Successful Hair
Restoration: A Case Report on Hair Transplant Part-I
Efficacy of Purified Protein
Derivative (PPD) in the Treatment of Genital Wart: A Case Presentation
Acrodermatitis
Enteropathica Rare
Hereditary Disorder: A Case Report
MOISTURIZER
A HEALTHY SKIN BARRIER
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Published for the period of August -2024
Seasonal Hair Loss
Seasonal hair loss is a natural phenomenon that affects many individuals. Hair loss can be influenced by various environmental factors, including changes in weather. Several factors contribute to this seasonal change, including variations in daylight hours, changes in temperature, and even shifts in hormonal levels. Maintaining a balanced diet, reducing stress, and using gentle hair care practices can help mitigate the effects of seasonal shedding.
During the rainy season, many individuals experience an increase in hair shedding. This phenomenon is often attributed to several key factors like humidity, sweat and moisture, hair care practices, nutritional changes, maintain scalp hygiene and use of gentle hair care products. High humidity levels can make the scalp more susceptible to fungal infections, which can weaken hair roots and lead to increased shedding. Prolonged exposure to moisture can make the scalp a breeding ground for bacteria and fungi, causing scalp issues like dandruff and itching, which in turn can contribute to hair loss.
If significant or prolonged hair loss, consulting a healthcare professional or dermatologist is advisable to rule out underlying conditions. We hope this information provides reassurance and practical advice for those navigating the natural ebb and flow of hair growth throughout the year.
In this issue, we have articles on hair transplant, purified protein derivative (PPD) in the treatment of genital wart and acrodermatitis enteropathica a rare hereditary disorder etc.
HOPE YOU HAVE A GREAT READ
Thanks & Cheers
- Dom Daniel
Executive Editor & Publisher
Successful Hair Restoration: A Case Report on Hair Transplant Part-I
Dr. Avinash Agrawal, MS (General Surgery)
Acrodermatitis Enteropathica Rare Hereditary Disorder: A Case Report
Dr. Sudarshan Pramod Gaurkar, MBBS, MD (Dermatology)
Dr. Aman Hooda, Senior Resident
Efficacy of Purified Protein Derivative (PPD) in the Treatment of Genital Wart: A Case Presentation
Dr. Dhavalkumar Shivram Bansode, MD (Dermatology)
Editorial Board
Dr. Avinash Agrawal
MS (General Surgery)
Hair Transplant Surgeon Director, Acube Aesthetics Clinic, Mumbai
Dr. Sudarshan Pramod Gaurkar
MBBS, MD (Dermatology)
Consulting Dermatologist Associate Professor, GMC Miraj, Maharashtra
Dr. Dhavalkumar Shivram Bansode
MD (Dermatology)
Assistant Professor Department of Skin and VD Ashwini Rural Medical College Solapur, Maharashtra
Dr. Aman Hooda
Senior Resident Department of Dermatology, GMC Miraj, Maharashtra
Advisory Board
DR. ABHISHEK RAMESH
DR. VENKATESH VINAYAK
DR. MANJUNATH HULMANI
DR. ARCHANA GULUR
DR. ARUN KUMAR
DR. ABDUL SAMAD
DR. DASARI SRINIVAS
DR. GURUPRASAD
DR. PRAVITA KANUNGO
DR. VINYASHREE MENE
DR. DINESH KAMATH
DR. SHYAM RAJ RAO
DR. ROOPASHREE M.
DR. KVT GOPAL
DR. NEETU CHOUDHARY
DR. P.RAMBABU
Successful Hair Restoration: A Case Report on Hair Transplant Part-I
Dr.
Avinash Agrawal
MS (General Surgery)
Hair Transplant Surgeon Director, Acube Aesthetics Clinic, Mumbai
Introduction
Hair loss, medically termed alopecia, is a widespread concern affecting millions worldwide, with androgenic alopecia (AGA), or patterned hair loss, being the most prevalent form. This condition manifests differently between genders, known as male pattern hair loss (MPHL) and female pattern hair loss (FPHL), respectively affecting approximately 67% of males and 24% of females. AGA involves the progressive miniaturization of hair follicles in genetically predisposed areas of the scalp, leading to visible thinning and loss of hair.1
Hair loss, or alopecia, presents with diverse clinical features depending on its underlying cause. Androgenetic alopecia, the most common form affecting both genders, manifests in males with initial hairline recession at the temples followed by crown thinning, resulting in a horseshoeshaped pattern of hair loss. Females typically experience diffuse thinning over the crown with preservation of the
frontal hairline. Progression is gradual over years due to genetic predisposition and hormonal influences, notably androgens. Scalp examination often reveals miniaturization of hair follicles, where hair become thinner and shorter. Alopecia areata, an autoimmune condition, is characterized by sudden onset of patchy hair loss that can resolve spontaneously but may recur unpredictably. Examination may show "exclamation mark" hair indicative of active disease. Telogen effluvium presents with diffuse shedding, usually triggered by physiological stressors like childbirth or illness, evident on scalp examination with increased telogen hair. Scarring alopecia results from irreversible damage and inflammation of hair follicles, seen with signs like erythema and follicular plugging, potentially confirmed by scalp biopsy showing scar tissue replacement of follicles. Other causes include trichotillomania, nutritional deficiencies, and
medication side effects. Accurate diagnosis involves comprehensive evaluation through history-taking, scalp examination, and occasionally diagnostic tests, guiding tailored management strategies to halt progression, promote regrowth, and address underlying conditions contributing to hair loss.2
Diagnosis of alopecia typically relies on clinical evaluation, including the recognition of characteristic patterns of hair loss, follicle miniaturization, and the absence of scalp inflammation. The Norwood classification system for males and the Ludwig classification for females are commonly used to categorize the extent and severity of hair loss, aiding in treatment planning and prognostication. While non-surgical treatments remain essential in managing hair loss, hair transplantation stands as a definitive solution for individuals seeking longterm restoration of hair density and appearance. As technologies and techniques continue to advance, the field of hair restoration offers hope and confidence to those affected by alopecia, improving both aesthetic outcomes and quality of life.2
Alopecia not only impacts physical appearance but also diminishes self-esteem and may lead to social withdrawal.
Fortunately, several nonsurgical treatments have emerged to manage hair loss effectively. These include minoxidil, finasteride, dutasteride, low-level laser light therapy, platelet-rich
plasma (PRP), adenosine, and ketoconazole. These treatments aim to slow down hair loss and stimulate new hair growth by various mechanisms, such as enhancing blood circulation to the scalp or inhibiting the hormone responsible for hair follicle miniaturization.2
Despite advancements in non-surgical treatments, many individuals with advanced or stable AGA seek more permanent solutions. This demand has led to the evolution of hair transplantation as a preferred surgical method for hair restoration. Hair transplantation involves the meticulous relocation of androgen-resistant hair follicles from the donor-rich occipital region to balding or thinning areas on the scalp. This procedure not only restores a natural hairline but also provides large coverage in areas affected by alopecia.1, 3
Hair transplantation serves as a powerful tool in restoring a more youthful appearance for individuals affected by AGA, reconstructing facial hair lost due to trauma or burns, and aiding in hair placement for transgender patients. Proper patient evaluation and meticulous execution of a comprehensive treatment plan are crucial in achieving safe, reliable, and satisfactory outcomes in hair transplantation procedures. Case report- 1
A 33-year-old female presented with male pattern hair thinning and opted for a full head shave in hopes
of improving hair density, a myth that did not yield results. Seeking effective solutions, she embarked on a comprehensive treatment plan tailored to address her specific needs. This included initiating hair cyclical therapy to enhance hair health through nutritional support, starting oral minoxidil at 2.5 mg daily to stimulate hair follicles, and regularly applying a serum containing redensyl, capixyl, and procapil to promote hair growth and improve follicle health. Concurrently, she underwent a meticulous hairline redesign procedure involving the transplantation of 1800 grafts, carefully crafted to complement her natural facial features. Following treatment, significant improvements were observed in hair density. Her hair noticeably thickened, indicating successful stimulation of hair follicles, while the redesigned hairline harmoniously blended with her facial proportions, achieving a natural and satisfying aesthetic enhancement.
