Aquagenic Syringeal Acrokeratoderma (ASA)

Aquagenic syringeal acrokeratoderma (ASA) is a rare skin condition. After a few minutes of touching water, small white, puffy, flat-topped bumps and soggy plaques suddenly appear on the palms (and sometimes soles). They often sting, burn, itch, or feel tight, and usually fade within minutes after drying. Doctors also call it aquagenic keratoderma or aquagenic wrinkling of the palms because the skin looks wrinkled and swollen right after water contact. ASA can happen by itself or together with other problems. It is strongly linked with cystic fibrosis (CF) and carriers of CF gene changes; it may also be triggered by certain medicines. Treatments are mostly based on small studies or case reports. Options include aluminium-salt antiperspirants, keratolytics (urea or salicylic acid), anticholinergics (like glycopyrronium), botulinum toxin, iontophoresis, and, rarely, surgery for sweat-nerve control. PMC+3PMC+3DermNet®+3

Many experts think water quickly enters the outer skin where the sweat ducts open. If the sweat is salty or the ducts are abnormal, water is pulled in even faster, which makes the skin swell and wrinkle. People with cystic fibrosis have very salty sweat and more water loss through skin, so ASA is common in them. Drugs that change salt handling in skin (for example, some NSAIDs or antibiotics) can also trigger ASA in some people. The exact cause can differ between patients, and several mechanisms may combine. PMC+2JAMA Network+2

Aquagenic syringeal acrokeratoderma (ASA) is a rare skin condition. After the hands (and sometimes the soles) touch water for a short time, small white, translucent bumps appear. The skin wrinkles more than normal, looks puffy, and the pores of the sweat glands look bigger. People often feel burning, tightness, itch, or pain. The changes usually fade after the skin dries. Doctors think the problem starts in the sweat-gland ducts and the top skin layer (stratum corneum). The condition is closely linked to how salt and water move in the skin, and it is often associated with cystic fibrosis (CF) or being a CF carrier. JAAD+2PMC+2

Why it happens

Water soaks into the top skin layer. In ASA, because of salt and water balance issues and sweat-duct changes, the stratum corneum swells quickly and wrinkling appears fast. In cystic fibrosis, abnormally salty sweat and CFTR-related water transport changes likely pull more water into the outer skin and around the sweat-duct openings. Under the dermoscope (a skin magnifier), doctors can see enlarged eccrine pores and special surface patterns like the “wood-bark sign.” Under the microscope (biopsy), common findings include hyperkeratosis (thick stratum corneum) and dilated sweat-duct openings. Non-invasive imaging (like reflectance confocal microscopy or optical coherence tomography) can also show sweat-duct and surface changes. PubMed+4JAMA Network+4PMC+4

ASA has several look-alike names in the medical literature. Some authors call it “aquagenic wrinkling of the palms” when the main change is quick wrinkling. Others use “transient reactive papulotranslucent acrokeratoderma,” “aquagenic palmoplantar keratoderma,” or simply “aquagenic keratoderma.” All of these labels describe the same pattern: water exposure triggers short-lived papules and wrinkling, most often on the palms. JAAD+2Oxford Academic+2

Other names

Doctors may use any of these names in reports or textbooks. They all point to the same core problem.

• Aquagenic wrinkling of the palms (AWP) — emphasizes the fast, strong wrinkling after brief water contact. PMC

• Transient reactive papulotranslucent acrokeratoderma (TRPA) — highlights the temporary, translucent bumps that appear with water and then fade. PubMed+1

• Aquagenic palmoplantar keratoderma (APPK) / aquagenic acrokeratoderma — focuses on thickening/keratoderma on palms (and rarely soles) that is triggered by water. PMC

• Aquagenic syringeal acrokeratoderma (ASA) — underlines changes around the “syringeal” (eccrine sweat-duct) openings. JAAD

ASA is a water-triggered skin reaction on the hands (and sometimes the feet). Within minutes of touching water, whitish, flat-topped bumps and excess wrinkling appear. The sweat-pore openings look larger. People may feel tightness, burning, itch, or pain. After the skin dries, these changes usually go away on their own. ASA is thought to come from abnormal handling of salt and water in the outer skin and functional changes in sweat-gland ducts. It is more common in females and is strongly linked to cystic fibrosis or carrying a CF gene change. JAAD+2PMC+2

