INTRODUCTION
In the most simplistic definition, hyperhidrosis is excessive sweating. However, it is largely misunderstood, often goes undiagnosed, and continues to be inadequately managed for many patients. Approximately half of those who self-identify as having excessive sweating do not discuss their symptoms with healthcare professionals despite the severe negative impact on their quality of life; reasons for this include the misconception that hyperhidrosis is not a medical condition and that no treatments exist.1 In one study, only half of patients who reported their symptoms to a healthcare professional were ultimately diagnosed with primary hyperhidrosis, which may reflect a reality of widespread underdiagnosis of the condition.1 In a survey conducted by the International Hyperhidrosis Society (IHhS), 48.9% of patients waited 10 or more years before seeking medical help for their excessive sweating.2
With the busy practitioner and dermatology resident in mind, here we provide a disease state primer for hyperhidrosis, a top-line review of the breadth of literature underscoring the overall burden of the disease, a practical guide to differential diagnosis, and an update on current treatment approaches.3, 4 In addition, a case study in primary axillary (underarm) hyperhidrosis is presented to provide a real-life perspective from the clinic on the importance of early and effective management strategies for those suffering with hyperhidrosis.
Hyperhidrosis Disease State Primer
Hyperhidrosis is a chronic medical condition characterized by excessive sweating beyond that which is necessary for thermoregulatory homeostasis.1 The excessive sweating of hyperhidrosis is thought to be produced by eccrine sweat glands (Figure 1), which are highly abundant in axillae, palms, soles, and craniofacial areas.4,5 Since no differences in histopathology, size, and number of eccrine sweat glands have been observed between patients with hyperhidrosis and those without the condition, it is thought that the disorder occurs due to abnormalities in the autonomic nervous system.5,6 The nerves that innervate sweat glands are sympathetic and utilize acetylcholine as the primary neurotransmitter.7 In hyperhidrosis, it is presumed that overstimulation of cholinergic receptors on eccrine sweat glands leads to overproduction of sweat.8,9,10
The condition is classified as either primary or secondary hyperhidrosis. Primary hyperhidrosis is idiopathic, tends to be concentrated in particular focal areas, often presents early in life, and is most often bilateral and symmetric in nature; patients with primary axillary hyperhidrosis do not typically experience excessive sweating while sleeping.1,4,5,8 Primary hyperhidrosis may have underlying genetic factors, as 5.7% to 65% of patients have a family history of the condition.2,11,12 Several genetic studies report primary hyperhidrosis inheritance as autosomal dominant or recessive, and identified loci for the condition on chromosome 2, 14, and 16; however, these results are heterogeneous and warrant further study to elucidate the disease etiology.2,11,12
Secondary hyperhidrosis occurs due to an underlying medical condition such as diabetes mellitus, hyperthyroidism, and lymphoma, or as a side effect of certain medications like some
With the busy practitioner and dermatology resident in mind, here we provide a disease state primer for hyperhidrosis, a top-line review of the breadth of literature underscoring the overall burden of the disease, a practical guide to differential diagnosis, and an update on current treatment approaches.3, 4 In addition, a case study in primary axillary (underarm) hyperhidrosis is presented to provide a real-life perspective from the clinic on the importance of early and effective management strategies for those suffering with hyperhidrosis.
Hyperhidrosis Disease State Primer
Hyperhidrosis is a chronic medical condition characterized by excessive sweating beyond that which is necessary for thermoregulatory homeostasis.1 The excessive sweating of hyperhidrosis is thought to be produced by eccrine sweat glands (Figure 1), which are highly abundant in axillae, palms, soles, and craniofacial areas.4,5 Since no differences in histopathology, size, and number of eccrine sweat glands have been observed between patients with hyperhidrosis and those without the condition, it is thought that the disorder occurs due to abnormalities in the autonomic nervous system.5,6 The nerves that innervate sweat glands are sympathetic and utilize acetylcholine as the primary neurotransmitter.7 In hyperhidrosis, it is presumed that overstimulation of cholinergic receptors on eccrine sweat glands leads to overproduction of sweat.8,9,10
The condition is classified as either primary or secondary hyperhidrosis. Primary hyperhidrosis is idiopathic, tends to be concentrated in particular focal areas, often presents early in life, and is most often bilateral and symmetric in nature; patients with primary axillary hyperhidrosis do not typically experience excessive sweating while sleeping.1,4,5,8 Primary hyperhidrosis may have underlying genetic factors, as 5.7% to 65% of patients have a family history of the condition.2,11,12 Several genetic studies report primary hyperhidrosis inheritance as autosomal dominant or recessive, and identified loci for the condition on chromosome 2, 14, and 16; however, these results are heterogeneous and warrant further study to elucidate the disease etiology.2,11,12
Secondary hyperhidrosis occurs due to an underlying medical condition such as diabetes mellitus, hyperthyroidism, and lymphoma, or as a side effect of certain medications like some
