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Focal hyperhidrosis
Focal hyperhidrosis
Focal hyperhidrosis
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Focal hyperhidrosis
Other namesprimary hyperhidrosis

Focal hyperhidrosis, also known as primary hyperhidrosis, is a disease characterized by an excessive sweating localized in certain body regions (particularly palms, feet and underarms). Studies suggest that this condition, affecting between 1% and 3% of the US population, seems to have a genetic predisposition in about two thirds of those affected.[1]

Focal hyperhidrosis is sometimes referred to as The Silent Handicap,[2] as it has a significant impact on the quality of life, affecting the individual socially, psychologically, emotionally and professionally.[3]

Genetics

[edit]

In 2006, researchers uncovered that primary palmar hyperhidrosis, referring to excess sweating on the palms of the hands and feet, maps to the gene locus 14q11.2-q13.[4]

Based on previous research using mice and rats, researchers looked towards the role of aquaporin 5 (AQP5), a water channel protein, in human individuals with primary focal hyperhidrosis.[5] AQP5 has been identified as a candidate gene in many hyperhidrosis studies. Using a family that had members with primary focal hyperhidrosis, researchers found that there was no connection between primary focal hyperhidrosis and AQP5. There was also no significant connection between the gene 14q11.2-q13 locus, which was linked to primary palmar hyperhidrosis, and primary focal hyperhidrosis in this family.[6]

The expression of the AQP5 protein and AQP5 mRNA was significantly higher in a patient group in comparison to the control group. In 2011, using a control group (individuals without primary focal hyperhidrosis) and a patient group (individuals with primary focal hyperhidrosis) researchers found that there was no difference between the number of sweat coils in the axillary sweat glands. This indicates that there is nothing morphologically different between individuals with and without primary focal hyperhidrosis. The discrepancies between the studies above call on further studies to confirm or deny the role of AQP5, and the role of other proteins, in hyperhidrosis.[7]

Beyond looking at the genes and individual proteins that play a role in primary focal hyperhidrosis, researchers have looked at the patterns of heredity for this trait. In a 2003 study, using multiple families, researchers found that primary focal hyperhidrosis was not a sex-linked gene, since male-to-male transmission was seen in multiple families. Instead evidence supported an autosomal dominant pattern of inheritance with an incomplete disease penetrance. 21 patients in this study reported a positive family history of hyperhidrosis (62%). Researchers were able to uncover this by creating pedigrees of all the participants in the study. Not every member of the pedigree exhibited forms of hyperhidrosis, which allowed the researchers to track the patterns of inheritance. The findings in this study indicated that primary focal hyperhidrosis is typically an hereditary disorder.[8]

Diagnosis

[edit]

Typical regions of excessive sweating include the hand palms, underarms, the sole of the foot, and sometimes groin, face, and scalp. Indeed, profuse sweating is present mostly in the underarms, followed by the feet, palms and facial region.[9]

Evidence demonstrates that a positive family history is also present (see the Genetics part).[10]

Treatments

[edit]

The Canadian Hyperhidrosis Advisory Committee has published a comprehensive set of guidelines which outlines key aspects of treatment related to this condition. Topical hyperhidrosis gels containing aluminum chloride hexahydrate are usually first choice treatments for this condition.[3]

In addition to topical antiperspirants (whose main active ingredients usually are aluminum or zirconium salts) treatment options include: iontophoresis (hands, feet), onabotulinum­toxinA (Botox) injections (underarms, hands, feet, and other localized areas),[11] electromagnetic/microwave energy thermolysis of underarm sweat glands (miraDry),[12] laser-assisted removal of the sweat glands (underarms),[13] other local procedures such as liposuction and curettage of the sweat glands (underarms), medications of the anticholinergic type that are taken by mouth, and sympathectomy surgery for sweating of the hands or head that can't be controlled by other means.[13]

Sofpironium bromide is approved for the treatment of primary axillary hyperhidrosis.[14]