Types

It helps to sort ASA into types so plans and expectations are clearer:

1. By cause

• Primary/idiopathic ASA — no clear trigger or disease is found. The skin still reacts to water with papules and wrinkling. Lippincott Journals

• Secondary ASA — occurs with another factor, most often cystic fibrosis or CF carrier status, or certain drugs (e.g., some NSAIDs or COX-2 inhibitors). JAMA Network+1

2. By body area

• Palms only — the classic and most common pattern.

• Palms and soles — less common; soles can be involved in some patients. Lippincott Journals

3. By frequency

• Intermittent — flares with water and settles quickly after drying.

• Persistent tendency — frequent episodes with daily activities involving water. PMC

4. By symptoms

• Wrinkling-dominant — wrinkling is main feature; little discomfort.

• Pain/itch-dominant — burning pain, sting, or itch with visible bumps. skin.dermsquared.com

5. By link to CFTR function

• CF/CF-carrier associated — higher rates of AWP/ASA, sometimes improving with CFTR-modulator therapy (e.g., ivacaftor).

• Non-CF ASA — same skin picture but without CFTR mutation. cysticfibrosisjournal.com+1

---

Causes

1. Cystic fibrosis (CF) — ASA/AWP is common in people with CF. The sweat is very salty and water handling in the skin is altered, making quick wrinkling and papules after water contact. JAMA Network+1

2. Carrier of a CF gene (CFTR heterozygote) — even one CFTR change can increase risk. Many carriers show rapid aquagenic wrinkling. PMC+1

3. COX-2 inhibitor drugs (e.g., celecoxib/rofecoxib class) — reported cases link these medicines to TRPA/ASA, probably by affecting sweat-gland or skin-barrier function. PubMed

4. Other NSAIDs — some non-steroidal anti-inflammatories have been linked to aquagenic wrinkling in case reports; stopping the drug may help. PMC

5. Hyperhidrosis (excess sweating) — more sweat and salt on the surface may draw water into skin faster and enlarge pores. JAAD

6. Sympathetic over-activity of sweat glands — suggested by good response to anticholinergic treatments (e.g., glycopyrronium). ResearchGate

7. Aquaporin-5 and water-channel changes — altered water channels in sweat glands have been described in AWP. DermNet®

8. Adolescence and young adult female sex — ASA often starts in teens/young adults and is more frequent in females, likely due to sweat/lipid and barrier differences. Lippincott Journals+1

9. Frequent water exposure (occupational/household) — repeated wet-work makes flares more common by constant swelling/drying cycles. PMC

10. High salt at skin surface — any setting that raises salt on the skin (e.g., CF) favors quick water uptake and wrinkling. JAMA Network

11. Topical products that impair barrier — harsh soaps or solvents can thin the lipid layer and speed water entry, revealing underlying ASA tendency. (General mechanism inferred from barrier science within AWP reports.) PMC

12. Heat and humidity — warm, humid conditions increase sweating and can worsen symptoms. PMC

13. Genetic background (non-CF) — some people without CF have idiopathic ASA, suggesting other genetic or barrier factors. Lippincott Journals

14. Atopy/eczema background — occasionally reported alongside ASA; barrier fragility may play a role (association noted in reviews). PMC

15. Certain antibiotics (e.g., reported with tobramycin in CF care) — proposed triggers in scattered reports; mechanism unclear. PMC

16. Salazopyrin + indomethacin combination — case reports of drug-associated aquagenic wrinkling. DermNet®

17. Minocycline/other medications — individual case links exist; individual de-challenge (stopping) may improve signs. DermNet®

18. Autonomic sweat-nerve dysfunction — sudomotor testing literature suggests sweat-gland nerve issues can change sweating; some ASA cases may overlap. (Supportive physiology from sudomotor reviews.) PubMed+1

19. COVID-era reporting increase — recent literature reviews note post-2014 case growth; whether COVID-19 itself causes ASA is unclear, but more cases were reported. PubMed+1

