Use of hyaluronidase as an adjuvant to ropivacaine to reduce axillary brachial plexus block onset time: a prospective, randomised controlled study.

When considering brachial plexus block as a practical alternative to general anaesthesia for upper limb surgery, the time to achieve complete sensory block is a clinically important variable. In this prospective randomised double-blind controlled trial, we investigated the hypothesis that addition of hyaluronidase to ropivacaine may reduce the time to achieve complete sensory block after axillary brachial plexus block. The patients were randomly assigned into a hyaluronidase group (n = 24) and a control group (n = 24). The hyaluronidase group received ropivacaine 0.5% with 100 IU.ml(-1) of hyaluronidase, and the control group received ropivacaine alone. The primary endpoint was the time to achieve complete sensory block. The hyaluronidase group demonstrated significantly shorter mean (SD) sensory block onset time (13.8 (6.0) min) compared with the control group (22.5 (6.3) min, p < 0.0001). Addition of hyaluronidase to ropivacaine resulted in a reduction in the time needed to achieve complete sensory block.

Alopecia neoplastica in a patient with gastric carcinoma.

A well-recognized but rare presentation of scalp metastasis is alopecia neoplastica, which occurs as a single or multiple areas of cicatricial alopecia. Alopecia neoplastica is usually a presentation of metastasis from breast cancer, and other primary sites are extremely rare. We report a 36-year-old woman with alopecia neoplastica due to metastasis from gastric carcinoma. She also had pelvic metastases. An asymptomatic erythematous alopecic plaque had developed 10 months before presentation and biopsy was consistent with scalp metastasis. Total abdominal hysterectomy and salphingo-oophorectomy was performed and chemotherapy was proposed.

Bowen's diseases and basal cell carcinomas in a patient.

Bowen's disease is a well-known precancerous lesion, in which invasive squamous carcinoma may develop. However, it is rare that Bowen's disease, basal cell carcinoma, and internal malignancy develop in a single patient. We report a case of a 54-year-old male patient with Bowen's disease, basal cell carcinoma of the skin, and squamous cell carcinoma of the lung. Multiple scaly erythematous patches had developed several years earlier and were diagnosed as Bowen's disease by skin biopsy. The number of lesions increased and, five months ago, a right lower lobectomy was done for squamous cell carcinoma which was detected on a chest X-ray. Skin biopsies of two different sites revealed Bowen's disease and basal cell carcinoma. The arsenic level was increased in his hair specimen. Cryotherapy was applied.

Arginine in the beginning of the 1A rod domain of the keratin 10 gene is the hot spot for the mutation in epidermolytic hyperkeratosis.

Keratin intermediate filaments are expressed in specific type I/type II pairs in the stage of differentiation of keratinocytes. The mutations in the keratin genes expressed in the epidermis are etiologically responsible for several epidermal genetic skin diseases, such as epidermolysis bullosa simplex, epidermolytic hyperkeratosis (EHK), ichthyosis bullosa of Siemens, palmoplantar keratoderma, pachyonchia congenita and white sponge nevus. The mutations of keratins 1/10 which are expressed in spinous and granular layers are confirmed to cause EHK. There are several trials to correlate between the clinical phenotypes and sites of mutations of the keratin genes. One of these is that EHK is divided into two groups: the palms and soles involvement (PS) group and the non-palms and soles (NPS) group. So far the PS group had the mutations in the keratin 1 and the NPS group in keratin 10. Most of the mutations of the NPS group were reported in the beginning of the 1A rod domain and over 2/3 of the mutations in the 1A rod domain were the base pair substitution of arginine. Here we find two different mutations in two unrelated Korean kindreds classified as NPS group-R156C and R156H-in the 1A rod domain of keratin 10. Our results are compatible with the above classification and suggest that the arginine in the beginning of the 1A rod domain is the hot spot for the mutation of the keratin 10 gene.