
0–18.
Sellheyer and coworkers showed that the ventral proximal fold in human nails expresses hair follicle
stem cell (hfSC) markers (eg, K15; keratin 19 [K19]; and pleckstrin homologylike domain, family A,
member 1 protein [PHLDA1]. during embryogenesis and contains very few Ki67+ cells (a nuclear
protein associated with cell proliferation), making them more quiescent similar to hfSCs,
suggesting that the proximal fold may represent the human NSC niche.

BMP signaling guides NPFSCs toward nail differentiation, and without this pathway, matrix cells
proliferate less, and a KZ is not observed above the matrix region (see Fig. 8-5).24 Also, proper nail
plate differentiation is compromised, and without BMP signaling, the nail adopts an epidermal fate
in vivo (see Fig. 8-5). It manifests the extension of the skin epidermis granular layer throughout the
nail with typical epidermal markers such as keratin 1 (K1) and loricrin expression observed in the
nail plate (see Fig. 8-5). In contrast, typical differentiation nail plate marker AE13 (keratin
expressed in both the hair cortex and nail plate) was undetectable (see Fig. 8-5).24 Interestingly, a
similar role of BMP signaling was observed in proper hair follicle differentiation.25 This observation
was also consistent, and the phenotype was even more severe than a phenotype of the Msx2 and
Foxn1 double mutant; both genes previously have been showed as downstream targets of BMP
signaling regulating normal nail differentiation.26 It was also similar to Foxn1 and Hoxc13 single
mutants, with aberrant extension of the epidermal stratum granulosum within the nail structure
(see Fig. 8-5).2,27 In addition, the role of BMP signaling is also required for maintenance of the LRC
characteristic of NPFSCs.

Taken together, a novel population of bifunctional stem cells within the NPF region displays plastic
homeostatic dynamics capable of responding to injury and suggests a common, coordinated
mechanism of protective barrier formation that could occur between the nail and adjacent
epidermis.

The nail matrix is a morphological continuation of the NPF cells that attach to each other through the IZ
wrapping around the proximal end of the nail plate (see Fig. 8-4). Thus, proliferating matrix
progenitor cells are found in the near vicinity of the NPF region and differentiate into cells of the KZ
to form the external nail plate.

BMP signaling guides NPFSCs toward nail differentiation, and without this pathway, matrix cells
proliferate less, and a KZ is not observed above the matrix region (see Fig. 8-5).24 Also, proper nail
plate differentiation is compromised, and without BMP signaling, the nail adopts an epidermal fate
in vivo (see Fig. 8-5). It manifests the extension of the skin epidermis granular layer throughout the
nail with typical epidermal markers such as keratin 1 (K1) and loricrin expression observed in the
nail plate (see Fig. 8-5). In contrast, typical differentiation nail plate marker AE13 (keratin
expressed in both the hair cortex and nail plate) was undetectable (see Fig. 8-5).24 Interestingly, a
similar role of BMP signaling was observed in proper hair follicle differentiation.25 This observation
was also consistent, and the phenotype was even more severe than a phenotype of the Msx2 and
Foxn1 double mutant; both genes previously have been showed as downstream targets of BMP
signaling regulating normal nail differentiation.26 It was also similar to Foxn1 and Hoxc13 single
mutants, with aberrant extension of the epidermal stratum granulosum within the nail structure
(see Fig. 8-5).2,27 In addition, the role of BMP signaling is also required for maintenance of the LRC
characteristic of NPFSCs.