20. Unknown causes — many patients have no clear trigger; they fit idiopathic ASA. Lippincott Journals

---

Symptoms

1. Fast wrinkling after water — appears within 2–7 minutes, much quicker than normal wrinkling. DermNet®

2. White, translucent bumps — flat-topped papules that merge into plaques. JAAD

3. Puffy, swollen look — the wet stratum corneum swells, giving a plump surface. PMC

4. Visible sweat-pore dots — eccrine openings look bigger or more numerous. PMC

5. Burning or stinging — many patients feel a mild burn when the skin is wet. skin.dermsquared.com

6. Itching — itch can accompany the papules during immersion. Lippincott Journals

7. Tightness — skin feels tight or “shrunken” while wet. PMC

8. Pain or tenderness — fingertip pain is reported in some cases. skin.dermsquared.com

9. Peeling after episodes — mild desquamation can follow repeated flares. PMC

10. Soggy/soft feeling — the top layer feels water-logged. PMC

11. Hyperhidrosis — some patients sweat more, and this worsens flares. JAAD

12. Symmetric on both palms — common pattern, though unilateral cases exist. PMC

13. Occasional sole involvement — less common but possible. Lippincott Journals

14. Short duration — changes usually fade within 10–60 minutes after drying. DermNet®

15. Daily-life impact — discomfort with washing, bathing, or wet-work tasks. PMC

---

Diagnostic tests

A) Physical examination

1. Bedside inspection before and after water
   Doctor looks at the dry hands, then again after brief water contact. The quick appearance of white papules and strong wrinkling after immersion supports ASA. PMC

2. Timed water-immersion (“hand-in-the-bucket”) test
   Hands are immersed (often 3–7 minutes). A positive test shows translucent papules, wrinkling, and prominent eccrine pores. Photos may be taken for comparison. PMC+1

3. Distribution mapping
   The doctor notes symmetry, palm vs. sole involvement, and fingertip prominence. Symmetric palmar disease is typical; soles may be involved in a minority. Lippincott Journals

4. Symptom provocation and recovery timing
   Clinician records how fast signs appear with water and how long they take to fade after drying (often within an hour). This pattern differentiates ASA from chronic keratodermas. DermNet®

5. Dermoscopy (hand-held skin scope)
   Under magnification, doctors may see enlarged sweat-duct pores and special surface patterns such as the “wood-bark sign.” This supports a sweat-duct-centered process. PMC+1

6. Differential diagnosis review
   Doctor rules out similar conditions (e.g., hereditary papulotranslucent acrokeratoderma, aquagenic urticaria), which have different timing and appearance. DermNet®

B) Manual/office tests

7. Standardized temperature and timing in immersion test
   Keeping water lukewarm and timing the test improves reliability and comparison over visits. This makes serial assessment more accurate. Open Access LMU

8. Starch–iodine (Minor’s) test for sweat
   Iodine is painted and starch is dusted; areas that sweat more turn dark. Many ASA patients also have focal hyperhidrosis, which this test can reveal. JAAD

9. Barrier-protection challenge
   Using petrolatum or barrier cream before immersion to see if wrinkling lessens can suggest a surface-barrier role (a practical clinic check reported in reviews). PMC

10. Glove occlusion trial
    Short periods of glove use during wet tasks can reduce water contact; improvement supports a water-triggered mechanism. PMC

11. Therapeutic trial as a diagnostic aid
    Improvement with aluminum chloride, topical anticholinergics (e.g., glycopyrronium), iontophoresis, or botulinum toxin supports eccrine involvement. ScienceDirect+2ResearchGate+2

C) Laboratory & pathological tests

12. Sweat chloride test
    A standard test for cystic fibrosis. High levels suggest CF, which is strongly linked to aquagenic wrinkling/ASA. JAMA Network+1

13. CFTR genetic testing
    Checks for mutations in the CFTR gene. Useful when ASA is the first clue to CF or when family history suggests carrier status. PMC

14. Medication review (pharmacovigilance approach)
    Systematic review of drugs (especially COX-2 inhibitors and some NSAIDs) and trial withdrawal if appropriate may identify a trigger. PubMed+1

