Miliaria and anhidrosis. II. The relationships between miliaria and anhidrosis in man.
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BACKGROUND: Previous studies have indicated that cutaneous bacteria, particularly coagulase-negative staphylococci, play a role in the pathogenesis of miliaria. An accumulation of periodic acid-Schiff (PAS)-positive material has been described as blocking the sweat duct in miliaria. Furthermore, a PAS-positive extracellular polysaccharide substance (EPS) has been identified as a product of some strains of Staphylococcus epidermidis. OBJECTIVE: We evaluated the relative ability of various species of coagulase-negative staphylococci to induce miliaria with particular reference to the potential role of EPS. METHODS: We inoculated various strains of coagulase-negative staphylococci on the volar forearms of subjects under an occlusive dressing coupled with thermal stimulation. Ability to induce miliaria as well as microbiologic, histologic, and immunostaining features were evaluated. RESULTS: Miliaria was induced only with strains of S. epidermidis; other species including S. haemolyticus, S. hominis, S. cohnii, S. saprophyticus, and S. simulans were not capable of inducing miliaria. Moreover, only S. epidermidis strains capable of producing EPS were capable of inducing miliaria. CONCLUSION: Our data indicate that EPS is the PAS-positive material that obstructs the delivery of sweat to the skin surface in miliaria and therefore demonstrate that the EPS produced by S. epidermidis plays a central role in the pathogenesis of miliaria. Furthermore, in a survey of staphylococcal flora isolated from 68 subjects, EPS-producing strains were found to be common.
This report documents a case series of miliaria rubra of the lower limbs in miners at a deep underground metalliferous mine in tropical arid Australia. During the summer months of February and March 1999, all cases of miliaria rubra of the lower limbs in underground miners seen at the mine's medical centre were clinically examined and administered a questionnaire. Twenty-five patients were seen, an incidence of 56.4 cases per million man-hours. Miliaria rubra was most often located between the ankle and knee (88% of cases). Twenty-four percent had concurrent folliculitis and 20% had concurrent tinea. Thirty-two percent had a personal history of asthma. Walking through ground-water and splashing of the legs was common. Three to 4 weeks of sedentary duties in air conditioning was generally required to achieve resolution of miliaria rubra. The incidence of miliaria rubra of the lower limbs is 38% of the incidence of heat exhaustion at the same mine. The length of disablement is greater, however. Atopics may be at increased risk of miliaria rubra. Control measures are discussed.
Generalized congenital miliaria crystallina occurred in a black newborn boy. Although miliaria crystallina occurring in infancy and beyond is well established, congenital occurrence is very rare. The pathogenesis of the disorder is not well understood. We discuss some hypotheses of pathogenesis in the context of our patient, as well as a differential diagnosis and a comparison with a previously reported case. Miliaria crystallina should be considered in the differential diagnosis of vesiculobullous eruptions in newborns.
Ten volunteers were heat acclimatized to 48.9 degrees C (Ta), 20% rh for 7 days to complete a 100-min walk on a level treadmill (1.56 m x s-1). Subjects were then divided into experimental (n = 6) and control (n = 4) groups. Miliaria rubra (heat rash) was then induced on the experimental subjects by wrapping them for 3 days in polyethylene plastic. All six developed marked miliaria with involvement of 40-70% of the total body surface area. All subjects were reexposed to walking in the heat on the 7th day after unwrapping, by which time rash was clinically indetectable, and again 14 days after unwrapping. On the first test (day 7) only one of the rashed group, and on the second test (day 14) only two could complete the 100-min walk; the control group finished without difficulty on both days. Body heat storage for the rash group was 2.5 times that of the control group on day 7 and 1.5 as great on day 14; measurements of mean body temperature (Tb) on the rash group indicated a much greater heat stress when compared to their own prerash-acclimatized values or those of the control group. These data demonstrate the potential of "healed" miliaria in the etiology of clinical heat illness.
Miliaria profunda is an uncommon but highly characteristic disorder that can be disabling. We describe a patient with miliaria profunda who responded to therapy with anhydrous lanolin and isotretinoin. Clinical features, pathogenesis, differential diagnosis, and therapy are reviewed.
A 4-month-old developed rapidly enlarging, white plaques up to several centimeters in diameter in areas where occlusive tape had been applied, almost all on the sites of venous or arterial punctures. Microscopy demonstrated the features of miliaria profunda, with sweat duct occlusion and evidence of extravasation of sweat into the dermis. This clinical entity has not been described previously, and we suggest the name giant centrifugal miliaria profunda.
