Allergic contact dermatitis from sorbitans in beer and bread.

Sorbitol-derived compounds have been increasingly recognized as a cause of delayed hypersensitivity reactions. We present a case of recurrent allergic contact dermatitis (ACD) that lasted 6 months in which the patient retrospectively correlated new lesion appearance with consumption of specific types of beer and bread. Patch testing using the North American Contact Dermatitis Group Standard Series with supplemental allergens was positive for sorbitan sesquioleate (SSO) and sorbitan monooleate (SMO). Avoidance of beer and bread led to complete clinical resolution. Sorbitol in beer and bread is not well documented but likely is related to the yeast cultures used for fermentation and leavening. Sorbitol is utilized as an osmotic stabilizer in yeast culture preparation and is found in commercially prepared brewer's and baker's yeasts. We propose that trace amounts of sorbitans in yeast-containing products can cause ACD. Systematized ACD poses a challenge for dermatologists to diagnose, as the pattern can be nonspecific and skin testing does not always produce meaningful results. Because it is difficult to elicit history and correlate exposures with worsening of skin symptoms, a trial of dietary avoidance may be necessary to determine the diagnosis of systematized ACD. When patch testing is positive for SSO and SMO, the dermatologist should inquire about dietary habits with attention to beer and bread.

Inflammatory tinea capitis mimicking dissecting cellulitis in a postpubertal male: a case report and review of the literature.

Tinea capitis in postpubertal patients is unusual and may be misdiagnosed as dissecting cellulitis. We report a case of a healthy 19-year-old Hispanic male presenting with a 2-month history of a large, painful subcutaneous boggy plaque on the scalp with patchy alopecia, erythematous papules, cysts and pustules. Although initially diagnosed as dissecting cellulitis, potassium hydroxide evaluation (KOH preparation) of the hair from the affected region was positive. A punch biopsy of the scalp demonstrated endothrix consistent with tinea capitis, but with a brisk, deep mixed inflammatory infiltrate as can be seen with chronic dissecting cellulitis. Fungal culture revealed Trichophyton tonsurans, and a diagnosis of inflammatory tinea capitis was made. The patient was treated over the course of 17 months with multiple systemic and topical antifungal medications, with slow, but demonstrable clinical and histopathological improvement. A rare diagnosis in adults, clinicians should have a high index of suspicion for this condition in an adult with an inflammatory scalp disorder not classic for dissecting cellulitis or with a recalcitrant dissecting cellulitis. Prompt, appropriate diagnosis and treatment is necessary to prevent the long-term complications of scarring alopecia.

The SWI/SNF chromatin remodeling complex influences transcription by RNA polymerase I in Saccharomyces cerevisiae.

SWI/SNF is a chromatin remodeling complex that affects transcription initiation and elongation by RNA polymerase II. Here we report that SWI/SNF also plays a role in transcription by RNA polymerase I (Pol I) in Saccharomyces cerevisiae. Deletion of the genes encoding the Snf6p or Snf5p subunits of SWI/SNF was lethal in combination with mutations that impair Pol I transcription initiation and elongation. SWI/SNF physically associated with ribosomal DNA (rDNA) within the coding region, with an apparent peak near the 5' end of the gene. In snf6Δ cells there was a ∼2.5-fold reduction in rRNA synthesis rate compared to WT, but there was no change in average polymerase occupancy per gene, the number of rDNA gene repeats, or the percentage of transcriptionally active rDNA genes. However, both ChIP and EM analyses showed a small but reproducible increase in Pol I density in a region near the 5' end of the gene. Based on these data, we conclude that SWI/SNF plays a positive role in Pol I transcription, potentially by modifying chromatin structure in the rDNA repeats. Our findings demonstrate that SWI/SNF influences the most robust transcription machinery in proliferating cells.

Xanthogranulomatous reaction to a ruptured galactocele.

We describe a case of a 34-year-old, healthy, lactating female with a 2-month history of breast pain and an enlarging, tender mass on her right nipple. Her right breast was firm and mildly engorged without mass, warmth or erythema. A tender, yellow nodule was located on the superior aspect of the nipple, obstructing the flow of milk from this portion of the nipple. A biopsy showed epidermal erosion, sheets of cells with massively distended, foamy cytoplasm in the dermis, and a hypertrophied and occluded glandular duct, consistent with reactive squamous metaplasia. Immunostaining for CD68 confirmed the foamy cells were macrophages, and anti-human milk fat globulin-1 (HMFG1) labeled the substance within the macrophages consistent with human breast milk. Therefore, the lesion could be identified as a xanthogranulomatous reaction to a ruptured galactocele.

Necrolytic acral erythema: a review of the literature.

Necrolytic acral erythema (NAE) has been described as an early cutaneous marker for hepatitis C virus (HCV) infection. It most commonly presents as a well-defined, dusky, erythematous eruption with marked hyperkeratosis and a dark red rim associated with pruritus or burning. Necrolytic acral erythema bears microscopic and clinical resemblance to other necrolytic erythemas, including necrolytic migratory erythema (NME) and several nutrient-deficient syndromes. It is distinct, however, in its predominantly acral distribution and strong association with HCV infection. The pathogenesis is unknown, but a relationship to metabolic alterations has been hypothesized. Optimal therapy appears to be treatment of the underlying HCV infection using a combination of ribavirin and interferon alfa; oral zinc therapy may be an alternative but useful therapy. Cases of NAE without HCV infection suggest that more work needs to be done defining NAE and its relationship to HCV.

A novel vaccine (Zostavax) to prevent herpes zoster and postherpetic neuralgia.

Varicella-zoster virus is the causal agent of varicella and herpes zoster in humans. Herpes zoster results from reactivation of latent varicella-zoster virus (VZV) within the sensory ganglia. The incidence and severity of herpes zoster increase with advancing age. More than half of all persons in whom herpes zoster develops are older than 60 years. The most frequent debilitating complication is postherpetic neuralgia, a neuropathic pain syndrome that persists or develops after the dermatomal rash has healed and can be prolonged and disabling. There are many limitations of current therapies for herpes zoster and postherpetic neuralgia. A live attenuated VZV vaccine has been developed and recently approved by the FDA for the prevention of herpes zoster in individuals 60 years of age and older. In a randomized, double-blind, placebo-controlled trial with 38,546 patients 60 years of age or older, the use of the zoster vaccine reduced the burden of illness due to herpes zoster by 61.1% (P < .001), reduced the incidence of postherpetic neuralgia by 66.5% (P < .001), and reduced the incidence of herpes zoster by 51.3% (P < .001). In this review, we will discuss the history of the use of the varicella vaccine in children, and the subsequent development of the new zoster vaccine.