15. Skin punch biopsy (H&E, PAS stains)
    Histology often shows hyperkeratosis and dilated eccrine ostia/ducts, supporting a sweat-duct process. Biopsy is not always needed but can confirm the diagnosis. PubMed

16. Basic labs when indicated
    Most patients need no routine blood tests. If a systemic link is suspected, CF-related evaluations are prioritized rather than general labs. (Guided by AWP/ASA reviews.) PMC

D) Electrodiagnostic sudomotor tests

17. QSART (Quantitative Sudomotor Axon Reflex Test)
    Measures sweat output after gentle electrical stimulation. Not required for most ASA cases, but it can document sweat-gland nerve function when autonomic involvement is suspected. Cleveland Clinic+1

18. Electrochemical skin conductance / sympathetic skin response
    Non-invasive tests of sweating used in autonomic labs; rarely needed but may support sudomotor dysfunction in complex cases. PMC

E) Imaging-based skin tools

19. Reflectance confocal microscopy (RCM)
    A “virtual biopsy” that shows sweat-duct and surface changes in vivo. Helpful when avoiding biopsy or tracking changes over time. PubMed+1

20. Optical coherence tomography (including line-field OCT)
    High-resolution imaging that can show surface ridges and duct changes during aquagenic wrinkling, supporting the diagnosis without cutting the skin. Wiley Online Library

Non-Pharmacological Treatments (Therapies & Others)

(Each item includes a short description, purpose, and mechanism in simple English.)

1. Short, smart water contact
   Keep hand-washing short; pat dry right away; use alcohol-based rubs if appropriate for hygiene. Purpose: reduce exposure time. Mechanism: less water enters swollen skin and sweat ducts, so fewer bumps appear. PMC

2. Cool water instead of warm
   Cooler water reduces swelling speed. Purpose: slow onset. Mechanism: cooler temps shrink vessels and reduce water uptake into the outer skin. PMC

3. Petrolatum barrier before wet work
   Apply a thin layer of plain petroleum jelly before dishwashing or bathing. Purpose: create a water barrier. Mechanism: occlusive film slows water entry into the stratum corneum. Lippincott Journals

4. Vinyl or nitrile gloves for wet tasks
   Wear cotton liners under waterproof gloves for dishes/cleaning. Purpose: limit soaking. Mechanism: physically blocks water while cotton improves comfort and wicks sweat. PMC

5. Frequent moisturizers after washing
   Use fragrance-free emollients after every wash. Purpose: restore skin barrier. Mechanism: replaces lipids and reduces transepidermal water loss. PMC

6. Keratolytic skincare routine (non-drug strength)
   Over-the-counter urea or salicylic-acid hand creams (low %). Purpose: smooth thickened lines. Mechanism: softens outer skin so water does not pool as easily. Lippincott Journals

7. Tap-water iontophoresis (device therapy)
   Hands placed on pads with mild current a few times weekly. Purpose: reduce sweating and water entry. Mechanism: temporarily blocks sweat ducts; widely used for hyperhidrosis, reported helpful in ASA. skin.dermsquared.com

8. Trigger-medicine review and deprescribing where possible
   Ask your clinician to check NSAIDs, COX-2, aspirin, macrolides, tobramycin, ACE inhibitors. Purpose: remove potential triggers. Mechanism: stopping a salt-handling drug can stop ASA in some cases. PMC+2ResearchGate+2

9. Sweat management habits
   Use breathable gloves, schedule breaks, cool environment. Purpose: limit hyperhidrosis. Mechanism: less sweat salt at ducts means less water pulling into skin. Indian J Dermatology

10. Dermoscopic/Wood’s lamp-guided monitoring
    Dermoscopic “wood-bark sign” and Wood’s lamp may help track response and confirm diagnosis in clinic. Purpose: structured follow-up. Mechanism: visual patterns correlate with changes in sweat duct openings and surface texture. Lippincott Journals+1

11. Gentle cleansers, avoid harsh soaps
    Use mild, pH-balanced cleansers. Purpose: protect barrier. Mechanism: less lipid stripping reduces TEWL spikes that accompany wrinkling. PMC

