Stevens-Johnson syndrome induced by carbamazepine

Stevens-Johnson syndrome (SJS) is a mucocutaneous disorder induced by an immune-complex-mediated hypersensitivity reaction. Nearly half of cases are caused by a reaction to drugs or appear during viral infections and malignancies. A very few cases are caused by a bacterial infection (Streptococcus) or Mycoplasma pneumoniae. Graft versus host disease is another well-established cause, independent of drugs. No specific etiology has been identified in up to half of cases. We report a 54-year-old man with SJS induced by carbamazepine. Reported patient had prodromal symptoms like fever, headache and polyarthralgia, which preceded mucocutaneous lesions by 3 days. Physical examination on admission, revealed asthenic male with a temperature of 37.2 degrees C and generalized dermatitis with positive Nikolsky sign, large erosions of the palms and soles, onychomadesis, numerous oral and vermilion border of the lips erosions. The patient was administered systemic steroidotherapy and carbamazepine dose was gradually decreased and finally replaced with valproic acid and valproate sodium. During the hospitalization, temperature normalized and the skin lesions disappeared after 3 weeks of treatment.     

Association of tetralogy of Fallot with a distinct region of del22q11.2

Congenital heart defects (CHDs) appear in greater frequency among relatives of patients and in individuals with DiGeorge syndrome (DGS) or velo-cardio-facial syndrome (VCFS). A majority of these patients and part of the apparently nonsyndromic CHD patients with conotruncal defects manifest hemizygous deletions within chromosome 22q11.2 (del22q11). We tested myocardial tissues of 31 CHD patients, 21 with tetralogy of Fallot (TOF) and 10 with a double-chamber right ventricle (DCRV). DNA isolated from tissues removed at corrective surgery was analyzed for homo- or heterozygosity of nine polymorphic short tandem repeat (STR) markers along the 22q11.2 region. DNA from the blood of 45 healthy individuals represented the general population. Ten of the 21 TOF patients (48%) showed homozygosity for three or more consecutive markers, indicating deletions of various sizes. No such indication was found for DCRV patients. Heterozygosity for markers D22S1648, D22S941, and D22S944 was lower in the TOF group than in normal controls, defining a minimal critical region (MCR) for the deletion. Our findings support an association between TOF and hemizygosity in 22q11.2, suggesting a distinct region, between markers D22S1638 and COMT, that may harbor TOF susceptibility genes.     

Definitions and use of the teach-back method in healthcare consultations with patients: A systematic review and thematic synthesis

ObjectiveTo review and synthesise definitions of the teach-back method in the literature. The second aim is to synthesise the barriers, facilitators and perceptions of teach-back use in healthcare consultations with patients.MethodsA systematic review and thematic synthesis following Braun and Clarke’s method.ResultsThe primary search found 1429 citations and the secondary search added 221 citations. Screening identified 66 citations eligible for data extraction. We contrasted and synthesised operational definitions of the teach-back method. The synthesis generated seven themes related to healthcare provider (HCP) and patient perceptions of teach-back (effectiveness, stigma and time-related perceptions), the universal application of teach-back, patient health outcomes and healthcare provider training.DiscussionOperational definitions of the teach-back method varied in the literature and contained implied steps. HCPs and patient perceptions of teach-back operated as both enablers and barriers to its use. HCPs training programs for the teach-back method were identified as beneficial for altering HCPs perceptions about the method and increased its use with patients.Practice implicationsStandardising operational definitions of the teach-back method can support replicability of research and enhance HCPs communication skills training programs. HCPs training on teach-back use can support the increased use of the technique with broader patient populations.     

Expression of p21WAF1 in Astler-Coller stage B2 colorectal cancer is associated with survival benefit from 5FU-based adjuvant chemotherapy

In several, but not all, previous studies, positive p21^WAF1 expression has been suggested as an indicator of a good prognosis in patients with stage III/IV colorectal cancer. However, it is not known whether the same is true for stage B2 patients. The purpose of this study is to assess the influence of p21^WAF1 expression in tumor cells on disease-free survival (DFS) and overall survival (OS) of Astler–Coller stage B2 and C patients with colorectal cancer who underwent 5-fluorouracil-based adjuvant chemotherapy. Nuclear p21^WAF1 was detected by immunohistochemistry in tissue microarrays from 275 colorectal cancers. The expression of p21^WAF1 was associated with DFS (p = 0.025) and OS (p = 0.008) in the subgroup of stage B2 patients that was treated with adjuvant chemotherapy. In multivariate analysis, it remained the only independent prognostic parameter in relation to DFS and OS (p = 0.035 and p = 0.02, respectively). In the subgroup of 72 stage B2 patients with positive p21^WAF1 expression but not in the subgroup of 61 stage B2 patients with negative p21^WAF1 expression, adjuvant chemotherapy was associated with better DFS (85% 5-year survival versus 65% without chemotherapy, p = 0.03) and OS (96% versus 82%, p = 0.014). In the combined stage B2 and C group of patients treated with adjuvant chemotherapy, positive p21^WAF1 expression was also associated with better DFS and OS (p = 0.03, p = 0.002, respectively). Expression of p21^WAF1 in colorectal tumor cells identifies a subgroup of Astler–Coller stage B2 patients who could benefit significantly from 5FU-based chemotherapy and may improve the selection of patients for adjuvant chemotherapy.