References

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Focal hyperhidrosis

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Focal , also known as primary , is a medical condition characterized by excessive sweating in localized areas of the body, such as the palms, soles, underarms, and face, that occurs independently of heat, exercise, or emotional stress. This form of is idiopathic, meaning it arises without an identifiable underlying medical cause, and primarily affects otherwise healthy individuals through overactivity of the eccrine sweat glands due to faulty signals. Unlike secondary hyperhidrosis, which results from systemic conditions like or disorders and often involves generalized sweating, focal hyperhidrosis is confined to specific regions and is bilateral, typically ceasing during . The condition affects approximately 2.8% to 3% of the general , with no significant predominance, though it is more prevalent among individuals of Japanese descent. Onset usually occurs during childhood or , with an average age of 25 years, and symptoms often peak in the second or third decade of life and typically persist, though some older reports suggest potential improvement in later years. Common sites include the axillae (underarms, affecting 51% of cases), feet (29%), palms (25%), and face or (20%), where sweating can be visible as beads of or lead to wet clothing and . A familial pattern is observed in 30% to 50% of cases, suggesting a that may involve hyperactivity of the . Symptoms manifest as profuse, uncontrollable sweating that interferes with daily activities, such as gripping objects, writing, or social interactions like handshaking, and may be exacerbated by triggers including anxiety, high humidity, , or physical exertion. Additional complications can include skin softening and peeling, chafing, secondary infections, or due to bacterial overgrowth in moist areas. The excessive sweating stems from overstimulation of receptors on eccrine glands, leading to increased release and impaired thermoregulatory feedback in the . This autonomic dysfunction results in sweating that exceeds the body's needs for temperature control, significantly impacting for those affected.

Overview and Classification

Definition and Characteristics

Focal , also known as primary hyperhidrosis, is defined as idiopathic excessive sweating confined to specific focal areas of the body, occurring at levels that exceed the physiological requirements for and without an identifiable underlying cause. This condition manifests in otherwise healthy individuals, with sweating episodes happening at least once per week and typically not during sleep. Key characteristics include a symmetric distribution affecting both sides of the body equally and an onset that usually begins in childhood or , often before the age of 25 years. Unlike generalized , which involves widespread sweating over the entire body, focal hyperhidrosis is limited to discrete regions and is not associated with systemic disorders. It is also distinct from secondary hyperhidrosis, where excessive sweating results from an underlying medical condition, medication, or external factor, often presenting more diffusely and potentially during sleep.

Types and Affected Areas

Focal hyperhidrosis is classified into subtypes based on the primary affected body regions, with the most common forms involving the palms, soles, axillae, face or , and areas around the triggered by . Palmar hyperhidrosis affects the hands, leading to excessive sweating on the palms; plantar hyperhidrosis impacts the feet, particularly the soles; axillary hyperhidrosis occurs in the underarm areas; craniofacial hyperhidrosis involves the face and ; and gustatory hyperhidrosis manifests as sweating around the or face during gustatory , such as spicy foods. Prevalence varies by subtype and age group, with axillary hyperhidrosis being the most common overall, affecting approximately 50-68% of cases in adults, while palmar and plantar forms predominate in adolescents, often with onset before age 18. Craniofacial hyperhidrosis accounts for about 20% of cases, and gustatory hyperhidrosis is less frequent at around 2%. These subtypes primarily involve the eccrine sweat glands, which are densely concentrated in apocrine-poor areas such as the palms and soles, where they produce a watery, odorless sweat in response to signals, independent of . Rare variants include isolated hyperhidrosis of the trunk or thighs, which may present as localized or segmental sweating without involvement of the typical sites.

Etiology and Pathophysiology

Genetic Factors

Focal hyperhidrosis exhibits strong familial aggregation, with studies reporting that up to 65% of affected individuals have a positive family history, indicating a significant hereditary component. This pattern suggests an autosomal dominant mode of inheritance with variable , as evidenced by multi-generational transmission observed in multiple pedigrees, without . The variable accounts for skipped generations and incomplete expression within families, supporting the genetic basis while highlighting the role of modifying factors. Genome-wide linkage analyses have identified specific chromosomal loci associated with focal , particularly primary palmar hyperhidrosis. One key locus maps to 14q11.2-q13, spanning approximately 6 cM between markers D14S1070 and D14S990, based on linkage studies in affected families showing maximum scores exceeding 3.0. This region is implicated in regulation, though no specific causative has been definitively identified within it. Additional loci, such as on 2q31.1, have been reported in other family cohorts, underscoring . Genetic associations extend to variants in genes involved in the signaling pathway, which regulates activity. For instance, polymorphisms in the (BCHE) gene, including the -116A variant (rs1126680) and K-variant (rs1803274), have been observed exclusively in patients with primary , suggesting a contributory role in cholinergic metabolism. Similarly, the alpha 1 subunit (CHRNA1) has been linked to enhanced responsiveness in affected individuals. Candidate genes such as 1,4,5-trisphosphate receptor type 2 (ITPR2) and forkhead box A1 (FOXA1) have also been implicated in regulation. Overall, focal hyperhidrosis is considered a polygenic disorder, arising from the interaction of multiple genetic variants rather than a single , which explains the variability in clinical presentation and the incomplete linkage to any one locus across all cases. This multifactorial genetic architecture likely interacts with environmental influences to trigger overactive eccrine glands in predisposed individuals.