Figure 1: Full shaved head due to male pattern thinning
2: Pre hair transplantMeticulous hair line design
Case report 2
A 26-year-old male presented with Norwood grade 4 male pattern hair loss, underwent a comprehensive treatment plan to address his concerns about hair thinning and achieve a more natural hairline. Patient opted for surgical intervention with a hair transplant procedure involving approximately which is meticulously placed grafts to redefine his hairline. At the seven-month follow-up, significant improvements in hair density were noted in the treated areas, particularly along the newly established
hairline. The result achieved a natural appearance that harmonized well with patient facial features, fulfilling his aesthetic goals.
Diagnosis
A proper clinical history is essential in evaluating hair loss and distinguishing conditions like telogen effluvium. Patients typically report chronic hair thinning over frontal, parietal, or vertex areas, often accompanied by itching and trichodynia. It's crucial to inquire about
systemic diseases, recent medications (especially within the past year), family history of androgenetic alopecia (AGA), and dietary habits to rule out nutrition-related effluvium. Lifestyle factors such as traction, smoking, and ultraviolet exposure can exacerbate alopecia. In female patients, assessing hormonal dysfunction is particularly important. During general scalp and hair examination, hair loss usually presents with a normal scalp, although aggravating factors like seborrheic dermatitis and photodamage should be noted. The primary goal is to identify any patterned hair loss.4
The "pull test" is a straightforward method for assessing hair loss severity. Approximately 60 hair are gently pulled; a negative test (six or fewer hair obtained) indicates normal shedding, while a positive test (more than six hair obtained) suggests active shedding, possibly indicating telogen effluvium. For accurate results, patients should refrain from shampooing for 24 hours before the test. The diagnosis of Norwood classification hair loss involves categorizing male pattern baldness based on distinct stages of hairline recession and vertex thinning. Beginning with Stage 1, characterized by minimal to no hairline recession, the classification progresses through stages of increasing severity. Stage 2 exhibits mild frontal recession, Stage 3 includes further hairline
Figure
Figure 3 : Post hair transplant of 1800 grafts
Figure 4 : Pre hair transplant (Temporal and frontal hair loss)
Figure 5 : Post hair transplant (After 7 months)
recession and initial vertex thinning, and Stage 3 Vertex features noticeable vertex hair loss. By Stage 4, there is significant hair loss on both the frontal and vertex regions, often separated by a bridge of hair. Stages 5 to 7 depict progressively more extensive balding, with Stage 7 being the most severe, showing only a horseshoe-shaped fringe of hair remaining. This standardized classification aids in diagnosing male pattern hair loss, guiding treatment decisions, and assessing response to interventions over time.4
During the physical examination, inspect the scalp for signs of inflammation, scarring, or scaling, which may indicate underlying dermatological conditions contributing to hair loss. Perform a hair pull test to assess for excessive shedding, systematically pulling on several handfuls of hair to gauge the extent of hair loss. Evaluate hair density and distribution across the scalp to identify areas of reduced hair volume or thinning. Using a magnifying tool, examine hair shafts for signs of miniaturization, a hallmark of androgenic alopecia where hair becomes finer and shorter over time.4
Trichograms involve plucking 60-80 hair after a five-day period without hair washing. The roots of these hair are examined immediately to evaluate parameters such as hair follicle density, proportion of anagen fibers, and hair shaft diameter in a defined area.4
Phototrichograms (PTG) are non-invasive methods that utilize close-up photographs of specific areas to assess hair growth rate, follicle density, and shaft thickness. Techniques like contrastenhanced PTG and automated PTG (Trichoscan) enhance accuracy and efficiency by capturing detailed images for analysis. Trimming hair over the selected area is essential for accurate measurement.4
Hair wash test, developed by Rebora et al., distinguishes between AGA and telogen effluvium (TE) based on the count of vellus and terminal telogen hair washed out after a five-day period of abstaining from washing and shampooing. This method, however, has drawbacks such as potential hair breakage leading to inaccurate counts, limitations in curly hair types, and being time-consuming.5
Laboratory investigations are generally not required for diagnosing alopecia in males, except possibly testing for Prostate Specific Antigen before initiating finasteride in men over 45. In women, the focus of laboratory tests is to rule out hormonal disorders like polycystic ovarian syndrome. Recommended tests include free androgen index, Dehydroepiandrosterone (DHEAS), and prolactin levels. Additional tests may be necessary to exclude rarer conditions such as congenital adrenal hyperplasia. The role of measuring serum ferritin levels in AGA remains unclear due to conflicting study
results.4
Scalp biopsy plays a limited but crucial role in the treatment of hair loss, particularly in cases where the diagnosis is unclear or when differentiating between various types of alopecia is necessary. This invasive procedure involves the extraction of tissue samples from the scalp's affected areas, which are then examined microscopically. Biopsy findings can reveal important information such as the ratio of terminal to vellus hair, follicular density, and the presence of inflammation or fibrosis, aiding in the accurate diagnosis of conditions like androgenetic alopecia, alopecia areata, and cicatricial alopecia. While scalp biopsy is not routinely recommended for every case of hair loss, its judicious use under appropriate clinical circumstances can provide valuable insights that guide targeted treatment strategies, ultimately improving outcomes for patients. Normally, the ratio of terminal to vellus hair is greater than 7:1, whereas in AGA, it tends to be less than 3:1. Additional findings in AGA biopsies may include increased follicular stelae, an elevated telogen to anagen ratio, and minimal perifollicular lymphohistiocytic infiltrate, sometimes with mild fibrosis around the upper follicle.4
Global photography of a patient's scalp with hair loss serves as a valuable tool for monitoring treatment response and follow-up evaluations. This method
requires a cooperative patient with clean, dry hair, and careful preparation of the hair by a skilled technician, maintaining consistency in style and color across visits. Multiple standardized images are taken, covering specific views such as vertex, midpattern, frontal, and temporal areas. Standardization of image magnification, position, and lighting is crucial for accurate evaluation, often achieved using stereotactic imaging apparatuses. Global photography is widely regarded as the most effective method for comprehensive assessment of hair growth and treatment outcomes.4
Accurate diagnosis of hair loss is pivotal in guiding effective management strategies. Through detailed clinical evaluation, diagnostic tests such as trichoscopy, and occasionally scalp biopsies where necessary, healthcare professionals can identify the underlying causes and tailor treatment plans accordingly. This holistic approach not only addresses the symptoms but also aims to improve overall scalp health and quality of life for individuals experiencing hair loss.
