Severe night sweating treated by oxybutynin.

Sleep hyperhidrosis is defined as profuse nocturnal sweating that disrupts sleep. Although the mechanism is unknown, some cases are secondary to hot flushes during the menopausal period, medical, mental and sleep disorders, and medication, while dysregulation of thermoregulation during sleep is suspected in primary cases. We present the case of a woman with severe primary sleep hyperhidrosis, occurring nightly for 23 years, which definitively resolved after brief treatment with oxybutynin (a muscarinic receptor-blocking anticholinergic). An ammoniacal odor in the sweat and a sensation of coldness on awakening during sweating episodes suggest that the mechanism of her night sweating was not an exacerbation of thermoregulation during the night but shares the mechanical properties of emotional/psychological sweating. This extreme case of sleep hyperhidrosis was treated with excellent efficacy and minimal side effects using oxybutynin, which could benefit other patients with nighttime discomfort. CITATION: Dias L, Martinot C, Vaillant G, Arnulf I. Severe night sweating treated by oxybutynin. J Clin Sleep Med. 2024;20(1):169-172.

Urinary retention and mydriasis secondary to topical glycopyrronium for axillary hyperhidrosis.

PURPOSE: Glycopyrronium, also known as glycopyrrolate, is an antimuscarinic competitive inhibitor of acetylcholine widely utilized topically for its anticholinergic properties in dermatology. A single topical glycopyrronium tosylate (GT) formulation is available on the market, and prescription of this medication has become increasingly popular among dermatologists. This medication has a relatively notable adverse effect profile and carries risks that patients need to be counseled on before initiation. SUMMARY: A 22-year-old female presented to our emergency department (ED) with a chief complaint of difficulty urinating for 48 hours and blurred vision for 2 weeks. Over the course of a week, she visited the ED once and urgent care multiple times due to complications associated with combination use of GT and cetirizine. Although these clinical effects were reversible, the patient impact in our case was profound given the time, cost, and invasive nature of these visits. CONCLUSION: The notable adverse effects of GT should be considered when prescribing this agent.

Mydriasis and anisocoria in a pediatric hyperhidrosis patient with interesting findings in the family cat.

Here, we report a case of unilateral ocular mydriasis in a pediatric patient with longstanding hyperhidrosis, as well as similar findings in her cat. The patient had been undergoing treatment of her hyperhidrosis with topical glycopyrrolate. This case highlights the potential side effect profile of topical antimuscarinics and the importance of counseling patients on proper precautions.

Anisocoria secondary to antiperspirant wipes in a pediatric population: a case series.

Acute-onset anisocoria or mydriasis in children carries a broad differential diagnosis and includes both benign and life-threatening causes, ranging from systemic or topical drug use to peripheral or central nervous system disease. The topical anticholinergic agent glycopyrronium (approved by the Food and Drug Administration in June 2018) is used to treat hyperhidrosis. We present the first case series of pediatric patients presenting with acute mydriasis due to exposure to glycopyrronium wipes. Six cases (ages 12-16) were identified: 3 presented emergently and 3 to a primary care physician. Additional symptoms included blurry vision (4/6) and unilateral headache (1/6). In 3 cases, use of glycopyrronium wipes was not elicited initially, neuroimaging was obtained, and ophthalmology (2/3) or neurology (1/3) was consulted. One patient remained undiagnosed and presented emergently again 2 months later. In all patients, symptoms resolved without further treatment.

Botulinum Toxin Type B for Hidradenitis Suppurativa: A Randomised, Double-Blind, Placebo-Controlled Pilot Study.