From argument and a few personal observations, the hypothesis has crystallised that the miliaria commonly occurring in unacclimatised Caucasians visiting hot climates is caused by exposure to ultraviolet irradiation, by an effect on the cells of the upper epidermis, which eventually allows a split to develop between them and the new stratum corneum that grows up beneath, into which sweat from the disrupted ducts can collect as microcysts. This dehiscence is the probable explanation of sunburn peeling and photo-onycholysis. It is concluded that duct disruption, not blockage or dysfunction, is the immediate cause of the miliarias.
Miliaria crystallina is characterized by intracorneal or subcorneal, 1 to 2 mm, clear, noninflammatory vesicles that typically appear in crops after a severe sunburn or during a febrile illness. They frequently occur in neonates, most likely due to lack of maturation of the sweat duct during the first few days following birth, but are rarely present at delivery. We describe here a patient with extensive miliaria crystallina that was present at birth and review possible theories of the pathogenesis of these lesions.
A case of miliaria crystallina occurring with isotretinoin therapy in a patient with lamellar ichthyosis is described. To our knowledge, the association of miliaria crystallina with isotretinoin therapy has not been previously reported.
Deletion 3q27----3qter in an infant is described. A chromosomal abnormality was suspected because of minor facial dysmorphism and closed parietal meningocele. On the first day of life, a large exudative inflammation appeared on the skin of her back, which completely resolved after 1 week. Biopsy showed dilated sweat gland openings resembling miliaria rubra, which has not been previously reported in this age group. It is unclear if the skin change was due to the chromosomal abnormality. The meningocele was repaired at age 8 months. At age 20 months, slight neurodevelopmental delay was evident, the main features being hypertonicity and inability to walk without support. The patient has two healthy sisters, and prometaphase chromosome studies in both parents were normal. This infant represents the first example of del3q27----3qter and the first reported association of meningocele with an abnormality of chromosome 3.
A retrospective study was undertaken to examine by interactive linear modeling a possible association between environmental conditions and the incidence of skin conditions (excluding athletes foot) in a coal mine following an increase in skin rashes, mainly 'prickly heat' (Miliaria rubra). An increase in the incidence was found with increasing surface temperature and underground air velocity; a decreased incidence with increased underground air quantity (air volume per unit time); whilst the relationship with underground temperature was found to be quadratic with incidence decreasing until 27 degrees C wet bulb (although this is not necessarily the optimum temperature for other purposes) and then increasing. The association between skin incidence and environmental factors was strongest (in terms of variance explained) when the incidence was associated with the environmental conditions of 4 to 8 weeks previously. The constant nature of relative humidity over the period prevented an examination of its relationship with rash incidence. Possible strategies for reducing the incidence of 'prickly heat' are discussed.
Anhidrosis was induced in volunteers by covering the skin with an impermeable plastic film. The degree of sweat suppression and miliaria after a thermal stimulus was directly proportional to the increase in the density of resident aerobic bacteria, notably cocci. No anhidrosis resulted when antibacterial substances were used to prevent the expansion of the microflora. Histological study showed a PAS-positive diastase resistant amorphous mass deep within the acrosyringium after 2 days of occlusion, accompanied by a periductal dermal infiltration of leukocytes. After another 2 days the duct became clogged by an amalgam of degenerating leukocytes. This impaction sloughed after about 3 weeks as a result of epidermal renewal. Colonies of bacteria were never found within the ducts. It is postulated that cocci secrete a toxin which injures luminal cells and precipitates a cast within the lumen. Infiltration by leukocytes creates an impaction which completely obstructs the passage of sweat for several weeks.
Twenty-four heat-acclimatized male volunteers were wrapped as previously described (Am. J. Physiol. 239 (Regulatory Integrative Comp. Physiol. 8): R226-R232, 1980) but to produce miliaria rubra (heat rash) in specific regions of the body. Three experimental rash groups were involved: 1) the torso (17% total skin surface rashed, n = 6), 2) torso and arms (38%, n = 8), or 3) legs (41%, n = 6), while four subjects served as controls. All subjects were reexposed to walking in the heat on the 7th day after unwrapping, and again 14, 21, and 28 days after unwrapping. When compared to responses for the last heat acclimatization day, tolerance time and sweat rate were lower and mean body temperature and delta heat storage significantly higher for experimental rash subjects contrasted to the controls for up to 21 days; however, no significant differences between the three rashed groups were found. The critical amount of surface area for heat intolerance from heat rash appears to be related to the specific region of the body and associated sweating responses; smaller rashed areas of the trunk, because they have greater potential for abundant sweating, may produce similar responses to heat stress as larger rashed areas of the limbs. Heat intolerance due to rash was not resolved until after 21 days.
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