References
1. Qi J, Garza LA. An overview of alopecias. Cold Spring Harb Perspect Med. 2014;4(3):a013615.
Published 2014 Mar 1. doi:10.1101/ cshperspect.a013615.
2. Phillips TG, Slomiany WP, Allison R. Hair Loss: Common Causes and Treatment. Am Fam Physician. 2017;96(6):371-378.
3. Ho CH, Sood T, Zito PM. Androgenetic Alopecia. In:
StatPearls. Treasure Island (FL): StatPearls Publishing; January 7, 2024.
4. Kaliyadan F, Nambiar A, Vijayaraghavan S. Androgenetic alopecia: an update. Indian J Dermatol Venereol Leprol. 2013;79(5):613-625. doi:10.4103/0378-6323.116730
5. Wall D, Meah N, Fagan N, York K, Sinclair R. Advances in hair growth. Fac Rev. 2022;11:1. Published 2022 Jan 12. doi:10.12703/r/11-1.
MOISTURIZER
Acrodermatitis Enteropathica Rare Hereditary Disorder: A Case Report
Dr. Sudarshan Pramod Gaurkar
MBBS, MD (Dermatology)
Consulting Dermatologist
Associate Professor, GMC Miraj, Maharashtra
Dr. Aman Hooda
Senior Resident
Department of Dermatology, GMC Miraj, Maharashtra
Introduction
Acrodermatitis enteropathica (AE) is a rare hereditary disorder, which is mainly caused by zinc deficiency. It is clinically characterised as dry scaly erythematous plaques, often localized periorificially on the face or anogenital region, irritability, growth retardation, and systemic complications such as anaemia, amenorrhea, and neuropsychiatric issues may manifest. It is classified into inherited (genetic) and acquired, the genetic zinc deficiency is primarily linked to impaired zinc absorption, often stemming from mutations within the zinc transporter gene SLC39A4. Consequently, the faulty absorption of zinc gives rise to hallmark
signs of zinc deficiency in affected individuals. Acrodermatitis enteropathica shares symptomatology with other zinc deficiency etiologies, including acquired deficiencies attributable to malabsorption syndromes, liver or kidney diseases, dietary insufficiencies, or iatrogenic influences. Moreover, mutations within the SLC30A2 gene in mothers may diminish zinc secretion into breast milk, potentially exacerbating acrodermatitis enteropathica in breastfed infants. The pathophysiology underlying acrodermatitis enteropathica centres on zinc's pivotal role in diverse cellular processes, encompassing nucleic acid and protein synthesis, wound
healing, immune function, and antioxidative defence mechanisms. Enteral zinc absorption predominantly occurs in the jejunum via the ZIP4 transporter protein. However, mutations within the gene encoding ZIP4 inhibit effective zinc absorption, precipitating deficiency and ensuing clinical presentations.1,2,3
Acrodermatitis enteropathica presents with a spectrum of clinical manifestations, primarily characterized by its dermatological features, systemic symptoms, and concurrent mucosal involvement. Dermatological symptoms include periorificial and acral dermatitis, marked by erythematous, scaly, and vesicular lesions predominantly affecting perioral, periocular, perinasal, and acral regions. If left untreated, these lesions can progress to erosions and crusting and are often accompanied by pruritus and discomfort. Alopecia, particularly diffuse or patchy hair loss on the scalp, eyebrows, and eyelashes, is a common feature of acrodermatitis enteropathica.3 Systemic symptoms, though less frequent, may manifest as gastrointestinal disturbances such as diarrhea, abdominal pain, and poor appetite, impaired wound healing due to zinc's crucial role in cellular proliferation and tissue repair, growth retardation especially notable in pediatric cases, and immunological
abnormalities predisposing to increased susceptibility to infections. Concurrent mucosal involvement includes angular cheilitis and less commonly, conjunctivitis. The comprehensive understanding of acrodermatitis enteropathica’s clinical presentation underscores the importance of prompt recognition and management to mitigate complications and optimize patient outcomes.3
Diagnosis of acquired acrodermatitis enteropathica requires a comprehensive approach, incorporating clinical evaluation, laboratory investigations, and sometimes histopathological examination. Additionally, skin biopsy is necessary in certain cases to confirm the diagnosis and rule out other dermatological conditions.4,5,6 Treatment for acquired acrodermatitis enteropathica focuses on zinc supplementation to address the deficiency and management of underlying conditions like nutritional deficiencies or gastrointestinal disorders, integral for comprehensive care.7 By comprehensively addressing the multifaceted nature of acquired acrodermatitis enteropathica, clinicians can adeptly navigate the diagnostic and therapeutic complexities associated with the condition, ultimately enhancing the quality of life for affected individuals.5
Case Report
A 25-year-old male patient,
presented with symptoms consistent with acrodermatitis enteropathica acquired. Upon examination, the patient showed typical dermatological manifestations of acrodermatitis enteropathica, including periorificial and acral dermatitis. Additionally, the presence of erythematous on the buttock and penile region, itchy patches with hair loss on the crown region of the scalp, flaky patches on the ears, and scaly and vesicular lesions around mouth, eye and nose region was noted. Based on the clinical presentation and physical examination findings, a provisional diagnosis of acrodermatitis enteropathica acquired was made. The patient was started on zinc supplementation as the initial treatment for acrodermatitis enteropathica. Zinc supplements were administered orally for a period of 5 days. Additionally, supportive measures were provided to address the symptoms of psoriasis and itching. After 5 days of zinc supplementation, the patient showed significant improvement in symptoms. The dermatological manifestations of acrodermatitis enteropathica, including periorificial and acral dermatitis, started to resolve. The psoriatic patches on the buttocks, scalp, ears, and around the eye region showed marked improvement, with reduced itching and flakiness.
