Cases reported "Sweat Gland Diseases"

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1/33. hidradenitis suppurativa occurring on the leg.

    The case of a patient with a recurrent, painful ulceration on the lower leg, clinically and histologically resembling hidradenitis suppurativa, is presented. The fact that this site is devoid of apocrine glands supports the concept that apocrine involvement in hidradenitis suppurativa is coincidental and that these glands are involved secondarily. It is suggested that in this patient the pathogenesis of the disease is follicular occlusion rather than selective apocrine poral closure.
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2/33. Eccrine angiomatous hamartoma: report of seven cases.

    Eccrine angiomatous hamartoma is a rare cutaneous lesion. Histologically it is characterized by the proliferation of eccrine glands, vascular structures and occasionally other elements in the middle and deep dermis; we now report seven further cases of this condition, two with lipomatous involvement and also discuss its nosology.
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3/33. hyperpigmentation caused by hyperthyroidism: differences from the pigmentation of Addison's disease.

    Two cases of hyperthyroidism with hyperpigmentation are presented. In both cases, hyperpigmentation was seen on the lower extremities, most strikingly on the shins, backs of the feet and the nail bed. histology of the pigmented skin showed basal melanosis and heavy deposition of haemosiderin around dermal capillaries and sweat glands. Treatment with mercazol in both cases resulted in no significant waning of pigmentation. Distribution of hyperpigmentation, haemosiderin deposition and poor response to the treatment may be characteristic features of the pigmentation caused by hyperthyroidism, and may represent differences from the pigmentation seen in Addison's disease.
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4/33. Eccrine angiomatous hamartoma: a report of symmetric and painful lesions of the wrists.

    Eccrine angiomatous hamartoma (EAH) is a rare, benign cutaneous lesion histologically defined as a proliferation of eccrine glands within a closely associated vascular stroma. Typically EAH presents as a solitary flesh-colored, hyperhidrotic, painful papule or plaque appearing at birth or during childhood. Only two previously reported cases have been described involving multiple, symmetrically located lesions. The occurrence of knuckle pads in patients with EAH has not been reported. We present an instance of multiple painful EAH lesions occurring symmetrically on the extensor wrists in a 14-year-old girl with knuckle pads.
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5/33. Acral erythrodysesthesia syndrome caused by intravenous infusion of docetaxel in breast cancer.

    Docetaxel-induced skin reactions include hypersensitivity, edema, skin toxicity with erythrodysesthesia syndrome, infusion site reactions, alopecia, nail onycholysis, nail pigmentation, photosensitivity, scleroderma, and others, for example, stomatitis and paresthesias. However, of all reported effects, the acral erythrodysesthesia syndrome has only rarely been described in the literature. We report on two female patients with breast cancer who on treatment with docetaxel developed acral erythrodysesthesia syndrome. It presented as bizarrely shaped, burning skin reactions at their hands and feet. histology of skin biopsies revealed microscopic damages to the eccrine sweat glands in both patients. skin patch testing with docetaxel was negative. None of the reports dealing with side effects of docetaxel chemotherapy has described acral erythrodysesthesia syndrome with the histologic features of syringo-squamous metaplasia and eccrine neutrophilic hidradenitis. We propose here that these characteristic histologic features are essential in the differentiation from fixed drug eruption and localized graft-versus-host disease.
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6/33. Treatment of facial chromhidrosis with botulinum toxin type A.

    BACKGROUND: hyperhidrosis is an idiopathic condition of exaggerated sweat production by the eccrine glands that affects approximately 1% of the population. There are many viable therapeutic options and the use of botulinum toxin has become an important treatment option and received FDA approval for this disorder in July 2004. The other forms of aberrant sweating; bromhidrosis (malodorous) and chromhidrosis (pigmented) are much rarer and more recalcitrant to treatment. METHOD: This is the first case report of dark-colored facial sweat in a young woman that was adequately controlled with botulinum toxin. CONCLUSION: Chromhidrosis is an unusual clinical entity with an ill-defined glandular etiology. The successful response to botulinum toxin supports the eccrine gland as a source of the sweat production and, furthermore, that the administration of this toxin should be considered as a form of therapy.
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7/33. Botulinum toxin a in the treatment of chromhidrosis.