12. After-water air-dry plus cool fan
    Air-dry with a fan to speed water evaporation. Purpose: shorten symptom time. Mechanism: faster drying reduces swelling duration. PMC

13. Hand-care schedule (plan baths, dishwashing)
    Do wet chores in one block, not many short exposures. Purpose: fewer flares. Mechanism: minimizes repeated water triggers. PMC

14. Occupational changes for severe cases
    If water exposure is unavoidable at work, seek accommodations. Purpose: reduce severity. Mechanism: less cumulative water contact lowers symptom load. PMC

15. Education on CF link; family screening when indicated
    Discuss CF symptoms (chronic cough, GI issues) and carrier testing as clinically appropriate. Purpose: do not miss CF. Mechanism: ASA can be an early clue to CF/CFTR issues. PMC+1

16. Photographic diary
    Take phone pictures before/after water. Purpose: document patterns. Mechanism: helps clinician tailor therapy and detect drug triggers. PMC

17. Limit hot tubs/long swims
    Prefer short pool sessions; apply barrier first. Purpose: reduce intense triggers. Mechanism: heat plus long immersion amplifies wrinkling. PMC

18. Mind-body stress reduction for sweat flares
    Breathing or relaxation can reduce stress-sweat bursts. Purpose: dampen hyperhidrosis triggers. Mechanism: sympathetic tone affects sweating. Indian J Dermatology

19. Regular follow-up for treatment tuning
    Because evidence is mostly case-based, care is trial-and-adjust. Purpose: find your lowest-risk, best-fit plan. Mechanism: iterative change based on response and side-effects. PMC

20. Sun-safe, fragrance-free routines
    Avoid irritants that can worsen burning/itching. Purpose: comfort. Mechanism: fewer irritants means calmer barrier under water stress. PMC

---

Drug Treatments

1. Topical aluminium chloride hexahydrate (20%)
   Class: antiperspirant. Dose/Time: apply nightly to dry palms, then reduce to maintenance. Purpose: first-line to reduce water-triggered changes. Mechanism: blocks sweat ducts and decreases water influx; many cases improve quickly. Side-effects: irritation, stinging, dryness; use on fully dry skin to limit sting. PMC+1

2. Topical aluminium lactate/aluminium-based roll-ons
   Class: antiperspirant. Dose/Time: daily or every other day. Purpose: maintenance after control. Mechanism: similar duct blocking with gentler feel. Side-effects: mild irritation. Lippincott Journals

3. Topical urea (10–20%)
   Class: keratolytic/humectant. Dose/Time: 1–2×/day. Purpose: smooth ridges, reduce pooling. Mechanism: softens outer skin and improves barrier. Side-effects: mild sting on cracked skin. Lippincott Journals

4. Topical salicylic acid (3–5%)
   Class: keratolytic. Dose/Time: 1×/day or every other day. Purpose: cut down thick lines. Mechanism: breaks down keratin to reduce water trapping. Side-effects: irritation; avoid overuse. PMC

5. Topical ammonium lactate (12%)
   Class: alpha-hydroxy acid emollient. Dose/Time: daily. Purpose: smoother texture, better barrier. Mechanism: gentle exfoliation plus moisturization. Side-effects: sting on cuts. Lippincott Journals

6. Topical glycopyrronium (glycopyrrolate)
   Class: anticholinergic. Dose/Time: wipes/compounded gel daily; adjust to effect. Purpose: reduce sweating and burning. Mechanism: blocks acetylcholine at sweat glands; case series show good responses in aquagenic keratoderma. Side-effects: dry mouth, blurry vision if systemic absorption; wash hands after use and avoid eyes. jaadcasereports.org+2ScienceDirect+2

7. Oral oxybutynin (5 mg/day, titrate)
   Class: anticholinergic. Dose/Time: start low (e.g., 2.5–5 mg once daily), titrate; clinician-guided. Purpose: for resistant cases with marked sweating. Mechanism: reduces sweat gland activity; reported helpful where topicals fail. Side-effects: dry mouth, constipation, drowsiness; caution in glaucoma/urinary retention. ScienceDirect