BACKGROUND: Botulinum toxin (BTX) is a potent neurotoxin with a long history of therapeutic application in neurological and dermatological conditions, with a strong efficacy and safety profile. OBJECTIVE: Our aim was to assess whether intradermal injection with BTX-B is an effective treatment for hidradenitis suppurativa (HS). METHODS: Twenty patients with HS stage I-III disease, according to Hurley's classification, were consecutively included for treatment with either a placebo or BTX-B. At the next intervention after 3 months, all participants received the active substance and another follow-up at 6 months. The primary outcome was quality of life, measured using the Dermatology Life Quality Index (DLQI), while secondary outcomes were the visual analogue scale (VAS) for pain in the worst boil and HS-related impairment of general health (VAS), as well as changes in physician-reported disease activity assessed as the number of total lesions, and reported adverse effects of treatment. RESULTS: The DLQI improved from a median of 17 at baseline to 8 at 3 months in the BTX-B group, compared with a reduction from 13.5 to 11 in the placebo group (p <0.05). Improvement of the patients' own ratings of symptoms and a reduction in total lesions supplemented the primary outcome. Fifty-five percent of the study population reported some degree of hyperhidrosis. CONCLUSION: BTX-B improves the quality of life in patients with HS. Furthermore, comorbidity between HS and hyperhidrosis is suggested. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT03103074.

A case report of sweating caused by hydromorphone.

Thermoregulatory control of shivering and sweating is a complex process that can be affected by centrally acting medications. Opioids, in particular fentanyl and methadone, have been associated with sweating, but it remains a relatively rare occurrence in clinical practice. Under-recognition of this medication side-effect may lead to patient discomfort as well as a potentially unnecessary work-up to determine the etiology of the sweating. Here, we discuss severe sweating caused by hydromorphone that resolved upon the medication's discontinuation.

[Aripiprazole-Induced Hyperhidrosis: Two Case Reports]. / Aripiprazol ile Tetiklenmis Asiri Terleme: Iki Olgu Sunumu.

Many drugs including anti-depressants and anti-psychotics are known to cause excessive sweating (hyperhidrosis). Hyperhidrosis may be caused by drugs acting at the hypothalamus, spinal thermoregulatory centres, and sympathetic ganglia or at the eccrine-neuroeffector junction. Hyperhidrosis can be distressing and embarrassing symptom, which if not addressed properly, may lead to non-concordance to medication. Two female patients are reported here who developed hyperhidrosis with aripiprazole. Both the patients stopped experiencing hyperhidrosis after their aripiprazole was discontinued. To the best of the knowledge of the author, no case of aripiprazole induced hyperhidrosis has been published in the literature.

Meta-analysis: Risk of hyperhidrosis with second-generation antidepressants.

BACKGROUND: Our goal was to quantify the risk of hyperhidrosis associated with commonly used antidepressant agents and examine the impact of medication class, pharmacodynamics, and dose on risk of hyperhidrosis. METHODS: We conducted a PubMed search to identify all double-blind, randomized, placebo-controlled trials examining the efficacy of second-generation antidepressant medications in the treatment of adults with a depressive disorder, anxiety disorders, or obsessive-compulsive disorder. We used a random-effects meta-analysis to examine the pooled risk ratio of hyperhidrosis reported as a side effect in adults treated with second-generation antidepressants compared to placebo. We used stratified subgroup analysis and metaregression to examine the effects of medication type, class, dosage, indication, and receptor affinity profile on the measured risk of hyperhidrosis. RESULTS: We identified 76 trials involving 28,544 subjects. There was no significant difference in the risk of hyperhidrosis between serotonin-norepinephrine reuptake inhibitors (SNRI) [risk ratio (RR) = 3.17, 95% CI: 2.63-3.82] and selective serotonin reuptake inhibitors (SSRI) (RR = 2.93, 95% CI: 2.46-3.47) medications compared to placebo. All antidepressant medications were associated with a significantly increased risk of hyperhidrosis except fluvoxamine (RR = 0.56, 95% CI: 0.12-2.53), bupropion (RR = 1.23, 95% CI: 0.57-2.67), and vortioxetine (RR = 1.35, 95% CI: 0.79-2.33). The dose of SSRI/SNRI medications was not significantly associated with the risk of hyperhidrosis. Increased risk of hyperhidrosis was associated with increased affinity of SSRI/SNRI medications to the dopamine transporter. CONCLUSION: Risk of hyperhidrosis was significantly increased with most antidepressant medications but was associated with dopamine transporter affinity.