Pathophysiological Mechanisms

Focal hyperhidrosis arises from the overstimulation of eccrine sweat glands by the , which is in this context, leading to excessive release at neuroglandular junctions independent of thermoregulatory demands. This neurogenic overactivity results in profuse in localized areas, driven by heightened sympathetic impulses that exceed normal physiological responses to emotional or stimuli. The eccrine glands themselves remain structurally normal, with no increase in gland number or histopathological changes, indicating that the disorder stems from functional hyperactivity rather than glandular abnormalities. Central nervous system involvement plays a key role, with dysregulation potentially originating in the , which serves as the primary sweat center integrating emotional and signals. Hyperactivity or reduced inhibition in hypothalamic pathways may lead to abnormal cortical control of emotional sweating, distinct from , as evidenced by the absence of sweating during in affected individuals. Projections from the descend to the spinal cord's intermediolateral cell column at levels T2-T3, where sympathetic preganglionic neurons exhibit increased activity, amplifying signals to postganglionic fibers. Peripheral components, including a larger number of cells and elevated expression in thoracic sympathetic chain ganglia, further contribute to this overexcitation. Aquaporin-5 (AQP5), a channel protein in the apical membrane of ductal cells, facilitates rapid water transport essential for sweat secretion and shows dysregulation in focal hyperhidrosis. Studies reveal upregulated AQP5 mRNA and protein expression in sweat glands of patients with palmar, axillary, and craniofacial subtypes compared to controls, correlating with enhanced acetylcholine-induced that boosts sweat production. This overexpression increases membrane water permeability without altering gland morphology, supporting AQP5's role in the functional excess of sweat output.

Clinical Presentation

Symptoms and Signs

Focal hyperhidrosis manifests primarily as visible, profuse sweating confined to specific areas of the body, such as the palms, soles, axillae, or craniofacial , where eccrine sweat glands are densely concentrated. This sweating is typically bilateral and symmetric, often appearing as beads of moisture or soaking through clothing and is not provoked by underlying medical conditions. It is frequently triggered by emotional stress, anxiety, , , or , though it can occur spontaneously without an identifiable stimulus. Notably, sweating does not occur during , distinguishing it from secondary forms. The excessive moisture leads to associated signs, including , where the affected areas become soft, wrinkled, pale, or fissured due to prolonged wetness. This environment promotes bacterial overgrowth, resulting in an unpleasant odor from the breakdown of sweat components. Secondary complications may include skin infections, such as or fungal issues, characterized by redness, swelling, peeling, or pain in the sweaty regions. Symptoms are often episodic or continuous, occurring at least once a week, with symptoms persisting for at least six months, and they tend to worsen with anxiety or emotional triggers. On , the condition is evident through direct observation of damp skin in focal areas, and a confirmatory starch-iodine test—applying iodine solution followed by powder—produces a blue-black discoloration precisely where sweating occurs, aiding in localization.