8. Botulinum toxin A (palmar injections)
   Class: neuromuscular blocker. Dose/Time: injected in grids across palms; effects last ~3–5 months. Purpose: strong option when antiperspirants fail. Mechanism: blocks acetylcholine release, suppressing sweat; multiple reports show symptom control. Side-effects: injection pain, temporary hand weakness, cost. Lippincott Journals+1

9. Topical antiperspirant combinations (aluminium + emollients)
   Class: compounded barrier/antiperspirant. Dose/Time: nightly then maintenance. Purpose: balance power and comfort. Mechanism: duct blockage + barrier repair. Side-effects: local irritation. Lippincott Journals

10. Tap-water iontophoresis (medical device with/without anticholinergic additive)
    Class: physical therapy (often grouped with treatments). Dose/Time: sessions several times/week then weekly maintenance. Purpose: reduce flares. Mechanism: creates temporary duct plugs; sometimes aided by anticholinergic additives. Side-effects: skin dryness, mild tingling. skin.dermsquared.com

11. Oral antihistamines (e.g., cetirizine at night)
    Class: H1 blocker. Dose/Time: typical allergy dosing. Purpose: ease itch/burning. Mechanism: dampens histamine-mediated sensations; sometimes used adjunctively. Side-effects: sleepiness (older agents), dry mouth. PMC

12. Topical barrier ointments (petrolatum) as “drug therapy” when scheduled
    Class: occlusive emollient. Dose/Time: before water exposure. Purpose: pre-emptive shield. Mechanism: slows water entry. Side-effects: greasy feel. Lippincott Journals

13. Topical aluminium chloride 15% for sensitive skin
    Class: antiperspirant. Dose/Time: nightly then reduce. Purpose: alternative when 20% stings. Mechanism: partial duct plugging. Side-effects: less irritation than 20% but may be weaker. PMC

14. Compounded topical glycopyrrolate low-dose (0.5–1%)
    Class: anticholinergic. Dose/Time: once daily; pharmacist compound. Purpose: step-down from stronger wipes. Mechanism: local sweat reduction. Side-effects: minimal if applied correctly. jaadcasereports.org

15. Topical glycerol-rich creams
    Class: humectant emollient. Dose/Time: multiple times/day. Purpose: improve barrier elasticity. Mechanism: binds water in the outer skin to stabilize barrier between immersions. Side-effects: rare irritation. Cureus

16. Topical lactic acid 5–10%
    Class: AHA keratolytic. Dose/Time: daily at night. Purpose: texture smoothing. Mechanism: gentle exfoliation limits maceration. Side-effects: sting, photosensitivity care needed. Lippincott Journals

17. Topical ammonium chloride/aluminium blends (clinic protocols)
    Class: antiperspirant blends. Dose/Time: clinic-guided schedules. Purpose: persistent control. Mechanism: combines duct occlusion and keratolysis. Side-effects: irritation risk. Lippincott Journals

18. Oral anticholinergics other than oxybutynin (specialist use)
    Class: anticholinergic (e.g., glycopyrrolate tablets). Dose/Time: individualized. Purpose: severe hyperhidrosis with ASA. Mechanism: systemic sweat reduction. Side-effects: dry mouth, constipation, blurred vision. ScienceDirect

19. Topical compounded aluminium + urea + salicylic “triple therapy”
    Class: combination topical. Dose/Time: nightly cycles. Purpose: multi-pathway control. Mechanism: duct block + keratolysis + humectancy. Side-effects: local irritation. PMC

20. Clinical trial enrollment when available
    Class: research therapies. Dose/Time: per protocol. Purpose: access new options, document outcomes. Mechanism: contributes to better evidence for this rare disease. Side-effects: study-specific. PMC

---

Dietary Molecular Supplements (Adjuncts)

(These do not “cure” ASA; they support skin barrier or sweating comfort. Always discuss with a clinician.)

