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• W3201466287 abstract "The human body contains approximately 3 million eccrine sweat glands. These glands are unevenly distributed and mediate thermoregulation through the evaporation of secreted sweat. This physiological function is disordered in hyperhidrosis (HH), a state of excessive sweating over and above what is physiological, and is a mysterious but common disorder. With an estimated prevalence of 4.8% of the US population,1 it probably afflicts approximately 1.2 million Australians in our nation of 26 million people. The impact on lives is substantial, with significant social isolation, poor self-esteem, decreased leisure activities, anxiety and depression in sufferers. This impairment of quality of life is equivalent to many chronic diseases such as rheumatoid arthritis, multiple sclerosis and end-stage renal failure.2 There is often a family history, implying a genetic susceptibility, sometimes autosomal dominant, with some loci identified in several studies.3, 4 Therefore, it is self-evident to most that this disease is poorly recognised. To some extent, the reason for this is patient embarrassment. They may not broach the problem, but often, when acknowledged by the clinician, it suffers from insufficient attributed importance, as patients are morbid rather than there being any threat to life. Under-recognition is also probably in no small part because the subject is poorly taught to clinicians, both at undergraduate and postgraduate level; the condition still appears to remain the realm of specialists such as neurologists, dermatologists and a sprinkling of other specialties such as endocrinology. Given the above, it is unsurprising that cosmetic clinics have stepped into the fray, offering treatments for various sweating body parts, as botulinum toxin injection already forms part of their suite of procedures. However, this does not obviate the need for a proper clinical evaluation of each patient with HH. One needs to be vigilant for secondary causes of HH; there are many including acute and chronic infection (e.g. TB, HIV), endocrinopathies (e.g. diabetes mellitus, states of hormonal excess such as thyroid, catecholamines, growth hormone, pituitary lesions, carcinoid), malignancy (haematological and solid), cardiac/respiratory failure, neurological conditions (e.g. stroke, Parkinson disease and myelopathy) and drugs both proprietary and recreational. The history is often sufficient to differentiate secondary causes.5 Clinical pointers to these include the presence of nocturnal as well as daytime sweating, and a generalised distribution although a focal or regional predilection is also possible.6 However, despite these caveats, the vast majority of abnormal sweating falls under the rubric of idiopathic focal, affecting the axillary, palmoplantar and craniofacial regions in descending order of prevalence. One suspects extremity sweating would be more problematic, but an audit of this disease conducted at our centre on 200 consecutive patients in an 11-month period in 2019 did not confirm that palmoplantar HH was more impactful on lifestyle than axillary HH, with quite similar HH disease severity scale (HDSS, range 1–4) scores for both (mean HDSS: palmoplantar alone 3.52 (n = 21), palmoplantar in combination 3.44 (n = 54), cf. axillary alone 3.50 (n = 95), P = NS).7 Frequent complaints from patients with HH include bodily discomfort, social anxiety and restricted choice of clothing (black being preferred). Peculiar to palmar HH is the impaired manual handling of objects and inability to shake hands. An encounter with a patient with severe palmar or plantar HH with literally dripping extremities, once witnessed is difficult to forget. In this issue of the Internal Medicine Journal, the authors retrospectively studied 30 palmar HH patients over a 4-year period, and analysed response rates to botulinum toxin injections into the palms.8 These treatments are delivered intradermally in a grid pattern spaced roughly 1 cm apart between injections. On average, their patients received two treatments. In summary, there was a 3-point reduction in the HDSS from 4 to 1, on a scale of 1–4. Studies have shown a 1-point reduction translates to a 50% reduction in sweating, and 2 points to approximately 80%.6 Therefore, as commonly observed, the effect of this therapy is dramatic, and provides strong evidence for its use, and it is supported by several randomised controlled trials to date.9, 10 However, the procedure is invasive. Many would advocate the prior use of topical antiperspirants containing high-dose aluminium and even iontophoresis11 (53% and 17% respectively in this study) before selecting toxin. The latter involves considerable time outlay for the patient, requiring immersion of the extremities in a tap water receptacle running a small DC current, sometimes mixed with a small amount of bicarbonate of soda or glycopyrrolate to increase efficacy. Botulinum toxin is no doubt