Excessive Sweating (Hyperhidrosis): Causes and Treatment

Sweating is regulated mainly by eccrine glands. Humans have several million of them, with the highest density on the palms, soles, underarms and face. They are stimulated by the sympathetic nervous system, but unusually the mediator at the nerve endings is acetylcholine, not noradrenaline. That is why drugs with anticholinergic action (both topical and oral) and botulinum toxin, which blocks acetylcholine release, effectively reduce sweating. Apocrine glands, concentrated in the underarms and genital area, secrete a thicker fluid that is itself odourless; the smell arises only when skin bacteria break it down. Odour (bromhidrosis) and hyperhidrosis are therefore two related but separate problems.

In primary hyperhidrosis the glands are usually normal in structure and number; what seems disturbed is an excessive response of the centres controlling sweating to stimuli that would produce only a small reaction in other people. Hence the typical features: symmetrical, focal sweating that worsens with emotion and stops during sleep. The exact mechanism is not fully understood, and in some families inheritance is observed, which confirms that this is not about 'poor hygiene' or 'weak nerves'.

A second level of explanation concerns the types of triggers. Thermoregulatory sweating involves the whole body and depends on core temperature. Emotional sweating (stress, anxiety, embarrassment) affects mainly the palms, soles, underarms and forehead. Gustatory sweating appears after spicy food and affects the face. People with primary hyperhidrosis usually describe a mix of these triggers, and simply expecting to sweat can be an additional trigger, creating a vicious circle: shame increases stress, stress increases sweat.

This is the most important distinction in the whole topic, because it decides whether we look for a disease or treat the symptom right away. Primary focal hyperhidrosis usually affects the underarms, palms, soles or face and head, is symmetrical (on both sides of the body), most often starts in childhood or youth, frequently runs in the family, and almost always stops during sleep. The secondary form can be focal or generalised, usually begins later, may be asymmetrical, also occurs at night and comes with other symptoms such as fever, weight loss, palpitations, tremor or abnormal test results.

In practice the doctor asks about age at onset, family history, the sites of sweating and whether the symptom continues at night. With a typical picture of the primary form, extensive testing is not necessary. Severity is assessed with the HDSS (Hyperhidrosis Disease Severity Scale), a four-point scale based on how much sweating interferes with daily life; the result helps choose treatment intensity. The Minor test, in which the skin is painted with iodine solution and dusted with starch so that areas of active sweating turn dark, is used to visualise the affected areas, for example before toxin injections.

The list of secondary causes is long, but a few groups appear most often. Hormonal and metabolic disorders: hyperthyroidism (sweating, palpitations, tremor, weight loss despite appetite), diabetes and hypoglycaemia (sweating as an adrenergic symptom), menopause and perimenopause (hot flushes, heavier sweating), and less often acromegaly and pheochromocytoma. Infections: tuberculosis, brucellosis, endocarditis, HIV, usually with fever and weakness. Cancers: lymphomas and other blood malignancies, which can cause night sweats, fever and weight loss. Neurological diseases and autonomic disorders, as well as anxiety disorders and obesity.

Drugs are a separate, often overlooked group. Sweating as a side effect can be caused by, among others, some antidepressants (SSRIs, SNRIs, tricyclics), opioids, some antidiabetic drugs (during hypoglycaemic episodes), drugs used in hormonal cancer therapy (tamoxifen, aromatase inhibitors), as well as excess caffeine, alcohol and withdrawal syndromes. If sweating appeared within a few weeks of starting a new drug, that is an important clue to report to the prescribing doctor; never stop a medication on your own.

Laboratory tests for suspected secondary hyperhidrosis are chosen according to the clinical picture, not from a single 'sweating panel'. Most often doctors consider TSH and thyroid hormones, glucose or HbA1c, a blood count with differential, inflammatory markers, and sometimes tests for infection or blood malignancy. We explain the interpretation of basic thyroid results in our knowledge base entry on TSH and thyroid hormones, and the role of sex hormones in sweating in the entry on menopause.

In most recommendations, treatment of focal hyperhidrosis starts with topical aluminium chloride. The review by Nawrocki and Cha (J Am Acad Dermatol, 2019) describes antiperspirants as first-line therapy for primary focal hyperhidrosis, and the review for family physicians (McConaghy and Fosselman, 2018) names topical aluminium chloride solution as the initial treatment in most cases. Aluminium salts form plugs in the sweat gland ducts that mechanically limit secretion, which is why the effect builds over a few days and fades after stopping.