Acrodermatitis Enteropathica Rare Hereditary Disorder: A Case Report
After treatment Before treatment
After treatment Before treatment
2 (a & b) : Flaky brown patches and vesicular lesion around eyes, mouth and nose region
After treatment Before treatment
Figure 3 (a & b) : Itchy patches with hair loss on the crown region of the scalp
Before treatment
After treatment
Figure 4 (a & b) : Erythematous patches on the buttock
Before treatment
Figure 1 (a & b) : Flaky brown patches on the ears and forehead
Figure
Fig. 1 (a)
Fig. 1 (b)
Fig. 2 (a)
Fig. 2 (b)
Fig. 3 (a)
Fig. 3 (b)
Fig. 4 (a)
Fig. 4 (b)
Fig. 5 (a)
After treatment
Diagnosis
Diagnosing acrodermatitis enteropathica involves a comprehensive approach, encompassing clinical, physical, and systemic diagnostic methods. The primary diagnostic hallmark of acrodermatitis enteropathica is the presence of characteristic dermatological manifestations. Clinically, periorificial and acral dermatitis are the most common findings. Periorificial dermatitis presents as erythematous, scaly, and vesicular lesions around the mouth, eyes, and nose, while acral dermatitis manifests similarly on the extremities, particularly the hands and feet. Patients may present with psoriasiform dermatitis, characterized by flaky patches resembling psoriasis, commonly observed on the buttocks, scalp, and ears. Alopecia or hair loss may also be evident, often occurring in a patchy or diffuse pattern,
especially on the scalp.4
In addition to dermatological findings, a thorough physical examination is conducted to assess for systemic symptoms associated with acrodermatitis enteropathica. This may include evaluating gastrointestinal symptoms such as diarrhea, vomiting, and abdominal pain, as well as signs of growth retardation or delayed development, particularly in pediatric patients. Patients may exhibit signs of immunological compromise, leading to increased susceptibility to infections. Assessing the patient's immune function and history of recurrent infections is important.5
Serum zinc level measurement stands as a pivotal diagnostic tool for acrodermatitis enteropathica. Zinc deficiency is conventionally confirmed by observing low serum zinc levels, typically defined as levels below 70 μg/dL. However, interpretation of these results warrants consideration of various factors, including the individual's age, sex, and recent dietary intake.4 Assessing a complete blood count (CBC) is crucial in suspected zinc deficiency to detect hematological abnormalities. Zinc is vital for red blood cell, white blood cell, and platelet production. Deficiency can cause hypochromic microcytic anemia, leukopenia, and
thrombocytopenia. Anemia shows as small, pale red cells, while leukopenia weakens immunity, and thrombocytopenia increases bleeding risk. CBC analysis, including hemoglobin, hematocrit, red and white blood cell counts, and platelet count, aids in identifying and monitoring these abnormalities, guiding zinc deficiency management.4
In acrodermatitis enteropathica, hair analysis may show uneven hair shaft diameter and atypical trichorrhexis nodosa with stretched fractures. Some hair fibers may exhibit nodal swellings of the pseudomonilethrix type. Polarization microscopy can reveal irregular alternating dark and bright bands in hair shafts. Although these anomalies may persist despite zinc therapy, longterm supplementation often resolves them. Hair probes may indicate low cystine content, suggesting underlying zinc deficiency.4
The normal range of zinc in urine is 0.3 to 2.5 milligrams per liter (mg/L) or 0.5 to 2.5 milligrams per gram (mg/g) of creatinine. Low urine zinc levels may suggest zinc deficiency, indicating inadequate dietary intake, impaired absorption, or increased excretion. Zinc deficiency can accelerate serum albumin degradation, leading to decreased levels. Additionally, zinc deficiency
Figure 5 (a & b) : Erythematous patches on penile region
Acrodermatitis Enteropathica Rare Hereditary Disorder: A Case Report
Fig. 5 (b)
triggers inflammation, increasing acute-phase proteins like C-reactive protein (CRP), indirectly impacting serum albumin levels. Characteristics include decreased levels, hypoalbuminemia, and symptoms like edema, impaired wound healing, and susceptibility to infections due to compromised immunity.4
In individuals suspected of zinc deficiency, the examination of alkaline phosphatase (ALP) levels offers valuable insights into both bone health and liver function. Alkaline phosphatase plays a crucial role in bone metabolism and liver function, reflecting the integrity of these systems. Zinc deficiency can disrupt bone metabolism, leading to changes in alkaline phosphatase levels that may indicate compromised bone mineralization or increased bone turnover. Additionally, zinc is essential for normal liver function, and deficiency can influence alkaline phosphatase levels, potentially indicating liver damage or dysfunction.4 In cases suspected to be due to inherited mutations affecting zinc transporters (genetic acrodermatitis enteropathica), genetic testing may be pursued to identify specific mutations in genes such as SLC39A4.5,6
In cases where the diagnosis is uncertain or to rule out other dermatological conditions, a skin biopsy may be
performed. Histopathological examination typically reveals nonspecific findings such as hyperkeratosis, parakeratosis, acanthosis, crust and perivascular lymphocytic infiltration.5,6
Treatment
In managing acrodermatitis enteropathica, zinc supplementation serves as the cornerstone of treatment, administered orally or intravenously depending on the severity and oral tolerance of the patient. The dosage and duration of zinc supplementation are tailored to individual factors such as age, weight, and treatment response. Oral zinc therapy, involving zinc sulfate or other salts, typically ranges from 1 to 3 mg/kg/day of elemental zinc, divided into multiple doses, preferred for mild to moderate cases.8
Intravenous zinc therapy becomes necessary for severe cases or when oral intake is hindered, allowing rapid replenishment of zinc stores under medical supervision. Additionally, managing underlying conditions like gastrointestinal disorders or malabsorption syndromes is crucial, which may involve treating inflammatory bowel disease or celiac disease.7 Nutritional support, including a balanced diet rich in zinc-containing foods, complements supplementation, aiding in acrodermatitis enteropathica management, especially
in cases of associated malnutrition.8
Topical zinc preparations, like zinc oxide ointment, address dermatological symptoms, providing relief and promoting healing, particularly in localized areas. For cases of genetic acrodermatitis enteropathica linked to zinc transporter gene mutations, genetic counseling is recommended, offering insights into inheritance patterns and family planning options for affected individuals and their families.8
Zinc ionophore
Zn- DTSM: Zinc diethyldithiocarbamate (ZnDTMS) is a compound that has garnered interest for its potential therapeutic applications, particularly in the realm of zinc deficiencyrelated disorders. As a dithiocarbamate compound, Zn-DTMS possesses chelating properties, meaning it has the ability to bind to metal ions, including zinc, forming stable complexes. In the context of zinc deficiency disorders such as acrodermatitis enteropathica, Zn-DTMS may play a role in addressing the underlying deficiency. By chelating zinc ions, Zn-DTMS could potentially enhance the bioavailability of zinc, aiding in its absorption and utilization within the body. This could be particularly beneficial in cases where traditional oral zinc supplementation may be ineffective or poorly tolerated.9
Diodoquin: As a zinc ionophore, diodoquin facilitates the transport of zinc ions across cell membranes, which may be beneficial in cases of acrodermatitis enteropathica where there is impaired zinc absorption. By enhancing zinc uptake into cells, diodoquin supplementation could potentially help address the underlying zinc deficiency characteristic of acrodermatitis enteropathica and alleviate associated symptoms.10
Discussion
Acrodermatitis enteropathica affects approximately 1 per 500,000 children, with no apparent predilection for race or sex. Zinc serves as a crucial trace element essential for cellular function, playing integral roles in protein, carbohydrate, and vitamin A metabolism. It acts as a cofactor for numerous metal enzymes, including alkaline phosphatases, alcohol dehydrogenase, RNA polymerase, and digestive enzymes. The factors which are responsible for zinc deficiency are prematurity, low birth weight, zinc insufficiency in maternal milk, exclusive parenteral nutrition, malabsorption disorders like Crohn's disease and celiac disease, alcoholism, low calcium and phytate diet, kwashiorkor. Inherited zinc deficiency, commonly termed "acrodermatitis enteropathica," stems from an autosomal recessive mutation
of the SLC39A4 gene on chromosome 8q24.3.11
The severe clinical symptoms in acrodermatitis enteropathica is skin lesions, with some becoming erosive or resembling a psoriatic rash. Additional mucous and cutaneous signs include diffuse alopecia, loss of eyelashes and eyebrows, glossitis, gingivitis, stomatitis, onychodystrophy, onycholysis, and pachyonychia.
