Chronic Spontaneous Urticaria – Diagnosis and Management

Chronic urticaria can be subclassified into chronic spontaneous urticaria and chronic inducible urticaria. Up to 30% of cases are associated with functional immunoglobulin G antibodies to the high affinity immunoglobulin E receptor FcεRIα or to immunoglobulin A. Pathogenic activation of mast cells and basophils gives rise to release of pro-inflammatory mediators that lead to development of hives. CSU is a debilitating disease with a relapsing course. It affects 0.5–1% of the population at any given time. The duration of CSU is generally 1–5 years but can be longer in cases associated with angioedema and autoreactivity. CSU has detrimental effects on life quality with sleep-deprivation and psychiatric disorders being the most frequent. In a great number of patients an underlying cause or eliciting factor cannot be identified. Among the patients in which an aetiology is suspected, infections, medication, food and psychological factors are most commonly associated. A potential autoimmune cause has been reported in up to 50% of patients. Chronic inducible urticaria is characterised by its ability to be triggered consistently and reproducibly in response to a specific stimulus (pressure, temperature, vibration, water, heat, light). Antihistamines form the mainstay of therapy. In recalcitrant chronic urticaria, a variety of other drugs have been tried

Focal Hyperhidrosis Associated with Recurrent Urinary Tract Infections

Hyperhidrosis affects almost 3% of the population and is characterized by sweating that occurs in excess of that needed for normal thermoregulation. It can occur as a primary disease or secondary to underlying clinical conditions. Hyperhidrosis can stem from neurogenic sympathetic over activity involving normal eccrine glands. We report the interesting case of a 75-year-old male patient with a 6-month history of new onset secondary focal hyperhidrosis of buttocks, pelvis, and upper thighs. Each time his symptoms worsened he was found to have culture positive urine samples for Escherichia coli (E. coli). He underwent urological investigation and was found to have urethral strictures and cystitis. The hyperhidrosis improved each time his urinary tract infection (UTI) was treated with antibiotics and continued to remain stable with a course of prophylactic trimethoprim. We hypothesize that the patient’s urethral strictures led to inhibition in voiding which in turn increased the susceptibility to UTIs. Accumulation of urine and increased bladder pressure in turn raised sympathetic nerve discharge leading to excessive sweating. We recommend that a urine dip form part of the routine assessment of patients presenting with new onset focal hyperhidrosis of pelvis, buttocks, and upper thighs. Timely urological referral should be made for all male patients with recurrent UTI. To the authors’ knowledge, there have been no other reports of UTI-associated focal hyperhidrosis