A Game-Changer for Diabetes: Polymer Delivers Insulin Painlessly Through Skin
November 25, 2025
Background
Herpes zoster is a painful viral infection caused due to varicella-zoster virus reactivation.Â
Symptoms start with pain in dermatome, that leads to vesicular eruption within days, with painful grouped herpetiform vesicles. Painful grouped herpetiform vesicles on red base.Â
Varicella-zoster virus reactivates from dorsal root ganglia decades after initial exposure to varicella.Â
It usually causes a rash and pain but can lead to serious complications like postherpetic neuralgia and economic burden.Â
Zoster commonly occurs due to immune system failure with latent VZV. Other triggers like radiation, trauma, meds, infections, and stress are uncertain.Â
Epidemiology
About 95% of U.S. adults and 99.5% of those >40 years old have antibodies to VZV.Â
Most individuals who had chickenpox can get shingles, especially as they get older and immunodeficiency.Â
Around 4% of patients experience later recurrences in immunosuppressed individuals. It is rare in children and young adults, common in those with AIDS, lymphoma, malignancies, immune deficiencies, or transplants.Â
About 50% of herpes zoster patients experience complications. Ophthalmic complications risk does not correlate with age, sex, or rash severity.Â
Anatomy
Pathophysiology
VZV infection causes chickenpox and shingles both distinct and contagious syndromes.Â
The host immune system suppresses viruses, Cutaneous rash from herpes zoster coincides with VZV-specific T-cells, followed but to interferon alfa production post-recovery. but VZV reactivates when containment fails.Â
Herpes zoster primarily affects dorsal root ganglia but can spread to CNS areas.Â
In very sick or immunocompromised patients, CNS involvement may present as meningoencephalitis or encephalitis.Â
Etiology
VZV infection causes herpes zoster, a disease from the Herpesviridae family with 70 encoded proteins.Â
Initial VZV infection in humans happens through contact with respiratory or conjunctiva mucosa.Â
VZV reactivation from dorsal root ganglia after initial varicella exposure causes herpes zoster.Â
Cellular immunity decline raises reactivation risk with age and immunocompromised individuals.Â
Genetics
Prognostic Factors
Good prognosis for younger, healthy patients, and higher risk for elderly complications.Â
Rarely fatal in healthy individuals, but it may be life-threatening for vulnerable patients.Â
Morbidity typically limited to varying levels of pain in dermatome.Â
Patients with lymphoproliferative malignancies have 5-15% mortality risk from disseminated herpes zoster.Â
Clinical History
Herpes zoster affects older adults in individuals more than age of 50 years old. Â
Physical Examination
Inspection for Rash and LesionsÂ
Neurological ExaminationÂ
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Red patches in affected area progress to clusters of blisters in 1-2 days. Severe acute neurotic pain accompanies rash, described as burning and stabbing, that impact patient’s quality of life.Â
Differential Diagnoses
Herpes Simplex Virus InfectionÂ
Dermatitis HerpetiformisÂ
ImpetigoÂ
Contact DermatitisÂ
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Treatment most effective for immunocompromised individuals and those >50 years old with severe or prolonged symptoms.Â
Transfer sick patients with advanced disease or compromised immunity to specialized care.Â
The topical treatments, including topical acyclovir cream, lidocaine, and capsaicin.Â
Acute herpes zoster causes pain that is usually the most severe symptom for patients.Â
Limited studies on specific treatments for acute zoster-associated pain despite established effectiveness for general neuropathic pain.Â
Consider nonpharmacologic therapies like nerve blocks and electrical stimulation for acute zoster pain.Â
Antiviral therapy shortens time for vesicle formation, crusting attainment, and acute discomfort during infection.Â
Antiviral treatment can stop the spread of acute herpes zoster in immunocompromised patients starting even after 72 hours.Â
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
use-of-a-non-pharmacological-approach-of-herpes-zoster