1. Ceramide-rich oral oils (e.g., wheat germ oil supplements)
   Dose: per product. Function/Mechanism: support skin lipid balance to reduce dryness peaks after water exposure. Evidence is indirect (barrier support), not ASA-specific. PMC

2. Omega-3 fatty acids
   Dose: common 1–2 g/day EPA+DHA. Function/Mechanism: anti-inflammatory support for itchy/burning hands; helps general skin barrier function. Evidence extrapolated from derm barrier data. PMC

3. Vitamin D (if deficient)
   Dose: as advised after testing. Function/Mechanism: supports epidermal differentiation and immune balance; indirect help for comfort. PMC

4. Biotin (only if deficiency suspected)
   Dose: clinician-guided. Function/Mechanism: cofactor in keratin production; evidence in ASA is lacking but sometimes used for brittle skin/nails. PMC

5. Niacinamide (vitamin B3) oral or topical
   Dose: topical 2–5% or oral per label. Function/Mechanism: reduces TEWL and strengthens barrier; may lessen stinging after water. PMC

6. Zinc (if low)
   Dose: per labs. Function/Mechanism: supports wound healing and epidermal turnover; avoid excess. PMC

7. Probiotics (general skin comfort)
   Dose: per product. Function/Mechanism: gut-skin axis modulation; only indirect evidence for skin sensitivity. PMC

8. Evening primrose oil (GLA)
   Dose: per label. Function/Mechanism: may ease skin dryness/itch; evidence variable; adjunct only. PMC

9. Collagen peptides
   Dose: 5–10 g/day. Function/Mechanism: general skin hydration/elasticity support; not ASA-specific. PMC

10. Electrolyte balance (adequate fluids and salt in heat)
    Dose: routine hydration. Function/Mechanism: supports comfortable sweating; avoids extremes that might irritate. PMC

Note: High-quality ASA-specific supplement trials are not available; these are general barrier-support ideas to discuss with your clinician. PMC

---

Immunity-Booster / Regenerative / Stem-Cell” Drugs

ASA is a skin barrier/sweat-duct phenomenon. There are no proven immune-booster, regenerative, or stem-cell drugs for ASA. Below are six categories often asked about; none are established for ASA, and they should not be used for this purpose outside of clinical trials.

1. Systemic corticosteroids
   Dose: not indicated. Function/Mechanism: broad immunosuppression; no evidence for ASA. Risks outweigh benefits. PMC

2. Biologic immunomodulators (e.g., dupilumab)
   Dose: not indicated for ASA. Function/Mechanism: targeted immune pathways; no ASA data. PMC

3. Stem-cell therapies
   Dose: none. Function/Mechanism: theoretical regeneration; no role in ASA. PMC

4. Platelet-rich plasma (PRP)
   Dose: none for ASA. Function/Mechanism: growth factors; no evidence for water-induced wrinkling disorders. PMC

5. Systemic “immune boosters” (herbal mixes)
   Dose: not recommended. Function/Mechanism: unproven; may interact with medicines. PMC

6. Systemic retinoids
   Dose: not standard for ASA. Function/Mechanism: keratinization control; insufficient evidence and potential adverse effects. PMC

---

Surgeries (Why and When)

1. Endoscopic Thoracic Sympathectomy (ETS)
   Procedure: clips/cuts thoracic sympathetic chain to reduce hand sweating. Why: last-line for severe, disabling palmar hyperhidrosis with ASA after all conservative care fails. Some reports show permanent ASA control when sweating is stopped. Risks: compensatory sweating, surgical risks. Indian J Dermatology+1

2. Sweat-gland–focused procedures (rare/experimental)
   Procedure: targeted treatments aimed at sweat output (e.g., energy-based). Why: considered only in research settings. Risks: scarring, nerve irritation. grimalt.net

3. Botulinum toxin injections (procedure-based, minimally invasive)
   Procedure: grid injections into palms in clinic. Why: strong non-surgical option when topicals fail. Risks: transient weakness, pain. Lippincott Journals

4. Iontophoresis in clinic (device procedure)
   Procedure: supervised sessions, then home unit. Why: reduce sweating non-invasively. Risks: skin dryness, irritation. skin.dermsquared.com

5. Biopsy (diagnostic, not therapeutic)
   Procedure: small skin sample if diagnosis is unsure. Why: rule out other palmoplantar keratodermas. Risks: small scar. Lippincott Journals