Impact on Quality of Life

Focal hyperhidrosis significantly impairs patients' quality of life, with up to 48% reporting poor or very poor overall well-being due to the condition's disruptive effects on daily activities. This impairment is comparable to that experienced in chronic conditions such as severe or advanced , as measured by validated quality-of-life instruments. Patients often describe a profound sense of limitation, where excessive sweating in focal areas like the palms, axillae, or face hinders routine interactions and personal choices, leading to a mean quality-of-life score of 52.4 on a 20-100 scale (higher indicating worse impact). Socially, focal hyperhidrosis fosters stigma and isolation, with 75% of patients experiencing impaired social lives, including avoidance of handshakes, , and social events due to visible sweating and fear of judgment. Approximately 64% report fearing negative reactions from others, such as glares or misunderstandings, which exacerbate (reported by 33.3%) and (25%). These experiences contribute to reduced self-confidence and a reluctance to engage in communal activities, further compounding emotional distress. Occupationally, the condition interferes with professional functioning, affecting 63% of patients through challenges in tasks requiring manual dexterity, such as typing or surgical procedures, or in roles involving customer interaction. Palmar hyperhidrosis, in particular, is associated with a mean loss of 7.24%, prompting 33% of individuals to select careers that accommodate their symptoms, like avoiding client-facing positions. Such limitations not only hinder career advancement but also influence clothing choices and daily work habits to mitigate visible sweating. Psychologically, focal hyperhidrosis elevates rates of anxiety (ranging from 0-49%) and depression (0-60%), with 11.6% of those with localized forms experiencing depression and a higher (39.2%) in moderate-to-severe cases. This often manifests as a "" of nervousness triggering further sweating, leading to diminished and , particularly among females. Studies utilizing the Hyperhidrosis Disease Severity Scale (HDSS) show that 70% of patients score 3 or 4, indicating severe disease, which strongly correlates with Dermatology Life Quality Index (DLQI) scores of 11-20, reflecting a very large effect on . For instance, median DLQI scores reach 13.5 in axillary cases, underscoring the condition's substantial psychological burden.

Diagnosis

Diagnostic Criteria

The diagnosis of focal hyperhidrosis, also known as primary , relies on established clinical guidelines from the International Hyperhidrosis Society (IHS), which emphasize focal, symmetric sweating without identifiable secondary causes. Key criteria include bilateral and focal excessive sweating that has persisted for at least 6 months, occurring in at least two episodes per week, with onset typically in childhood or (though craniofacial involvement may begin later). The sweating must cease during , show no continuous pattern, and not be attributable to underlying medical conditions, medications, or physiological triggers alone; additionally, it should impair daily activities to warrant . Severity is assessed using the Hyperhidrosis Disease Severity Scale (HDSS), a validated four-point qualitative tool that evaluates the impact of sweating on daily life.03534-5/fulltext) Patients rate their condition by answering: "How would you rate the severity of your hyperhidrosis?" with options ranging from grade 1 (never noticeable and never interferes with daily activities) to grade 4 (intolerable and always interferes with daily activities). Scores of 3 or 4 indicate severe requiring intervention, while a one- or two-point improvement post-treatment correlates with approximately 50% or 80% sweat reduction, respectively. A thorough is essential for confirming the and guiding . This includes documenting the age of onset, family history (reported in up to two-thirds of cases), emotional or environmental triggers, and patterns of sweating to exclude secondary . Objective confirmation involves gravimetric testing, which quantifies sweat production by weighing the increase in weight of an absorbent material (e.g., ) applied to or wiped across the affected area before and after a standardized period, such as 1 minute, under controlled conditions. Results are often normalized by to assess severity. This method is reproducible and useful for baseline assessment and monitoring treatment efficacy.