Lifestyle modification like intake of healthy nutritional supplements and proper hydration should be followed by patients.Â
Proper education and awareness about herpes zoster should be provided and its related causes, and how to stop it with management strategies.Â
Consistent using emollients maintains hydration to prevent cracking and apply sunscreen on skin.Â
Appointments with a dermatologist and preventing recurrence of disorder is an ongoing life-long effort.Â
Use of antivirals
Acyclovir:Â
It is a synthetic purine nucleoside analogue, that inhibits human herpes viruses including HSV-1, HSV-2, VZV, Epstein-Barr, and CMV.Â
Famciclovir:Â Â
It turns into penciclovir when consumed and activated by viral thymidine kinase.Â
Use of Corticosteroids
It requires metabolization to active prednisolone metabolite, potentially impaired in liver disease.Â
Use of Analgesics (Topical)
Capsaicin from Solanaceae plants is a TRPV1 agonist used for neuropathic pain like PHN.Â
Use of Analgesics
Oxycodone:Â Â
It is used for moderate to severe pain relief, common in patients with herpes zoster.Â
Ibuprofen:Â Â
It is a NSAID used for mild to moderate pain treatment when there are no contraindications.Â
Use of Anticonvulsants
Gabapentin:Â
It acts on α2δ1 and α2δ2 subunits of calcium channels to treat neuropathic pain and provide sedation.Â
Use of Antidepressants
It inhibits spinal neurons to reduce pain perception effectively.Â
intervention-with-a-procedure
Surgical care is not indicated, but it may be required to treat certain complications. E.g., necrotizing fasciitis Â
Rhizotomy is surgical separation of pain fibers that may be indicated in cases of intractable pain.Â
use-of-phases-in-managing-herpes-zoster
In acute phase, initiate antiviral therapy within 72 hours then manage pain and provide skin care to patient.Â
In chronic phase, focus should be on managing chronic pain for improving quality of life includes use of pharmacological and non-pharmacological therapies.Â
The regular follow-up visits with the dermatologist are schedule to check the improvement of patients along with treatment response.Â
Medication
Acute treatment: 800 mg taken orally five times a day (7–10) for four hours each time you're awake
patients with weakened immune systems:
Intravenous 10 mg/kg every 8 hours for 7 days
Use ideal body weight while treating obese individuals (IBW):
Full recommended IV dose every 12 hours (CrCl 25–50 mL/min)
CrCl 10–25 mL/min: Once daily, provide the entire prescribed IV dosage
CrCl 0–10 mL/min: 50% of the suggested daily IV dosage
Dose Adjustments
Renal dose adjustments
dose modification in accordance with standard dosage guidelines and renal clearance
200 milligrams every four hours:
200 mg every 12 hours; 0–10 mL/min/1.73 m²
More than 10 mL/min/1.73 m²: 200 mg five times a day every four hours
400 mg every 12 hours :
200 mg every 12 hours for 0–10 mL/min/1.73 m²
Exceeding 10 mL/min/1.73 m²: 400 mg per 12-hour period
800 mg every 4 hours :
0–10 mL/min/1.73 m²: 800 mg every 12 hours
800 mg every 8 hours at 10–25 mL/min/1.73 m²
More than 25 mL/min/1.73 m²: 800 mg five times a day every four hours
Changing the dosage according to the dosage form:
Renal impairment (IV)
Administer prescribed dose every 12 hours when CrCl is 25–50 mL/min/1.73 m²
10–25 mL/min/1.73 m² of CrCl: Administer the prescribed dosage once every 24 hours
Give 50% of the recommended dose every 24 hours if the CrCl is less than 10 mL/min/1.73 m²
Renal impairment (Oral)
When the CrCl is less than 10 mL/min/1.73 m², the normal dosage of 200 mg every 4 hours or 400 mg every 12 hours should be reduced to 200 mg every 12 hours
CrCl 10–25 mL/min/1.73 m² and the usual dosage of 800 mg every 4 hours: Reduce to 800 mg every 8 hours
If the CrCl is less than 10 mL/min/1.73 m², reduce the normal dosage to 800 mg every 12 hours
Take a dose of 1 gm orally every eight hours for seven days
Dosage Modifications
Herpes labialis
1 g orally every 12 hours for a day with creatine clearance 30-49 mL/min
Creatinine clearance 10-29 mL/min: 500 mg orally every twelve hours for one day
Creatinine clearance 10 mL/min: once-only 500 mg orally
Herpes zoster
1 g orally every 12 hours, creatinine clearance 30-49 mL/min