Effectiveness depends on technique. Higher-strength preparations (available in pharmacies, often as solutions or gels containing aluminium chloride) are usually applied in the evening to completely dry skin, when glands are less active and the substance can enter the ducts, and washed off in the morning. At first they are used daily or every other day, then less often as maintenance once the effect is achieved. Damp skin after a shower increases the risk of irritation, so it is worth waiting until it is fully dry. The most common problem is irritation and itching, relieved by using the product every other day, shorter contact time, or a mild corticosteroid cream prescribed by a doctor.

The evidence for this method is largely clinical experience and expert consensus rather than large randomised trials, which is worth remembering when assessing the many promises found online. Ordinary deodorants mask odour but do not reduce sweating; classic drugstore antiperspirants contain lower concentrations of aluminium salts and may be enough only in mild cases. On the palms and soles aluminium chloride usually works less well than in the underarms, and the skin there is thicker, which reduces penetration.

Iontophoresis passes a weak direct current through the hands or feet immersed in trays of water. The exact mechanism remains unclear; hypotheses include a change in the pH of the gland ducts and their temporary blockage. According to the review by Nawrocki and Cha it is the primary remedy for palmar and plantar hyperhidrosis, and the overview in Deutsches Ärzteblatt likewise lists tap water iontophoresis among the non-surgical options.

For home use, iontophoresis devices are available to patients, and a typical regimen is several sessions a week for two to three weeks, then maintenance sessions every few days or weeks. The effect is reversible, so sweating returns after stopping. Side effects include dryness and peeling of the skin, tingling, and occasionally minor burns at very high current. Contraindications include a pacemaker or other implanted electronic devices, metal implants in the treated area, and pregnancy; it is worth discussing this with a doctor before buying a device.

Since sweat is driven by acetylcholine, a logical step is to block its receptors locally in the skin. Topical glycopyrrolate (glycopyrronium) is a drug that has been approved in some countries for axillary hyperhidrosis, and the review for family physicians describes it as first-line treatment for excessive facial sweating. Its availability in Poland depends on registration and reimbursement, so it is worth checking with a doctor or pharmacist rather than assuming it is a routinely available option.

Typical side effects of anticholinergic drugs include dry mouth, pupil dilation and difficulty with near vision (for example after accidental transfer of the drug to the eyes), and when used over larger areas also urinary retention and headaches. For this reason these drugs are used cautiously in people with angle-closure glaucoma, prostate enlargement with urinary retention, and some heart conditions.

When topical treatment is not enough, the next step is botulinum toxin. It blocks the release of acetylcholine at the nerve endings of the glands, so sweating at the injection site decreases, usually for a few months, after which the procedure has to be repeated. The review in Deutsches Ärzteblatt places it after aluminium chloride and anticholinergic drugs in axillary hyperhidrosis, and the review for family physicians describes it as a first- or second-line treatment for hyperhidrosis of the underarms, palms, soles and face. On the palms the injections are painful and may temporarily weaken grip, so anaesthesia is often used.

Oral drugs (oxybutynin, glycopyrrolate, methantheline) are reserved for resistant cases or generalised hyperhidrosis. The systematic review by Cruddas and Baker (2017), covering 23 publications, shows that for oxybutynin symptom improvement was reported in an average of 76.2% of patients, but dry mouth was reported by an average of 73.4% of those taking 10 mg daily, and on average 10.9% of participants stopped treatment because of it. The authors stress that the evidence is limited, mostly observational studies and small trials, and that efficacy goes hand in hand with a considerable number of adverse events.

The remaining methods are energy-based technologies (microwave, ultrasound, radiofrequency), local surgical procedures for axillary hyperhidrosis (excision, curettage, liposuction) and, as a last resort, thoracoscopic sympathectomy for palmar hyperhidrosis. Its serious limitation is compensatory sweating, that is, increased sweating of other body areas (trunk, back, thighs), which in some patients is more troublesome than the original problem and is permanent. The meta-analysis by Cai et al. (2015), covering 11 randomised trials and 1079 patients, did not confirm that restricting or lowering the level of sympathectomy meaningfully reduces compensatory sweating, so this method should be considered only after conservative options have been exhausted and after an honest discussion of the risks.

It is also worth naming honestly what proven methods do not promise: none of them 'cures' primary hyperhidrosis for good, apart from the surgical last resort, and all of them relieve the symptom. A realistic goal is therefore to reduce sweating to a level that no longer interferes, ideally with the lowest possible burden of side effects. Before buying quick, expensive 'miracle' regimens from the internet, consult a doctor and check whether they have any clinical trials at all.

The most important practical lesson from the literature is this: first work out what you are dealing with, and only then choose a therapy. Typical primary hyperhidrosis of the underarms, palms or soles rarely needs extensive testing and usually responds to stepwise treatment, from cheap and safe methods to more advanced ones. New, generalised or night sweats, however, especially with fever, weight loss or palpitations, should be a reason for tests rather than for another antiperspirant.