Differential Diagnosis and Tests

Focal hyperhidrosis must be differentiated from secondary hyperhidrosis caused by underlying medical conditions, which can mimic its focal presentation but often involves generalized sweating or additional systemic symptoms. Key differentials include endocrine disorders such as , diabetes mellitus, , and ; neurological conditions like neuropathy, , or ; infectious or neoplastic causes including tuberculosis or lymphoma; and medication-induced sweating from antidepressants like SSRIs or antipsychotics. Anxiety disorders can also present with excessive sweating as part of heightened autonomic arousal, particularly in social situations, warranting consideration in the differential. Dermatological conditions like palmoplantar pustulosis may mimic palmoplantar focal hyperhidrosis due to associated sweat leakage and inflammatory changes on the palms and soles. To exclude secondary causes, initial laboratory tests are essential, including (e.g., TSH levels) to rule out , fasting blood glucose or hemoglobin A1c for , and pregnancy tests in women of childbearing age to identify hormonal influences. A , , sedimentation rate, and testing help detect infections, malignancies, renal dysfunction, or disorders. Additionally, a assesses for autonomic dysfunction, such as asymmetric reflexes or sensory deficits suggestive of neuropathy or central lesions. Advanced confirmatory tests focus on sweat gland function and pattern to distinguish primary focal hyperhidrosis from mimics. The thermoregulatory sweat test involves applying indicator solution to the skin and exposing the body to thermal stress, revealing anhidrotic or hyperhidrotic patterns that indicate eccrine gland abnormalities or autonomic neuropathy. The quantitative sudomotor axon reflex test (QSART) measures sweat output in response to iontophoresis of pilocarpine, quantifying nerve-mediated sweat production to evaluate postganglionic sudomotor function and exclude small-fiber neuropathy. These tests are particularly useful when clinical history suggests possible neurological involvement. Red flags prompting investigation for secondary causes include asymmetric or unilateral sweating, onset after age 25, , or accompanying systemic symptoms like , fever, or , which deviate from the typical bilateral, symmetric, and diurnal pattern of primary focal hyperhidrosis.

Treatment and Management

Topical and Conservative Therapies

Topical antiperspirants represent the first-line treatment for focal hyperhidrosis, particularly for mild to moderate cases affecting the axillae, palms, or soles. Aluminum hexahydrate, typically in 20% concentrations such as Drysol, works by precipitating metal ions with mucopolysaccharides in the sweat ducts, forming a temporary plug that blocks without halting sweat gland production. Patients are advised to apply the solution to completely dry skin at bedtime, allowing it to remain for 6-8 hours before washing off in the morning, starting with nightly use until improvement occurs and then tapering to maintenance applications once or twice weekly. Clinical studies indicate that this approach can achieve up to 82% patient satisfaction for axillary sweating and reduce transepidermal water loss by 30% after four weeks for palmar involvement, though skin irritation may occur and requires application avoidance after . Topical anticholinergic agents offer an additional first-line option, especially for axillary . Sofpironium bromide gel 12.45% (Sofdra), approved by the in June 2024 for primary axillary in adults and pediatric patients aged 9 years and older, is applied once daily at bedtime to each using a provided applicator and allowed to dry for at least 5 minutes. Phase 3 clinical trials (CARDIGAN-1 and CARDIGAN-2) involving over 700 patients showed that 49% to 64% of treated patients achieved at least a 2-point improvement on the Hyperhidrosis Disease Severity Measure for Axillae (HDSM-Ax-7) scale at week 6, compared to 29% to 48% with vehicle control; more than 60% experienced at least 50% reduction in gravimetric sweat production. Common adverse effects include dry mouth (14%), (9%), (7%), and application-site reactions such as pain (8%) and (7%). Lifestyle modifications complement topical therapies by addressing environmental and behavioral triggers that exacerbate focal symptoms. Recommendations include wearing breathable fabrics like or moisture-wicking materials to facilitate and reduce moisture buildup, along with using absorbent powders or insoles in shoes to manage plantar sweating. Individuals are encouraged to avoid known triggers such as spicy foods, , alcohol, and emotional stressors, which can stimulate eccrine glands; maintaining a sweat journal helps identify personal precipitants for targeted avoidance. These non-pharmacological strategies improve daily comfort and can enhance , particularly when combined with severity assessments from diagnostic evaluations. Iontophoresis offers a device-based conservative option primarily for palmar and plantar focal , utilizing a mild electrical current passed through or solutions like glycopyrrolate to temporarily disrupt function, possibly by inducing in the ducts. Sessions typically last 20-30 minutes, conducted 2-3 times per week initially with hands or feet immersed in shallow trays connected to the device, followed by maintenance once weekly. data from clinical observations show reductions in sweating by 81-91% in responsive patients, with minimal side effects like transient dryness or tingling, though long-term adherence is necessary for sustained benefits. Home remedies such as sage tea or baking soda applications have been explored for symptom relief in focal hyperhidrosis but lack robust scientific validation and are not recommended as primary interventions. Sage, consumed as tea or applied topically, may contain that constrict sweat glands, yet evidence is anecdotal with unknown efficacy and potential for interactions. Baking soda can absorb moisture when used as a but risks irritation or post-inflammatory , particularly in darker tones, without proven long-term reduction in sweating. Consultation with a healthcare provider is essential before incorporating these, as they do not substitute for evidence-based conservative therapies.