Methadone-Induced Hyperhidrosis Treated With Oxybutynin.

OBJECTIVES: This case report aims to help healthcare providers and methadone clinic patients to recognize one of the less recognized adverse effects of methadone, hyperhidrosis, and to suggest oxybutynin as a possible solution. METHODS: A 35-year-old man on methadone maintenance therapy presented with excessive sweating, which began promptly after methadone was introduced. Urine toxicology was conducted every 2 weeks to rule out other illicit substances that may have contributed to the sweating. RESULTS: Oxybutynin (5 mg PO QID) resulted in cessation of the methadone-induced hyperhidrosis within 2 days of starting the medication. CONCLUSIONS: Methadone-induced excessive sweating is an adverse effect of the medication that reportedly affects up to 45% of those prescribed methadone, and oxybutynin is a potent treatment for methadone-induced excessive sweating.

Cutaneous adverse reactions of imatinib therapy in patients with chronic myeloid leukemia: A six-year follow up.

Imatinib is a tyrosine kinase inhibitor used in the treatment of chronic myeloid leukemia (CML). Cutaneous adverse reactions of imatinib therapy have been reported in 7%-88.9% patients. We sought to evaluate the prevalence rates of cutaneous adverse reactions of imatinib therapy and to investigate the clinical and pathological characteristics of these reactions. Sixty-six patients (36 men, 30 women; age range 19-83 years) with CML treated with imatinib between 2008 and 2014 were included in the study. Clinical and pathological features of the adverse reactions were investigated. Cutaneous adverse reactions were the most common adverse effects of imatinib therapy and were seen in nine patients with a prevalence rate of 13.6%. The second most common adverse effect was musculoskeletal pain (12.1%). The following cutaneous reactions were observed in patients: edema, rash, pigmentary changes, aphthous stomatitis, alopecia, cutaneous dryness, hyperhidrosis and cheilitis. Imatinib therapy was discontinued in four patients because of various adverse effects. Although the prevalence rate of cutaneous adverse reactions in our study was lower than that in several other studies, cutaneous reactions were common in our study. The relatively low prevalence rate of adverse reactions may be related to the low dosage of imatinib (400 mg/day) used to treat our patients and may have been affected by pharmacogenetic characteristics of our population.

Glycopyrrolate-induced craniofacial compensatory hyperhidrosis successfully treated with oxybutynin: report of a novel adverse effect and subsequent successful treatment.

Hyperhidrosis, or abnormally increased sweating, is a condition that may have a primary or secondary cause. Usually medication- induced secondary hyperhidrosis manifests with generalized, rather than focal sweating. We report a 32-year-old woman with a history of palmoplantar hyperhidrosis for 15 years who presented for treatment and was prescribed oral glycopyrrolate. One month later, the palmoplantar hyperhidrosis had resolved, but she developed new persistent craniofacial sweating. After an unsuccessful trial of clonidine, oxybutynin resolved the craniofacial hyperhidrosis. To our knowledge, this is the first case of compensatory hyperhidrosis secondary to glycopyrrolate reported in the literature. The case highlights the importance of reviewing medication changes that correlate with new onset or changing hyperhidrosis. It also demonstrates a rare drug adverse effect with successful treatment.

Prediction of compensatory hyperhidrosis with botulinum toxin A and local anesthetic.