    BACKGROUND: Chromhidrosis is an uncommon disorder characterized by secretion of colored sweat by apocrine glands, typically localized to the face or axilla. The current treatments available for chromhidrosis are time consuming and frequently ineffective. OBJECTIVE: Our purpose is to demonstrate a novel approach to the treatment of apocrine chromhidrosis. methods: We report a case of apocrine chromhidrosis successfully treated with botulinum toxin A (BTX-A; Botox). RESULTS: BTX-A therapy successfully controlled facial chromhidrosis, and the effects were visible at 19 weeks post-treatment. The therapeutic benefits may be attributed to its inhibitory effects on cholinergic stimulation, adrenergic stimulation, and substance p release, although further studies are necessary to elucidate the precise mechanism of action. CONCLUSION: This report demonstrates a new therapeutic approach to patients suffering from chromhidrosis.
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8/33. Late-onset eccrine angiomatous hamartoma on the forehead.

    A 71-year-old Korean man presented with a solitary erythematous plaque on his forehead (Fig. 1). It was first noticed by the patient 1 year previously and had slowly increased in size over that time. physical examination revealed a slightly elevated, 1.5 cm x 1.5 cm erythematous plaque on the upper midline of the forehead. sweating was not evoked by physical work or emotional stress. There was no pain or tenderness associated with the lesion. The patient had no history of trauma to the forehead. Histopathologic examination of the lesion showed increased numbers of eccrine glands, as well as dilated vascular channels in the deep dermis and subcutaneous tissue (Fig. 2). An immunohistochemical study showed that these eccrine glands stained positively for S-100 and carcinoembryonic antigen (CEA), and the vascular channels for the antifactor VIII-related antigens. These findings are consistent with eccrine angiomatous hamartoma. There was no change in the lesion during the 1-year follow-up period.
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9/33. Cold-induced sweating syndrome: a report of two cases and demonstration of genetic heterogeneity.

    OBJECTIVES: To characterize the specific autonomic disturbances underlying the cold-induced sweating syndrome (CISS), and to describe a novel genetic variant of this rare recessive disorder. The two not previously reported patients had similar dysmorphic features: abnormal facial appearance, high arched palate, low set rotated ears, flexion deformities of elbows and fingers and scoliosis. Most noticeable were their paradoxical sweat responses: cold ambient temperature induced a profuse sweating over the face, arms and trunk but not over the lower limbs; while in the heat very little sweating occurred primarily on the legs. Testing of autonomic functions demonstrated normal cardiovascular reflexes and postganglionic sympathetic efferent functions. sural nerve morphology and number of unmyelinated fibers was normal and skin biopsies showed normal appearing eccrine sweat glands. MRI scans revealed no structural brain abnormalities. Oral clonidine, prescribed in one patient, completely suppressed cold-induced sweating. Observed clinical features matched those of two sisters reported from israel and of two brothers reported from norway. All six cases presented a similar phenotype. The Norwegian, Israeli and Canadian cases were homozygous or compound heterozygous, respectively, for mutations in the CRLF1 gene on chromosome 19p12 (CISS1). The Australian case, however, had no pathogenic sequence variants in the CRLF1 gene, but was compound heterozygous for mutations in the CLCF1 gene on chromosome 11q13.3 (CISS2). CONCLUSION: The rare cold-induced sweating syndrome is genetically heterogeneous and is probably caused by central and peripheral impairment of sudomotor functions. This is the first detailed report on the clinical consequences of mutations in the CLCF1 gene in humans. Directions for medical therapies are outlined to achieve long term symptom control.
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10/33. CO2 laser for suppurative hidradenitis of the vulva.

    Chronic suppurative hidradenitis is a disease of the apocrine glands occurring predominantly in the axillae of the anogenital region. Treatment, to date, has been frustrating. Prolonged antibiotic therapy and multiple incisions and drainage have been the usual form of therapy, but those surgical procedures leave patients with ugly scars; retracted, hypertrophic skin edges; and pitted, indurated and disfiguring abscesses. The only successful treatment to date has been wide excision of the entire apocrine gland-bearing tissues, such as radical vulvectomy, which often necessitates grafts to cover the surgically exposed areas. That has left patients with unsatisfactorily functioning vaginas and a mutilated appearance. Recently we instituted the use of the CO2 laser to treat these patients with the goal of eradicating the suppurative sinus tracts and the infected apocrine glands without removing large volumes of adjacent, unaffected tissue. Over the past eight years we treated 11 patients who had extensive, chronic hidradenitis of the anogenital area with the CO2 laser. The use of laser therapy for these patients has produced effective and less-mutilating results. Such treatment has been a successful option for treating this debilitating disease.
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