Interventional and Pharmacological Options

For patients with focal hyperhidrosis refractory to topical therapies, injections represent a key interventional option by temporarily inhibiting release at the , thereby reducing stimulation. OnabotulinumtoxinA (Botox) is FDA-approved for severe primary axillary hyperhidrosis in adults when antiperspirants are inadequate, with intradermal administration of 50-100 units per axilla distributed across 10-20 sites. Clinical studies demonstrate significant efficacy, with 80-90% reduction in axillary sweat production lasting 4-12 months, though duration may extend to 9-12 months with repeated treatments. Common side effects include injection-site pain and transient , but the procedure is generally well-tolerated and reversible. Oral s offer systemic pharmacological control by blocking muscarinic receptors to suppress eccrine gland secretion, suitable for multifocal or widespread focal . Glycopyrrolate, at doses of 1-2 mg twice daily (up to 4 mg/day), or , at 5-10 mg/day (titrated to 15-20 mg if needed), achieve 50-70% sweat reduction in responsive patients, particularly for palmar or plantar involvement. Efficacy varies by individual tolerance, with studies showing improvement in severity scores within 2-4 weeks of initiation. However, anticholinergic side effects such as dry mouth (affecting up to 70% of users), , , and limit long-term adherence, necessitating dose adjustments or discontinuation in some cases. Microwave thermolysis using the miraDry system provides a for permanent axillary sweat reduction by delivering targeted electromagnetic energy to destroy eccrine glands through thermolysis, sparing surrounding tissues via a hydro-cooling mechanism. FDA-cleared for primary axillary , it typically requires 1-2 sessions spaced 3-6 months apart, each lasting about 60 minutes under . Pivotal trials report 80-82% average sweat reduction persisting beyond 12 months, with high patient satisfaction due to its durability compared to injectables. Adverse effects are mostly transient, including swelling, numbness, and discomfort resolving within 1-2 weeks, though axillary and altered sensation may occur. For exacerbated by emotional triggers, of beta-blockers like (10-40 mg as needed) or (0.1-0.4 mg/day) can modulate sympathetic outflow to reduce episodic sweating, though evidence remains limited to case series and small studies. Beta-blockers inhibit adrenergic stimulation of sweat glands, showing modest efficacy in stress-induced palmar or craniofacial cases without significant cardiac risks at low doses. , an alpha-2 agonist, similarly attenuates central sympathetic activity, with reports of 50-75% symptom relief in focal subtypes, but monitoring for and is advised. These agents are often trialed briefly before escalating to more definitive interventions.

Surgical Interventions

Surgical interventions are reserved for patients with severe, treatment-resistant focal hyperhidrosis, typically those scoring 3 or 4 on the Hyperhidrosis Disease Severity Scale (HDSS) after failure of conservative and pharmacological options. These procedures aim to provide permanent relief by disrupting function or sympathetic innervation, though they carry risks of irreversible side effects such as compensatory hyperhidrosis. Endoscopic thoracic sympathectomy (ETS) is the most established surgical approach for palmar and axillary , involving video-assisted thoracoscopic interruption of the sympathetic chain, usually by clipping or cutting at the T2-T4 levels. Success rates for achieving dryness or significant reduction in targeted areas range from 85% to 95%, with long-term efficacy reported at 94.5% for palmar and axillary symptoms. However, compensatory occurs in 60% to 80% of cases, often affecting the trunk or lower body, leading to dissatisfaction in up to 20-30% of patients over time. Other risks include (1-2.5%), gustatory sweating (up to 50%), and compensatory anhidrosis, with procedural complications like occurring in less than 5%. For axillary , local excision or targets eccrine sweat glands directly through minimally invasive techniques such as tumescent liposuction-assisted removal or subcutaneous scraping (Shelley's procedure). These methods yield good to excellent results in 82-90% of cases, with sustained sweat reduction in over 80% at one-year follow-up and minimal impact on surrounding tissues. Risks are generally low, including , scarring, or in under 10%, making this suitable for localized disease without systemic effects. Emerging options like , particularly with Nd:YAG lasers, offer focal destruction of sweat glands in the axillae via subdermal energy delivery. Studies report 65-70% sweat reduction immediately post-treatment, with 83% of achieving good to excellent outcomes (>50% improvement) after multiple sessions. Side effects are mild and transient, such as pain (90%), irritation (25%), or (100%), with no reports of compensatory in small cohorts. Patient selection emphasizes younger individuals (<25 years), low BMI (<28), early-onset symptoms, and absence of sleep-related sweating to optimize outcomes and minimize complications across all procedures.