OBJECTIVE: Compensatory hyperhidrosis (CH) is one of the most problematic complications of sympathectomy, which occurs often and is hard to treat. A predictive procedure (PP) for CH can help patients experience compensatory sweating before sympathectomy to determine whether or not to perform sympathectomy. Our study aimed to evaluate the CH after the PP and sympathectomy in patients with primary palmar hyperhidrosis using multiple drugs. METHODS: We reviewed 83 patients who underwent a PP between July 2009 and August 2013 with primary palmar hyperhidrosis. In group A, we used levobupivacaine (n = 39). In group B, we used botulinum toxin A plus ropivacaine for the PP in group B (n = 44). RESULTS: The CH rate after the PP was 44 % (group A) and 25 % (group B), and after sympathectomy 80 % (group A) and 75 % (group B). The prediction value between the PP and the sympathectomy was statistically significant in group A (p < 0.05). The positive prediction rate was 73 % and the negative prediction rate was 27 % in group A. CONCLUSIONS: Local anesthetic alone has a better predictive value. From our finding, patients should be made aware that CH after sympathectomy is less severe in 73 % of cases than that experienced in the PP.

Excessive sweating induced by interaction between agomelatine and duloxetine hydrochloride: case report and review of the literature.

OBJECTIVE: In this case report, we describe a case in which the clinical pharmacy team was asked to provide recommendations on possible continued use of combination antidepressants in a 62-year-old Slovenian female patient with major depressive disorder following agomelatine and duloxetine hydrochloride-induced excessive sweating. When agomelatine was administered as an additional treatment, drug-induced excessive sweating was observed after a daily intake of 90 mg of duloxetine hydrochloride and 25 mg of agomelatine. After thorough discussion, it was decided not to rechallenge with agomelatine because of the serious adverse effect. After agomelatine discontinuation and switching to trazodone, symptoms immediately improved. DISCUSSION: Duloxetine hydrochloride-induced sweating has been reported frequently, but excessive sweating induced by agomelatine and duloxetine hydrochloride has not been reported in the literature. The adverse effect was determined by a clinical pharmacist using the Naranjo probability scale and was probably associated with agomelatine use (6 points) and possibly associated with duloxetine hydrochloride use (4 points). The exact mechanism for this adverse effect in this patient is not known, but we believe that a pharmacodynamic drug-drug interaction between agomelatine and duloxetine hydrochloride had occurred. CONCLUSION: Such a case has not yet been described in literature; however, an adverse effect associated with drug-drug interaction can occur, as this report clearly demonstrates. The benefits of this antidepressant combination need to be carefully balanced with the risks associated with its use. This case report also highlights the increased potential for adverse reactions when prescribing antidepressant combinations and importance of clinical pharmacists' involvement in the psychiatric patients' pharmacotherapy.

Antidepressant-induced excessive sweating: clinical features and treatment with terazosin.

BACKGROUND: Antidepressant-induced excessive sweating (ADIES) occurs in 5% to 14% of patients taking antidepressants, usually persists throughout treatment, and causes subjective distress and functional impairment. We conducted the first clinical trial of any treatment for ADIES. METHODS: Clinical features of ADIES were assessed using a semi-structured form. Twenty-three patients with moderate or greater ADIES were assessed for a 2-week baseline period , followed by 6 weeks of open-label treatment with flexible dose terazosin, 1 to 6 mg/d. Improvement in ADIES was measured by the Clinical Global Impressions (CGI) scale and other measures. RESULTS: ADIES commonly was prominent in the scalp (62%), face (95%), neck (48%), and chest (57%); usually occurred either episodically or with episodic bursts (82%); and was persistent (median 63 months). Twenty-two of the 23 patients responded to terazosin (CGI-I scores 1 or 2), with CGI-Severity improving from median of 5 to median of 2 (P < .0001). Patient-rated daytime and nighttime severity of ADIES and proportion of time in ADIES also improved significantly. The most common adverse effects of terazosin therapy were dizziness/lightheadedness (n = 9) and dry mouth (n = 4). No patient dropped out because of adverse effects. Sitting and standing systolic blood pressure decreased by median values of 3 (P = .044) and 5 (P = .063) mm Hg, respectively. CONCLUSIONS: Terazosin may be an effective treatment for ADIES. Although dizziness/lightheadedness may occur in some patients, the treatment generally was well tolerated.