Neuropsychiatric disorders, hypogonadism, growth restriction, and immune dysfunction are among the more severe manifestations that may develop in advanced cases. Untreated acrodermatitis enteropathica can lead to multiple organ failure and death, often complicated by secondary bacterial infections.1, 2
Diagnosis of acrodermatitis enteropathica is mainly relies on, low plasma/serum zinc levels, and identification of pathogenic mutations. However, some patients may exhibit typical skin rash despite normal zinc levels, possibly due to intermittent zinc supplementation. The differential diagnosis for the presented case includes contagious impetigo, candidiasis, psoriasis, and other skin diseases associated with pathogens. The confirmed diagnosis for this patient was a cutaneous mycosis. Skin mycosis was ruled out as these specific characteristics were not
observed in the patient. Additional potential diagnoses to consider include seborrheic dermatitis, StevensJohnson syndrome, atopic dermatitis, and erythema multiforme.4,5 Oral zinc supplementation usually yields swift therapeutic outcomes, though some cases may require prolonged high-dose regimens. A recommended lifelong dose of elemental zinc is 3 mg/kg/day, with variations in efficacy noted between zinc sulfate and zinc gluconate formulations.6,7,8,9 Zinc diethyldithiocarbamate (ZnDTMS) possesses chelating properties, suggesting a potential role in enhancing zinc bioavailability in acrodermatitis enteropathica. Although research on ZnDTMS in acrodermatitis enteropathica is limited, its chelating properties hint at symptom alleviation by addressing zinc deficiency.9 Diodoquin, or clioquinol, has been explored for its potential as a zinc ionophore. Acting as a facilitator for zinc ion transport across cell membranes, diodoquin may enhance zinc uptake, addressing the underlying deficiency in acrodermatitis enteropathica.10
Conclusion
In conclusion, acrodermatitis enteropathica can typically be diagnosed relatively easily, with prompt treatment centered on zinc therapy being essential. Failure to promptly address the condition may result in
Acrodermatitis
Acrodermatitis Enteropathica Rare Hereditary Disorder: A Case Report
complications, potentially leading to more severe conditions such as fungal infections. Adequate nutrition rich in zinc is crucial to prevent the onset or recurrence of acrodermatitis enteropathica. Additionally, regular follow-up appointments are necessary to monitor progress and ensure the effectiveness of treatment. In closing, proactive management and adherence to treatment protocols are paramount in mitigating the impact of acrodermatitis enteropathica and promoting optimal outcomes for affected individuals.
References
1. Kurt BÖ, Urican CM, Ünal B, Çiftçiogllu MA, Uzun S. Acquired acrodermatitis enteropathica secondary to sleeve gastrectomy. Indian J Dermatol Venereol Leprol. 2019;85(2):220-223. doi:10.4103/ ijdvl.IJDVL_337_18
2. Kelly S, Stelzer JW, Esplin N, Farooq A, Karasik O. Acquired Acrodermatitis Enteropathica: A Case Study. Cureus. 2017;9(9):e1667. Published 2017 Sep 8. doi:10.7759/cureus.1667
3. Nistor N, Ciontu L, Frasinariu OE, Lupu VV, Ignat A, Streanga V. Acrodermatitis Enteropathica: A Case Report. Medicine (Baltimore). 2016;95(20):e3553. doi:10.1097/ MD.0000000000003553
4. Van Wouwe JP. Clinical and laboratory diagnosis of acrodermatitis enteropathica. Eur J Pediatr. 1989;149(1):2-8. doi:10.1007/BF02024322
5. Schmidt H, Riemann JF, Grosse KP. Klinik, Diagnostik und Therapie der Acrodermatitis enteropathica [Clinical aspects, diagnosis and therapy of acrodermatitis enteropathica]. Leber Magen Darm.
1982;12(6):239-244.
6. Dev T, Sethuraman G. Diagnosis of acrodermatitis enteropathica in resource limited settings. BMJ Case Rep. 2017;2017:bcr2017220928. Published 2017 Aug 2. doi:10.1136/ bcr-2017-220928
7. Lungarotti MS, Rufini S, Calabro A, Mariotti G, Ghebregzabher M, Monaldi B. Treatment of acrodermatitis enteropathica with zinc sulphate. Rerport of 3 cases. Helv Paediatr Acta. 1976;31(2):117120.
8. Der Kaloustian VM, Musallam SS, Sanjad SA, Murib A, Hammad WD, Idriss ZH. Oral treatment of acrodermatitis enteropathica with zinc sulfate. Am J Dis Child. 1976;130(4):421-423. doi:10.1001/ archpedi.1976.02120050079015
9. Bray L, Volitakis I, Ayton S, Bush AI, Adlard PA. Zn-DTSM, A Zinc Ionophore with Therapeutic Potential for Acrodermatitis Enteropathica?. Nutrients. 2019;11(1):206. Published 2019 Jan 21. doi:10.3390/nu11010206
10. DILLAHA CJ, LORINCZ AL, AAVIK OR. Acrodermatitis enteropathica; review of the literature and report of a case successfully treated with diodoquin. J Am Med Assoc. 1953;152(6):509-512. doi:10.1001/ jama.1953.03690060025009
11. Martínez-Bustamante ME, Peña-Vélez R, Almanza-Miranda E, Aceves-Barrios CA, VargasPastrana T, Morayta-Ramírez Corona ARR. Acrodermatitis enteropática [Acrodermatitis enteropathica]. Bol Med Hosp Infant Mex. 2017;74(4):295-300. doi:10.1016/j.bmhimx.2017.05.002
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Efficacy of Purified Protein Derivative (PPD) in the Treatment of Genital Wart: A Case Presentation
Dr. Dhavalkumar Shivram Bansode
MD (Dermatology)
Assistant Professor
Department of Skin and VD
Ashwini Rural Medical College
Solapur, Maharashtra
Introduction
Genital warts, clinically known as condylomata acuminata (CA), are a common sexually transmitted infection caused primarily by human papillomavirus (HPV) types 6 and 11. These benign growths typically appear as clusters or singular lesions in the genital or anal areas, resulting from skin-to-skin contact during sexual activity. The incidence of genital warts is influenced by factors such as early sexual debut and multiple sexual partners, contributing to their widespread occurrence.1
Clinically, genital warts present as flesh-colored growths with a distinctive cauliflower-like or papular appearance. They can vary in size and number, causing discomfort, itching, or pain in affected individuals. Despite HPV types 6 and 11 being classified as lowrisk for cancer development, they are responsible for the majority of genital wart cases,
highlighting their significant clinical impact. HPV is a nonenveloped, double-stranded DNA virus belonging to the Papovaviridae family.2 It replicates within the basal cell layer of surface tissues and infects basal keratinocytes of the epidermis following penetration of cutaneous and mucosal epithelium. Infections can occur along the genital tract, including the vulva, vagina, cervix, perianal regions in females, and penile shaft, scrotum, periurethral, and perianal regions in males, characterized by viral DNA proliferation and the formation of papules or plaques.1, 2
The diagnosis of genital warts commonly entails a visual inspection conducted by a healthcare provider. Additional diagnostic methods may include applying acetic acid to the lesions (acetowhite test) to enhance visualization. In cases where diagnosis is uncertain,
techniques such as biopsy, electron microscopy, or immunohistochemical staining may be employed to confirm the presence of HPV particles within infected cells.3 Treatment strategies for genital warts aim to remove visible lesions, alleviate symptoms, and prevent recurrence. Options include topical therapies like podophyllotoxin or imiquimod, which directly target wart tissue, as well as physical methods such as cryotherapy (freezing) or surgical excision for larger or persistent warts. Depending on individual circumstances, systemic medications or laser therapy may also be recommended.4
Genital warts represent a notable public health issue owing to their widespread occurrence and associated potential complications. Early detection, prompt treatment, and preventive measures such as vaccination against HPV (where available) are essential in managing this condition effectively. Seeking medical advice for diagnosis and treatment is crucial for individuals experiencing symptoms or concerns related to genital warts, ensuring proper management and reducing the risk of transmission.