effective, but the treatment trade-off can be a weakness from diffusion of toxin from the intradermal injections to the small muscles of the hand.12 This is seen in only one-quarter of patients in most studies including this one, and mirrors our experience of this technique. This particular side-effect is often short-lived, and we have found it unusual for a patient to cite this as a reason for discontinuation of this form of therapy. Nevertheless, consideration of oral medications is occasionally warranted, as many of these sufferers also suffer from HH in other areas; they are usually deployed after toxin. Oral medications come from a few classes, and one of the most frequently used are anticholinergic agents, which often carry systemic side-effects especially in the doses required to effect euhydrosis. This is with the notable exception of craniofacial HH where it is usually more efficacious. There are also concerns, at least in the elderly, of long-term development of mild cognitive impairment,13 therefore favouring the use of agents such as glycopyrrolate, which does not cross the blood–brain barrier. Despite such results, the number of patients treated with botulinum toxin for palmar sweating is still not half of those on axillary treatment in Australia, despite it being about half as prevalent.14 Some of the aforementioned side-effects are important, but there are other particular factors that are also likely to contribute to the lack of uptake. First, the treatment is not presently available on the Pharmaceutical Benefits Scheme (PBS), and there is no rebatable billing item for the injection procedure under the Medicare Benefits Schedule (MBS). This is unlike severe axillary HH where this treatment is permissible, provided the patient has tried and failed high-dose aluminium containing topical agents.15 Therefore, costs of toxin itself, as well as the necessary expertise for injection, can be high. Second, and this is directly related to the first point, is the duration of effect. Usually, a longer duration of more than 4 months is frequently achieved,11 but the study does recapitulate an experience that many injectors have noticed, that the duration appears to increase when more treatments are rendered. This phenomenon would appear not to be peculiar to this region, being observed in axillary sites as well. Last, the mode of delivery bears consideration which has not been extensively discussed in this study. Many patients rate the injections as painful without adequate analgesia, which may contribute to their reticence to have regular treatment. Topical anaesthetic creams, ice and vibration interferential modalities have been used, but are somewhat cumbersome. Nerve blockade, which can involve more than just median and ulnar nerves at the wrist, should probably only be undertaken with the assistance of ultrasound, as is the prevailing practice these days to reduce the risk of inadvertent intraneural injection. We have found the use of methoxyflurane-inhaled anaesthesia, the so-called ‘green stick’ often used by paramedical and acute responder staff, to be a safe and effective way to deliver toxin in an acceptable fashion. In the discussion, the authors cite an interesting observation in a previous study of improvement of plantar HH in a subset of patients with palmar HH that are treated with toxin.16 Both palmar and plantar HH often co-exist, and this observation not only permits the understanding of the central neural and psychological factors that contribute to perpetuation of inordinate sweating, but also allows a more limited regional initial treatment strategy restricted to the palms. This is desirable as frequently, very high doses of toxin are required in plantar HH. Psychological counselling can be a beneficial adjunctive therapy. This study serves to highlight the importance of botulinum toxin in the armamentarium of clinicians treating HH. Toxin assumes greater importance in more severe cases, as recognition of all the complications of sympathectomy has relegated such a procedure to an option of last resort. Unfortunately, promising new but expensive therapies like microwave thermolysis are not recommended in the extremities, because of the risk of neurovascular injury in these adipose-thin areas. It would be desirable if there is greater public and policy-making recognition soon that palmar and plantar HH are just as much a curse as axillary HH, and that could pave the way for a much-needed future listing of toxin treatment on the PBS/MBS. Dr Jordan Weastell, neurophysiology fellow, for conducting the Sydney North Neurology and Neurophysiology (SNNN) audit." @default.
• W3201466287 created "2021-09-27" @default.
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• W3201466287 date "2021-09-01" @default.
• W3201466287 modified "2023-10-17" @default.
• W3201466287 title "Time to sweat the small stuff: hyperhidrosis, a problem of epidemic proportions" @default.
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