1 g/day of creatinine clearance at 10-29 mL/min orally
500 mg/day, orally for creatinine clearance 10 mL/min
Genital herpes (initial episode)
1 g/day orally for creatinine clearance 10-29 mL/min
Creatinine clearance 10 mL/min: 500 mg every day, orally every day
Genital herpes (recurrent episodes)
500 mg/day, orally for creatinine clearance 29 mL/min
500 mg orally every 8 hours for 7-10 days
Children:
Immunocompromised children under 12 years old: 20 mg/kg IV every 8 hours for 7 days
Use ideal body weight while treating obese individuals (IBW):
If immunocompetent and older than 12 years old, take 800 mg orally every 4 hours while awake, five times a day for seven to ten days
Elderly (immunocompromised) than 12 years old: 30 mg/kg/day IV given every 8 hours for a duration of 7–10 days
Future Trends
Herpes zoster is a painful viral infection caused due to varicella-zoster virus reactivation.Â
Symptoms start with pain in dermatome, that leads to vesicular eruption within days, with painful grouped herpetiform vesicles. Painful grouped herpetiform vesicles on red base.Â
Varicella-zoster virus reactivates from dorsal root ganglia decades after initial exposure to varicella.Â
It usually causes a rash and pain but can lead to serious complications like postherpetic neuralgia and economic burden.Â
Zoster commonly occurs due to immune system failure with latent VZV. Other triggers like radiation, trauma, meds, infections, and stress are uncertain.Â
About 95% of U.S. adults and 99.5% of those >40 years old have antibodies to VZV.Â
Most individuals who had chickenpox can get shingles, especially as they get older and immunodeficiency.Â
Around 4% of patients experience later recurrences in immunosuppressed individuals. It is rare in children and young adults, common in those with AIDS, lymphoma, malignancies, immune deficiencies, or transplants.Â
About 50% of herpes zoster patients experience complications. Ophthalmic complications risk does not correlate with age, sex, or rash severity.Â
VZV infection causes chickenpox and shingles both distinct and contagious syndromes.Â
The host immune system suppresses viruses, Cutaneous rash from herpes zoster coincides with VZV-specific T-cells, followed but to interferon alfa production post-recovery. but VZV reactivates when containment fails.Â
Herpes zoster primarily affects dorsal root ganglia but can spread to CNS areas.Â
In very sick or immunocompromised patients, CNS involvement may present as meningoencephalitis or encephalitis.Â
VZV infection causes herpes zoster, a disease from the Herpesviridae family with 70 encoded proteins.Â
Initial VZV infection in humans happens through contact with respiratory or conjunctiva mucosa.Â
VZV reactivation from dorsal root ganglia after initial varicella exposure causes herpes zoster.Â
Cellular immunity decline raises reactivation risk with age and immunocompromised individuals.Â
Good prognosis for younger, healthy patients, and higher risk for elderly complications.Â
Rarely fatal in healthy individuals, but it may be life-threatening for vulnerable patients.Â
Morbidity typically limited to varying levels of pain in dermatome.Â
Patients with lymphoproliferative malignancies have 5-15% mortality risk from disseminated herpes zoster.Â
Herpes zoster affects older adults in individuals more than age of 50 years old. Â
Inspection for Rash and LesionsÂ
Neurological ExaminationÂ
Red patches in affected area progress to clusters of blisters in 1-2 days. Severe acute neurotic pain accompanies rash, described as burning and stabbing, that impact patient’s quality of life.Â
Herpes Simplex Virus InfectionÂ
Dermatitis HerpetiformisÂ
ImpetigoÂ
Contact DermatitisÂ
Treatment most effective for immunocompromised individuals and those >50 years old with severe or prolonged symptoms.Â
Transfer sick patients with advanced disease or compromised immunity to specialized care.Â
The topical treatments, including topical acyclovir cream, lidocaine, and capsaicin.Â
Acute herpes zoster causes pain that is usually the most severe symptom for patients.Â
Limited studies on specific treatments for acute zoster-associated pain despite established effectiveness for general neuropathic pain.Â