Typically, genital warts can appear as single lesions or clusters, appearing as single lesions or clusters that range from small papules to larger masses. They may be flat, raised, or have a rough, textured surface, often flesh-
colored, pink, or whitish depending on the individual's skin tone and the stage of development. Many genital warts exhibit a clustered growth pattern, with surfaces that can be smooth or rough, sometimes featuring fingerlike projections. Symptoms such as itching, discomfort, or pain may occur, particularly in areas prone to friction or moisture, and warts may bleed if irritated during activities like sexual intercourse or scratching. The presentation can vary significantly, from a solitary lesion to multiple growths covering a significant area, and their size can range from less than 1 millimetre to several centimetres in diameter, depending on their maturity and duration. In some cases, they may regress spontaneously, especially in individuals with strong immune responses. It's important to note that genital warts may coexist with other sexually transmitted infections like HSV or HIV, underscoring the need for comprehensive screening. Monitoring may be necessary for individuals infected with high-risk HPV strains due to their potential association with precancerous or cancerous conditions. Beyond physical symptoms, the emotional and psychological impact of genital warts can be significant, causing distress, embarrassment, and anxiety that affect sexual relationships and overall well-being. Understanding these clinical features is crucial for accurate diagnosis and effective
management.2
Case Report
A 50-year-old female patient presented with multiple genital warts with no risk behaviour, which were discovered due to her husband's concurrent diagnosis. Upon examination, flesh-colored and whitish genital warts of varying sizes were observed on the vulva and perianal area, ranging from small papules to larger masses, accompanied by mild itching and discomfort. Laboratory tests including HIV (Human Immunodeficiency Virus), HBV (Hepatitis B Virus), HCV (Hepatitis C Virus), VDRL (Venereal Disease Research Laboratory), and TPHA (Treponema Pallidum Hemagglutination Assay) yielded negative results, ruling out concurrent infections. Based on the clinical presentation and laboratory findings, a provisional diagnosis of genital warts was made. The patient was initiated on treatment with 0.1 ml purified protein derivative (PPD) injections administered via insulin syringe every 15 days. After completing the prescribed course of five doses, significant improvement was noted, and complete clearance of genital warts was achieved. This successful outcome underscores the efficacy of PPD injection therapy in treating genital warts caused by HPV infection in individuals with no high-risk behaviours.
Efficacy of Purified Protein Derivative (PPD) in the Treatment
Before treatment
Before treatment
After 5 doses (3 months) of treatment
After 5 doses (3 months) of treatment
2 : Flesh-colored and whitish genital warts observed on the perianal area
Diagnosis
Diagnosing genital warts begins with a comprehensive medical history assessment. Healthcare providers will inquire about any symptoms such as unusual growths or changes in the genital area, as well as patients sexual history, including the number of partners and any previous STIs. Discussions may also cover HPV vaccination history and past treatments for genital warts. Following this, a crucial step involves a thorough physical examination of the genital area, where healthcare providers look for visible warts or abnormal skin changes. Genital warts can vary widely in appearance, ranging from small, flesh-colored bumps to clusters resembling cauliflowerlike growths. In women, a pelvic exam may be conducted to check for warts on the cervix or inside the vagina. If the
diagnosis remains uncertain or if atypical symptoms are present, additional laboratory tests may be recommended. These could include an Acetic Acid (Vinegar) Test, where a solution is applied to the genital area to make warts turn white and more visible, a biopsy to examine tissue samples under a microscope, or an HPV DNA test to detect high-risk HPV types.3
Colposcopy, utilizing a magnifying colposcope, offers detailed examination of the cervix, vagina, vulva, and sometimes the urethral meatus. It enhances visualization to detect small or subtle genital warts, crucial for accurate diagnosis and treatment planning. It helps differentiate genital warts from other lesions, assess their extent for targeted therapy, guide biopsy or surgical procedures in uncertain cases, and supports long-term surveillance for recurrence or progression to dysplasia or cancer, especially in high-risk HPV or immunocompromised patients.3
Microscopy plays a crucial role in the diagnosis and management of genital warts, offering detailed insights into lesion morphology and aiding in treatment decisions. Dermatoscopes, often used for this purpose, provide magnification and illumination, enhancing visualization of genital warts' characteristic features such as their papillomatous or verrucous appearance. This tool allows clinicians to differentiate between genital warts
Figure 1 : Flesh-colored and whitish genital warts observed on the vulva
Figure
and other dermatological conditions with similar presentations, such as benign nevi or molluscum contagiosum. Additionally, microscopy facilitates precise assessment of lesion extent, aiding in the selection of appropriate treatment modalities, including topical therapies, cryotherapy, or surgical excision. In cases where the diagnosis is uncertain or atypical features are suspected, microscopic examination guides the decision-making process for biopsy or referral to further specialist evaluation. Overall, microscopy in the context of genital warts supports accurate diagnosis, targeted treatment strategies, and comprehensive patient care, ensuring optimal outcomes and patient satisfaction.3
Screening for other STIs such as chlamydia, gonorrhea, syphilis, and HIV is also typically advised due to the nature of HPV being a sexually transmitted infection. Once diagnosed, healthcare providers discuss treatment options and provide counselling on preventing HPV transmission and minimizing the risk of complications. Early detection and prompt medical attention are crucial for effective management of genital warts and prevention of further spread.
