S3-Leitlinie: Analabszess

Background

Anal abscesses are relatively frequent and most common in young men.

Methods

A systematic review of the literature has been undertaken.

Results

The origin of the abscess is usually the proctodeal gland in the intersphincteric space. There are different types of abscesses: intersphincteric, ischioanal and supralevatory abscesses. Anamnesis and clinical examination are sufficient to indicate surgery. Further examinations such as endosonography or magnetic resonance tomography (MRT) should be considered in recurrent or supralevatory abscesses. The timing of surgical intervention depends on clinical symptoms, whereas the acute abscess is an emergency indication. Surgery is the primary therapy approach for anal abscess. Surgical access (transrectal or perianal) depends on the localization of the abscess. The aim of surgery is to broadly drain the infection and protect anal sphincter structures. The wound should be rinsed regularly (showering with clear water). Treatment with local antiseptics carries the risk of zytotoxicity. Antibiotic treatment is necessary only in selected cases. Any attempt to locate a fistula intraoperatively should be undertaken with great care; proven evidence of a fistula is not mandatory. Although the risk of recurrent abscess or secondary fistula is low, these may be caused by insufficient drainage. The primary fistulotomy of superficial fistulas should only be performed by an experienced surgeon. In the case of ambiguous findings or high fistulas, treatment should be carried out in a second surgical procedure.

Conclusion

For the first time in Germany, this clinical S3 guideline provides instructions for the diagnosis and treatment of anal abscesses based on a systematic review of the literature.     

3-Hydroxy-3-methylglutaric aciduria combined with 3-methylglutaconic aciduria: A new case

The urinary organic acids of a new case of 3-hydroxy-3-methylglutaryl-CoA lyase deficiency have been analysed by gas chromatography-mass spectrometry. This patient's fibroblasts showed a reduced ability to oxidize leucine.     

V3: HIV's switch-hitter

The third variable region, V3, of the gp120 surface envelope glycoprotein is an approximately 35-residue-long, frequently glycosylated, highly variable, disulfide-bonded structure that has a major influence on HIV-1 tropism. Thus the sequence of V3, directly or indirectly, can determine which coreceptor (CCR5 or CXCR4) is used to trigger the fusion potential of the Env complex, and hence which cells the virus can infect. V3 also influences HIV-1's sensitivity to, and ability to escape from, entry inhibitors that are being developed as antiviral drugs. For some strains, V3 is a prominent target for HIV-1 neutralizing antibodies (NAbs); indeed, for many years it was considered to be the "principal neutralization determinant" (PND). Some efforts to use V3 as a vaccine target continue to this day, despite disappointing progress over more than a decade. Recent findings on the structure, function, antigenicity, and immunogenicity of V3 cast new doubts on the value of this vaccine approach. Here, we review recent advances in the understanding of V3 as a determinant of viral tropism, and discuss how this new knowledge may inform the development of HIV-1 drugs and vaccines.     

3-Hydroxy-3-methylglutaryl-coenzyme A lyase deficiency: A review

Children with 3-hydroxy-3-methylglutaryl-CoA lyase deficiency (HMG-CoA-LD; McKusick 24645), have inherited two areas of metabolic weakness. Firstly, they are unable to metabolize fully the carbon skeleton of leucine, and secondly, they cannot make ketone bodies in response to prolonged fasting. In the first year of life infants with HMG-CoA-LD run a high risk of developing severe hypoglycaemia which can lead to death if prompt intervention does not occur. The metabolic crisis develops when the infant is first introduced to dietary protein soon after birth, or later, when a reduced intake of glucose, often during a viral infection, results in a drain on the infant's circulating glucose levels. However, where diets are adequately adjusted to limit protein and fat intake, the metabolic handicaps of individuals with HMG-CoA-LD are not exposed and they are virtually symptomless. As children with HMG-CoA-LD grow older the incidence of hypoglycaemic attacks diminishes and they usually develop normally. This article reviews literature on cases of HMG-CoA-LD and interprets data on altered metabolism in these children.