Consider nonpharmacologic therapies like nerve blocks and electrical stimulation for acute zoster pain.Â
Antiviral therapy shortens time for vesicle formation, crusting attainment, and acute discomfort during infection.Â
Antiviral treatment can stop the spread of acute herpes zoster in immunocompromised patients starting even after 72 hours.Â
Dermatology, General
Lifestyle modification like intake of healthy nutritional supplements and proper hydration should be followed by patients.Â
Proper education and awareness about herpes zoster should be provided and its related causes, and how to stop it with management strategies.Â
Consistent using emollients maintains hydration to prevent cracking and apply sunscreen on skin.Â
Appointments with a dermatologist and preventing recurrence of disorder is an ongoing life-long effort.Â
Dermatology, General
Acyclovir:Â
It is a synthetic purine nucleoside analogue, that inhibits human herpes viruses including HSV-1, HSV-2, VZV, Epstein-Barr, and CMV.Â
Famciclovir:Â Â
It turns into penciclovir when consumed and activated by viral thymidine kinase.Â
Dermatology, General
It requires metabolization to active prednisolone metabolite, potentially impaired in liver disease.Â
Dermatology, General
Capsaicin from Solanaceae plants is a TRPV1 agonist used for neuropathic pain like PHN.Â
Dermatology, General
Oxycodone:Â Â
It is used for moderate to severe pain relief, common in patients with herpes zoster.Â
Ibuprofen:Â Â
It is a NSAID used for mild to moderate pain treatment when there are no contraindications.Â
Dermatology, General
Gabapentin:Â
It acts on α2δ1 and α2δ2 subunits of calcium channels to treat neuropathic pain and provide sedation.Â
Dermatology, General
It inhibits spinal neurons to reduce pain perception effectively.Â
Dermatology, General
Surgical care is not indicated, but it may be required to treat certain complications. E.g., necrotizing fasciitis Â
Rhizotomy is surgical separation of pain fibers that may be indicated in cases of intractable pain.Â
Dermatology, General
In acute phase, initiate antiviral therapy within 72 hours then manage pain and provide skin care to patient.Â
In chronic phase, focus should be on managing chronic pain for improving quality of life includes use of pharmacological and non-pharmacological therapies.Â
The regular follow-up visits with the dermatologist are schedule to check the improvement of patients along with treatment response.Â
Herpes zoster is a painful viral infection caused due to varicella-zoster virus reactivation.Â
Symptoms start with pain in dermatome, that leads to vesicular eruption within days, with painful grouped herpetiform vesicles. Painful grouped herpetiform vesicles on red base.Â
Varicella-zoster virus reactivates from dorsal root ganglia decades after initial exposure to varicella.Â
It usually causes a rash and pain but can lead to serious complications like postherpetic neuralgia and economic burden.Â
Zoster commonly occurs due to immune system failure with latent VZV. Other triggers like radiation, trauma, meds, infections, and stress are uncertain.Â
About 95% of U.S. adults and 99.5% of those >40 years old have antibodies to VZV.Â
Most individuals who had chickenpox can get shingles, especially as they get older and immunodeficiency.Â
Around 4% of patients experience later recurrences in immunosuppressed individuals. It is rare in children and young adults, common in those with AIDS, lymphoma, malignancies, immune deficiencies, or transplants.Â
About 50% of herpes zoster patients experience complications. Ophthalmic complications risk does not correlate with age, sex, or rash severity.Â
VZV infection causes chickenpox and shingles both distinct and contagious syndromes.Â
The host immune system suppresses viruses, Cutaneous rash from herpes zoster coincides with VZV-specific T-cells, followed but to interferon alfa production post-recovery. but VZV reactivates when containment fails.Â
Herpes zoster primarily affects dorsal root ganglia but can spread to CNS areas.Â
In very sick or immunocompromised patients, CNS involvement may present as meningoencephalitis or encephalitis.Â