Treatment
Human papillomavirus (HPV) infection is persistent and cannot be completely eradicated; removal of visible warts does not ensure eradication of the
underlying viral infection spontaneous clearance of HPV occurs in approximately 80% of individuals within 18 to 24 months. Treatment approaches vary depending on the number, size, and location of warts. Ablative treatments such as vaporization, resection, coagulation, or excision effectively physically remove warts. However, these methods may result in permanent depigmentation, itching, pain, and scarring. Warts situated at the urethral meatus are best managed through surgical intervention to reduce potential longterm complications. Despite their typically lower efficacy compared to ablative treatments, patients often prefer topical agents initially, particularly for smaller lesions.4
1. Topical agents
A. Podophyllotoxin 0.05% solution or 0.15% cream/ gel: Podophyllotoxin, an extract from the podophyllum plant, acts by binding to cellular microtubules, thereby inhibiting mitotic division and causing necrosis of warts within 3 to 5 days postapplication. This results in shallow erosions that heal over several days. The treatment is widely considered safe, effective, and suitable for selfadministration. Application involves twice daily use for three consecutive days weekly, for up to four weeks. Penile lesions are typically treated with the solution, while cream or gel formulations are preferred for anal or vaginal lesions due to enhanced
comfort.5
B. Imiquimod 5% cream: Imiquimod is a topical immune response modifier cream applied locally to the affected area. It enhances the immune response by increasing cytokine production, including tumor necrosis factor-alpha (TNF-a) and interferon alfa, which stimulate a cytotoxic immune reaction mediated by T cells. The application of imiquimod 5% cream is recommended three times per week. It is associated with lower rates of wart recurrence compared to podophyllinbased therapies and typically promotes non-scarring healing.6
C.Sinecatechins: .........: Sinecatechins, formulated as a 15% ointment derived from catechins found in green tea, exhibit superior effectiveness in clearing warts compared to podophyllotoxin. This botanical treatment is noted for its immuno-stimulatory, anti-proliferative, and anti-tumor properties. Its mechanism of action involves reducing the expression of HPV gene products E6 and E7, which are essential for the viral replication and persistence that characterize human papillomavirus infections. This targeted action against HPV gene products contributes to sinecatechins' efficacy in treating genital warts, making it a valuable therapeutic option for patients seeking effective and well-tolerated treatment.4
D. Isotretinion: Isotretinoin, primarily known for its use in treating severe acne, has been explored as an
adjunctive therapy in the management of genital warts, particularly in cases where conventional treatments have been inadequate or when warts are extensive. The rationale behind its use lies in isotretinoin's ability to modulate cell differentiation, reduce sebum production, and exert anti-inflammatory effects. These properties may contribute to its potential efficacy in enhancing the response to other topical treatments aimed at eliminating warts.4
E. Trichloroacetic Acid (TCA) : Trichloroacetic acid demonstrates lower efficacy compared to cryosurgery and is contraindicated for use on the vagina, cervix, or urinary meatus due to its elevated recurrence rate and potential for local tissue damage. TCA application should be performed exclusively by healthcare professionals to mitigate these potential adverse effects.4
2. Electronics - Based Therapy
A. Liquid nitrogen cryosurgery ablation: Liquid nitrogen cryosurgery ablation is a widely used technique for treating genital warts. This procedure involves applying liquid nitrogen directly to the warts, causing freezing and destruction of the affected tissue. It is considered safe during pregnancy and typically does not result in significant scarring. Cryosurgery is performed in an outpatient setting and may require local anesthesia to manage discomfort. This method is effective due to its
ability to destroy wart tissue by freezing, leading to sloughing off of the wart over time.4
B. Electrocauterization:
This therapeutic technique is commonly employed in the treatment of genital warts. This procedure utilizes high-frequency electrical currents to burn and destroy wart tissue. It is particularly effective for small to mediumsized warts located on sensitive areas such as the genitalia. Electrocauterization is performed under local anaesthesia to minimize discomfort for the patient. The electrical current heats up and cauterizes the tissue, effectively removing the wart. This method aims to completely eradicate visible warts and reduce the viral load responsible for the infection.4
C. Laser vaporization: Laser vaporization is a specialized treatment modality commonly utilized for genital warts. This technique employs a concentrated beam of laser light to precisely target and vaporize wart tissue. It is particularly suitable for extensive or difficult-toaccess areas where surgical excision may be challenging. Laser vaporization is performed under local or general anaesthesia depending on the extent of treatment required and patient comfort. The laser beam effectively destroys wart tissue by heating and vaporizing it, which promotes healing and minimizes bleeding.4
D. Surgical removal under general anaesthesia: Surgical removal under
general anaesthesia is a definitive treatment option for extensive or deep-seated genital warts that require precise and extensive removal. This approach involves the complete excision of warts using surgical instruments while the patient is under general anaesthesia to ensure comfort and immobility. It is particularly indicated for large or multiple warts that are difficult to manage with other less invasive methods. Surgical removal under general anaesthesia allows for thorough removal of visible warts and potentially reduces the viral load responsible for the infection.4
E. Photodynamic therapy: Photodynamic therapy (PDT) treats genital warts by applying a photosensitizing agent like aminolevulinic acid (ALA) to the wart area. After absorption, the agent is activated by light, creating reactive oxygen species that damage and destroy wart cells. This targeted approach effectively eliminates external genital warts with minimal invasiveness and reduced risk of scarring compared to surgical methods.4
3. Vaccination
A. Human Papillomavirus
Vaccine: This is the first FDA-approved quadrivalent HPV vaccine designed to prevent infections caused by HPV types 6, 11, 16, and 18. These types are implicated in cervical, vulvar, and vaginal cancers, as well as genital warts (condyloma acuminata) in females aged 9-26. HPV vaccine effectively stimulates
Efficacy
the production of host antibodies against these HPV subtypes, which collectively account for approximately 90% of genital warts and 70% of cervical malignancies. Administration of three doses of HPV vaccine in HPV-naive individuals has demonstrated up to 99% efficacy in preventing genital warts.4
B. Human Papillomavirus
Bivalent (Types 16 and 18)
Vaccine, Recombinant:
On the other hand, this is a bivalent HPV vaccine targeting HPV types 16 and 18, both recognized as carcinogenic and associated with cervical cancer, cervical intraepithelial neoplasia (CIN) grade 1 or worse, and in situ malignancies. Like HPV vaccine induces immune responses against these specific HPV types. Adverse effects reported with human papillomavirus bivalent vaccine include injection site reactions (e.g., pain, redness, and swelling) and general symptoms such as fatigue, headaches, and muscle pain (myalgia). Variations in vaccine preparation, particularly adjuvant components enhancing immune response to vaccine antigens, may influence the immunological reactions observed between the two vaccines.4
Discussion
Genital HPV infections have an estimated prevalence of 10% to 20%, with clinical manifestations appearing in about 1% of cases. The incidence of HPV infection is on the rise, particularly affecting individuals aged 17 to 33 years, with the highest
rates observed among those aged 20 to 24. HPV infection is strongly implicated as the primary cause of anal cancer (approximately 90% of cases) and nearly all cases of cervical cancer in women, with HPV type 16 responsible for approximately half of cervical cancer cases. Cervical cancer ranks as the fourth most common cancer among women. HPV infections are also associated with a significant proportion of vulvar cancers (29% to 43%) and are implicated in about 70% of vaginal cancer cases, predominantly linked to HPV. Genital warts are typically diagnosed based on visual examination, and biopsies for confirmation are generally unnecessary. These warts appear as exophytic lesions due to enlargement of dermal papillae and are characterized by hyperplastic squamous epithelium displaying koilocytes, which are squamous cells with an eccentric, hyperchromatic nucleus displaced by a large perinuclear vacuole.1
HPV is primarily transmitted through penetrative sexual intercourse, although transmission via nonpenetrative sexual activities is less common. The effectiveness of condoms in preventing HPV transmission is uncertain based on conflicting evidence.1 Approximately 30% of genital warts resolve spontaneously within four months of appearing. However, most warts recur within three months after completing initial therapy,
regardless of treatment adherence. Recurrence rates vary based on factors such as the patient's overall health, immune status, prior HPV vaccinations, specific HPV strain, and frequency of sexual contact with an infected partner, condom use, and viral load. Smoking increases the risk of acquiring genital warts. Around threequarters of partners who initially do not have warts develop them within eight months of contact with an affected individual. Although 90% of HPV infections clear within two years, latency periods can occur, leading to the first occurrence or recurrence months to years later. Latent HPV infections are transmissible, with a 70% likelihood of transmission during unprotected sex with an infected partner.2, 3
The patient presents with several dermatological concerns, necessitating a comprehensive differential diagnosis. Firstly, condyloma lata, characteristic of secondary syphilis, manifests as wart-like growths in moist areas, including the genitals. This possibility underscores the need for serological testing to confirm or rule out syphilis. Secondly, familial benign pemphigus, a rare condition, may present with superficial blisters and erosions, typically without systemic involvement. Thirdly, herpes simplex infection, marked by painful vesicles and ulcers, requires consideration due to its recurrent nature and characteristic symptoms. Benign nevi, commonly seen
Efficacy of Purified Protein Derivative (PPD) in the Treatment of Genital Wart:
on the skin, may resemble other more concerning lesions, highlighting the importance of careful examination and possibly biopsy for definitive diagnosis. Lastly, vulvar neurofibromatosis, associated with café-au-lait spots and neurofibromas, should be evaluated given its potential for variable presentation and association with systemic neurofibromatosis type
1. Differential diagnosis is crucial in this context to guide appropriate management and treatment decisions tailored to the specific condition identified.3
Genital warts frequently exhibit treatment resistance and recurrence, exacerbated by repeated exposure to HPV through sexual contact and its prolonged incubation period. Ensuring patient adherence to therapy, switching therapeutic agents as necessary, and incorporating isotretinoin adjunctively are effective strategies.3 The morbidity associated with genital warts arises from symptoms such as pruritus, bleeding, and the substantial psychosocial impact of genital lesions.4 Additionally, the potential for malignant transformation into squamous cell carcinoma underscores the disease's significance in terms of mortality. Immunocompromised ........... patients typically present with more refractory lesions compared to the general population, often experiencing frequent recurrences. They also face an elevated risk of malignant transformation to squamous cell carcinoma.