Epidemiology

Prevalence and Incidence

Focal hyperhidrosis, also known as primary , affects an estimated 1-5% of the global , with rates varying across studies due to differences in diagnostic criteria and reporting methods. In the United States, the condition is reported in approximately 4.8% of individuals, equating to about 15.3 million people, though this figure may underestimate the true burden as many cases remain undiagnosed. The is considered underreported globally owing to associated , which discourages individuals from seeking medical evaluation or participating in surveys. Incidence rates for focal hyperhidrosis are lower, ranging from 0.13% in the to 0.28% , reflecting the typically early-life onset rather than frequent new cases in adulthood. The condition most commonly begins during , with average onset ages of 13 years for palmar and axillary forms, though it can emerge as early as childhood or up to 25 years. Once established, focal hyperhidrosis tends to remain stable throughout adulthood without spontaneous progression or resolution in most cases. Geographic variations in have been observed, with higher rates reported in warmer s such as tropical or subtropical regions, where environmental factors may exacerbate sweating and influence reporting. For instance, studies indicate a of 4.8% in compared to around 5.5% in , though broader European estimates sometimes fall lower at 1-2% in certain populations. In Asian urban settings like , self-reported reaches 14.5%, potentially linked to both and higher awareness. Prevalence estimates have remained relatively stable across studies, though increased awareness since the early has likely led to higher rates.

Demographic Patterns

Focal , a form of primary characterized by excessive sweating in localized areas such as the palms, soles, axillae, or face, typically manifests early in life. The condition most commonly begins during childhood or , with mean ages of onset reported between 14 and 20 years across multiple studies. peaks in younger adults, particularly those under 30 years of age, where rates can reach 8.8% in the 18–39 age group, and declines sharply thereafter, dropping to 4.2% in the 40–64 age group and 2.1% in those under 18 or over 65. This age-related pattern holds in diverse populations, including outpatients in and , with odds ratios indicating up to sixfold higher likelihood in individuals younger than 30 compared to those over 60. Gender distribution in focal hyperhidrosis shows variability across studies, with no consistent predominance. In a cohort of medical students in , prevalence was similar between males (23.1%) and females (19.4%), suggesting comparable risk. However, clinic-based studies from the and report a slight female majority, with 62.8% of patients being , potentially reflecting differences in healthcare-seeking behavior or site-specific involvement, such as higher plantar sweating in women. Males, in contrast, may experience greater or involvement in some populations. Overall, gender ratios hover near parity in community surveys but tilt toward females in treatment-seeking groups. Ethnic and racial patterns reveal geographic and population-specific differences, with Caucasians demonstrating higher rates of certain subtypes, particularly axillary hyperhidrosis, at 2.5 to 5 times the prevalence seen in Chinese populations. Individuals of Japanese descent show particularly high rates of palmoplantar hyperhidrosis, reportedly up to 20 times more frequent than in other ethnic groups. In the United States, over 87% of affected individuals in clinical samples are Caucasian, alongside smaller proportions of African-American (8.4%) and Asian (1.7%) patients, which may reflect both genetic predispositions and access to care. Conversely, in , non-white and mixed-race groups exhibit higher prevalence (24.2%) compared to whites (19.3%), indicating potential environmental or genetic modifiers. Global variations persist, with overall primary hyperhidrosis rates ranging from 3.2% in Indian populations to 16.3% in German cohorts, underscoring the influence of and regional factors. A notable familial component affects demographics, with 35–65% of cases reporting positive family history, suggesting hereditary influences that may cluster within certain ethnic or age groups. has been linked to late-onset forms but not typically to early-onset focal hyperhidrosis. These patterns highlight the interplay of genetic, environmental, and socioeconomic elements in the distribution of the condition.

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