VZV infection causes herpes zoster, a disease from the Herpesviridae family with 70 encoded proteins.Â
Initial VZV infection in humans happens through contact with respiratory or conjunctiva mucosa.Â
VZV reactivation from dorsal root ganglia after initial varicella exposure causes herpes zoster.Â
Cellular immunity decline raises reactivation risk with age and immunocompromised individuals.Â
Good prognosis for younger, healthy patients, and higher risk for elderly complications.Â
Rarely fatal in healthy individuals, but it may be life-threatening for vulnerable patients.Â
Morbidity typically limited to varying levels of pain in dermatome.Â
Patients with lymphoproliferative malignancies have 5-15% mortality risk from disseminated herpes zoster.Â
Herpes zoster affects older adults in individuals more than age of 50 years old. Â
Inspection for Rash and LesionsÂ
Neurological ExaminationÂ
Red patches in affected area progress to clusters of blisters in 1-2 days. Severe acute neurotic pain accompanies rash, described as burning and stabbing, that impact patient’s quality of life.Â
Herpes Simplex Virus InfectionÂ
Dermatitis HerpetiformisÂ
ImpetigoÂ
Contact DermatitisÂ
Treatment most effective for immunocompromised individuals and those >50 years old with severe or prolonged symptoms.Â
Transfer sick patients with advanced disease or compromised immunity to specialized care.Â
The topical treatments, including topical acyclovir cream, lidocaine, and capsaicin.Â
Acute herpes zoster causes pain that is usually the most severe symptom for patients.Â
Limited studies on specific treatments for acute zoster-associated pain despite established effectiveness for general neuropathic pain.Â
Consider nonpharmacologic therapies like nerve blocks and electrical stimulation for acute zoster pain.Â
Antiviral therapy shortens time for vesicle formation, crusting attainment, and acute discomfort during infection.Â
Antiviral treatment can stop the spread of acute herpes zoster in immunocompromised patients starting even after 72 hours.Â
Dermatology, General
Lifestyle modification like intake of healthy nutritional supplements and proper hydration should be followed by patients.Â
Proper education and awareness about herpes zoster should be provided and its related causes, and how to stop it with management strategies.Â
Consistent using emollients maintains hydration to prevent cracking and apply sunscreen on skin.Â
Appointments with a dermatologist and preventing recurrence of disorder is an ongoing life-long effort.Â
Dermatology, General
Acyclovir:Â
It is a synthetic purine nucleoside analogue, that inhibits human herpes viruses including HSV-1, HSV-2, VZV, Epstein-Barr, and CMV.Â
Famciclovir:Â Â
It turns into penciclovir when consumed and activated by viral thymidine kinase.Â
Dermatology, General
It requires metabolization to active prednisolone metabolite, potentially impaired in liver disease.Â
Dermatology, General
Capsaicin from Solanaceae plants is a TRPV1 agonist used for neuropathic pain like PHN.Â
Dermatology, General
Oxycodone:Â Â
It is used for moderate to severe pain relief, common in patients with herpes zoster.Â
Ibuprofen:Â Â
It is a NSAID used for mild to moderate pain treatment when there are no contraindications.Â
Dermatology, General
Gabapentin:Â
It acts on α2δ1 and α2δ2 subunits of calcium channels to treat neuropathic pain and provide sedation.Â
Dermatology, General
It inhibits spinal neurons to reduce pain perception effectively.Â
Dermatology, General
Surgical care is not indicated, but it may be required to treat certain complications. E.g., necrotizing fasciitis Â
Rhizotomy is surgical separation of pain fibers that may be indicated in cases of intractable pain.Â
Dermatology, General
In acute phase, initiate antiviral therapy within 72 hours then manage pain and provide skin care to patient.Â
In chronic phase, focus should be on managing chronic pain for improving quality of life includes use of pharmacological and non-pharmacological therapies.Â
The regular follow-up visits with the dermatologist are schedule to check the improvement of patients along with treatment response.Â

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