Optimal management for these patients involves combining therapies, early introduction of isotretinoin, extended treatment duration, and timely consideration of surgical interventions when indicated.5 Prevention through HPV vaccination before exposure, alongside education on safe sexual practices and regular screening, remains crucial in reducing the incidence and impact of genital warts. These approaches aim to achieve better clinical outcomes and mitigate the complications associated with genital warts in immune-compromised individuals.5, 6
Conclusion
Genital warts present a multifaceted clinical challenge characterized by their persistence, recurrence, and potential for complications. Effective management requires a tailored approach that addresses both the physical symptoms and the psychological impact on patients. Prevention through vaccination against HPV remains paramount in reducing the incidence of genital warts and associated malignancies. For those already affected, prompt diagnosis, patient education, and comprehensive treatment strategies including topical therapies, immunomodulators, and surgical options are essential. Continued research into novel treatments and improved strategies for HPV control will further enhance our ability to manage and prevent genital warts effectively.
References
1. Leslie SW, Sajjad H, Kumar S. Genital Warts. In: StatPearls. Treasure Island (FL): StatPearls Publishing; May 30, 2023.
2. Yanofsky VR, Patel RV, Goldenberg G. Genital warts: a comprehensive review. J Clin Aesthet Dermatol. 2012; 5(6):2536.
3. Wiley DJ, Douglas J, Beutner K, et al. External genital warts: diagnosis, treatment, and prevention. Clin Infect Dis. 2002;35 (Suppl 2):S210-S224. doi:10.1086/ 342109
4. Kore VB, Anjankar A. A Comprehensive Review of Treatment Approaches for Cutaneous and Genital Warts. Cureus. 2023;15 (10) :e47685. Published 2023 Oct 25. doi:10.7759/cureus.47685
5. Mohanty KC. The cost effectiveness of treatment of genital warts with podophyllotoxin. Int J STD AIDS. 1994; 5 (4) : 253-256. doi: 10.1177 /095646249400500405
6. Bilu D, Sauder DN. Imiquimod: modes of action [published correction appears in Br J Dermatol. 2006 Jun;154(6):1220. Bilu, Donna [added]]. Br J Dermatol. 2003;149 Suppl 66:5-8.doi:10.1046/j.0366-077 x.2003.05628.x
Efficacy
In Some Patients, Antiseizure Medications Can Cause Severe Skin Reactions
Avoiding severe skin reactions to antiseizure medications (ASMs) requires assessing patient risk factors and prescribing lower-risk drugs wherever possible, according to authors of a recent review. And if putting higher-risk patients on drugs most associated with human leukocyte antigen (HLA)–related reaction risk before test results are available, researcher advised starting at low doses and titrating slowly.
The incidence of benign skin reactions such as morbilliform exanthematous eruptions,which account for 95% of cutaneous adverse drug reactions (CADRs), ranges from a few percent up to 15%. It’s a somewhat common occurrence. Fortunately, the reactions that can lead to morbidity and mortality are fairly rare.
Among the five ASMs approved by the Food and Drug Administration since 2018, cenobamate has sparked the greatest concern. In early clinical development for epilepsy, a fast titration schedule (starting at 50 mg/day and increasing by 50 mg every 2 weeks to at least 200 mg/day) resulted in three cases of drug reaction with eosinophilia and systemic symptoms (DRESS, also called drug-induced hypersensitivity reaction/DIHS), including one fatal case. Based on a phase 3 trial, the drug’s manufacturer now recommends starting at 12.5 mg and titrating more slowly.
DRESS/DIHS appears within 2-6 weeks of drug exposure. Along with malaise, fever, and conjunctivitis, symptoms can include skin eruptions ranging from morbilliform to hemorrhagic and bullous. “Facial edema and early facial rash are classic findings,” the researcher added. DRESS also can involve painful lymphadenopathy and potentially life-threatening damage to the liver, heart, and other organs.
Stevens-Johnson syndrome (SJS), which is characterized by detached skin measuring less than 10% of the entire body surface area, typically happens within the first month of drug exposure. Flu-like symptoms can appear 1-3 days before erythematous to dusky macules, commonly on the chest, as well as cutaneous and mucosal erosions. Along with the skin and conjunctiva, SJS can affect the eyes, lungs, liver, bone marrow, and gastrointestinal tract.
Often, researcher added, all hope is not lost for future use of the medication after a minor skin reaction. A case series and literature review of mild lamotrigine-associated CADRs showed that most patients could reintroduce and titrate lamotrigine by waiting at least 4 weeks, beginning at 5 mg/day, and gradually increasing to 25 mg/day.
More Illnesses Possible Related Linked to Counterfeit Botulinum Toxin Reported
Botulinum toxin is a medication used to manage and treat therapeutic and cosmetic purposes. Medicinal uses include chronic migraine, spastic disorders, cervical dystonia, and detrusor hyperactivity. Botulinum toxin is in the neurotoxin class of medications.
Recently published study showed after receiving botulinum neurotoxin (BoNT) injections in nonmedical settings, and four of the women required hospitalization — two in the intensive care unit. None of the cases required intubation, according to an announcement of an investigation into these reports in by the Centers for Disease Control and Prevention (CDC).
This study reports that the four patients received counterfeit BoNT, while product information was not available for the three cases. However, one person reported paying less than wholesale acquisition cost for the administered product, and another reported that the product had been purchased overseas, the authors of the report wrote. The development underscores that BoNT injections “should be administered only by licensed and trained providers using recommended doses of FDA [Food and Drug Admininstration]-approved products.
This report follows a CDC advisory published in April 2024 of at least 22 people from 11 states who reported serious reactions after receiving botulinum toxin injections from unlicensed or untrained individuals or in nonhealthcare settings, such as homes and spas.
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