---

Preventions

1. Plan short water contact; dry quickly. PMC

2. Use cool water when possible. PMC

3. Apply petrolatum or aluminium-based antiperspirant before wet work. PMC

4. Wear cotton liners under waterproof gloves. PMC

5. Keep a simple emollient by every sink. PMC

6. Avoid known trigger medicines when safe/approved. PMC

7. Cool rooms, fans, breaks to limit sweating. Indian J Dermatology

8. Prefer gentle cleansers; avoid harsh soaps. PMC

9. Document flares with photos for pattern spotting. PMC

10. Seek CF evaluation if symptoms/history suggest risk. PMC

---

When to See a Doctor

See a clinician if: the hand pain, burning, itching, or tightness is frequent or limits daily tasks; bumps last long after drying; there is heavy sweating, cough or GI symptoms suggesting CF; you started a new medicine before symptoms; home steps do not help; or you have job-related water exposure and need accommodations. A dermatologist can confirm the diagnosis (often clinically), consider CF assessment, review medicines, and tailor a safe treatment plan. PMC+1

---

What to Eat & What to Avoid

What to eat: a balanced diet with enough protein and healthy fats to support skin barrier (fish, eggs, legumes, nuts), fruits/vegetables rich in antioxidants, and adequate fluids—especially in heat—to keep sweating comfortable. What to avoid: extreme dehydration or excessive caffeine that can spike sweat in some people; very spicy foods if they trigger sweating; and any supplement or herb that interacts with your medicines. These tips support comfort but do not cure ASA. PMC

---

Frequently Asked Questions

1. Is ASA dangerous?
   No. It is uncomfortable but not life-threatening. The main concern is its link to cystic fibrosis or CF carrier state in many patients, so evaluation matters. PMC+1

2. How is it diagnosed?
   Usually by history and exam after brief water exposure (“hand-in-bucket” sign). Dermoscopy and sometimes Wood’s lamp can help; biopsy is rarely needed. JAMA Network+2Lippincott Journals+2

3. How common is it in cystic fibrosis?
   Reports suggest very high rates in CF and increased rates in carriers. This is why doctors think about CF when ASA appears. PMC+1

4. What medicines can cause ASA?
   Case reports link celecoxib, rofecoxib, aspirin, tobramycin, and occasionally others like clarithromycin or ACE inhibitors. Stopping the trigger can help. PMC+2ResearchGate+2

5. Why does water do this?
   Water rushes into the outer skin, especially around sweat ducts; saltier sweat or duct changes pull in more water, making white, puffy plaques. PMC

6. Does it happen only on palms?
   Mostly palms; sometimes soles, rarely other sites. PMC

7. What is the first treatment to try?
   Topical aluminium chloride at night on completely dry skin is often first. Add emollients and smart water exposure control. PMC

8. What if aluminium burns my skin?
   Use lower strengths, apply to dry skin, reduce frequency, or switch to other options like urea/salicylic creams or topical glycopyrronium with clinician advice. Lippincott Journals+1

9. Is botulinum toxin safe for hands?
   It can help a lot, but injections may hurt and cause temporary weakness. Effects last months and then wear off. Lippincott Journals

10. Will iontophoresis help?
    Yes, for some people. It is a low-risk device that reduces sweating and can lessen flares; it needs a schedule. skin.dermsquared.com

11. Do I need surgery?
    Almost never. ETS is only for severe, disabling cases tied to hyperhidrosis after all other treatments fail. Indian J Dermatology

12. Can children have ASA?
    Yes; it has been reported in children, especially with CF. Pediatric evaluation is important. PMC

13. How long do lesions last after water?
    Usually minutes to tens of minutes after drying, but it varies. jaadcasereports.org

14. Can ASA be cured?
    There is no universal cure. Many people manage it well with antiperspirants, keratolytics, anticholinergics, and procedural options. PMC

15. What research is new?
    Recent reviews (2014–2025) discuss updated case counts, CF links, diagnostic aids, and responses to glycopyrronium and other therapies. PubMed+1

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: September 21, 2025.

PDF Documents For This Disease Condition References