Repair of large midline incisional hernias with polypropylene mesh: Comparison of three operative techniques

Polypropylene mesh is widely used for the reconstruction of incisional hernias that cannot be closed primarily. Several techniques have been advocated to implant the mesh. The objective of this study was to evaluate, retrospectively, early and late results of three different techniques, onlay, inlay, and underlay. The records of 53 consecutive patients with a large midline incisional hernia — 25 women and 28 men, mean age 60.4 (range 28–94) — were reviewed. Polypropylene mesh was implanted using the onlay technique in 13 patients, inlay in 23 patients, and underlay in 17 patients. Either the greater omentum or a polyglactin mesh was interponated between the mesh and the viscera. The records of these 53 patients were reviewed with respect to: size and cause of the hernia, pre- and postoperative mortality and morbidity, with special attention to wound complications. Patients were invited to attend the outpatient clinic at least 12 months after implantation of the mesh for physical examination of the abdominal wall. Postoperative complications occurred in 14 (26.4%) patients. The onlay technique had significantly more complications, as compared to both other techniques. Reherniation occurred in 15 (28.3%) patients. The reherniation rate of the inlay technique was significantly higher than after the underlay technique (44% vs 12%, P=0.03) and tended to be higher than the onlay technique (44% vs 23%, P=0.22). Repair of large midline incisional hernias with the use of a polypropylene mesh carries a high risk of complications and has a high reherniation rate. The underlay technique seems to be the better technique.     

The Scimitar syndrome: CT findings in partial anomalous pulmonary venous return

An anomalous pulmonary vein draining into the subdiaphragmatic inferior vena cava was initially demonstrated on computed tomographic (CT) scans. The diagnosis of scimitar syndrome was confirmed with digital subtraction angiography. In retrospect, the anomalous vein and dextroposition of the heart were shown on chest radiographs.     

Folic acid in the treatment of acute watery diarrhoea in children: a double-blind, randomized, controlled trial

One-hundred and six male children aged 6-23 months with a history of acute watery diarrhoea of less than 72 h duration were randomized to receive either folic acid in a dose of 5 mg at 8-h intervals or placebo for 5 d. There were 54 children in the folic acid group and 52 in the placebo group. The admission characteristics were comparable between the two groups. No significant differences were observed in the intake of oral rehydration solution or stool output between the groups. The mean ± SD of total stool output (g kg⁻¹) was 532 ± 476 vs 479 ± 354 and the duration (h) of diarrhoea was 108 ± 68 vs 103 ± 53 in the folic acid vs placebo group, respectively. The findings, therefore, should have a positive influence on preventing the inappropriate use of folic acid in acute diarrhoea.     

Quantitative trait loci controlling allergen-induced airway hyperresponsiveness in inbred mice

Identification of the genetic loci underlying asthma in humans has been hampered by variability in clinical phenotype, uncontrolled environmental influences, and genetic heterogeneity. To circumvent these complications, the genetic regulation of asthma-associated phenotypes was studied in a murine model. We characterized the strain distribution patterns for the asthma-related phenotypes airway hyperresponsiveness (AHR), lung eosinophils, and ovalbumin (OVA)-specific serum immunoglobulin (Ig) E induced by allergen exposure protocols in A/J, AKR/J, BALB/cJ, C3H/HeJ, and C57BL/6J inbred strains and in (C3H/HeJ x A/J)F1 mice. Expression of AHR differed between strains and was sometimes discordant with lung eosinophils or serum IgE. Furthermore, we identified two distinct quantitative trait loci (QTL) for susceptibility to allergen-induced AHR, Abhr1 (allergen-induced bronchial hyperresponsiveness) (lod = 4. 2) and Abhr2 (lod = 3.7), on chromosome 2 in backcross progeny from A/J and C3H/HeJ mice. In addition, a QTL on chromosome 7 was suggestive of linkage to this trait. These QTL differ from those we have previously found to control noninflammatory AHR in the same crosses. Elucidation of the genes underlying these QTL will facilitate the identification of biochemical pathways regulating AHR in animal models of asthma and may provide insights into the pathogenesis of human disease.     

Correction of a suppressor cell deficiency in four patients with familial mediterranean fever by in vitro or in vivo colchicine

We have previously reported that three patients with familial Mediterranean fever (FMF) had deficient concanavalin A (Con A) activated suppressor cell inhibition of the proliferation of healthy volunteers' phytohaemagglutinin stimulated responder cells. When these three FMF patients were treated with long term oral colchicine (2 mg/day), their Con A activated suppressor cell deficiency was corrected and FMF attacks prevented. In the present report, the effect of in vitro as well as in vivo colchicine treatment on the suppressor cell function of these three FMF patients as well as one more FMF patient was tested to determine whether colchicine can directly increase suppressor cell function rather than colchicine's preventing FMF attacks by unknown mechanisms which only indirectly results in a correction of the suppressor cell deficiency. Long term oral colchicine treatment corrected the suppressor cell deficiency in the four FMF patients (5±2%, 35±5%, and 46±4% for mean ±s.e.m.% suppression for 0, 1 and 2 mg/day of oral colchicine, respectively). Oral colchicine treatment corrected their suppressor cell deficiency within one week of commencing treatment and even corrected one of the FMF patient's suppressor cell deficiency while he still had some FMF attacks on 1 mg/day of colchicine. Suppressor cells from two of the in vivo untreated FMF patients cultured with 10^-5 M colchicine plus Con A significantly (P<0·01) suppressed proliferation (36±5%) as compared to their suppressor cells cultured only with Con A (4±7%). Furthermore, these in vivo untreated FMF patients' suppressor cells cultured with 10^-5 M colchicine (without Con A) often suppressed as compared to their suppressor cells cultured in medium. Thus colchicine appears to directly correct these FMF patients' suppressor cell deficiency. These observations raise the possibility that colchicine may be therapeutically useful in treating patients with other diseases associated with an absolute or relative deficiency of suppressor cell function.     

Elastin point mutations cause an obstructive vascular disease, supravalvular aortic stenosis

Supravalvular aortic stenosis (SVAS) is an inherited obstructive vascular disease that affects the aorta, carotid, coronary and pulmonary arteries. Previous molecular genetic data have led to the hypothesis that SVAS results from mutations in the elastin gene, ELN. In these studies, the disease phenotype was linked to gross DNA rearrangements (35 and 85 kb deletions and a translocation) in three SVAS families. However, gross rearrangements of ELN have not been identified in most cases of autosomal dominant SVAS. To define the spectrum of ELN mutations responsible for this disorder, we refined the genomic structure of human ELN and used this information in mutational analyses. ELN point mutations co-segregate with the disease in four familial cases and are associated with SVAS in three sporadic cases. Two of the mutations are nonsense, one is a single base pair deletion and four are splice site mutations. In one sporadic case, the mutation arose de novo. These data demonstrate that point mutations of ELN cause autosomal dominant SVAS.      

Effect of colchicine on T cell subsets of healthy volunteers

We examined the effect of oral colchicine (1-2 mg/day) on four healthy volunteers' T cell subsets. Colchicine significantly (P less than 0.01) decreased the mean (+/- SD) percent of OKT3+ total T cells (from 70 +/- 16 to 47 +/- 13), OKT4+ helper/inducer T cells (from 44 +/- 9 to 24 +/- 6), and OKT8+ suppressor/cytotoxic T cells (from 27 +/- 7 to 17 +/- 7), but did not significantly affect the OKT4:OKT8 ratio (from 1.64 +/- 0.21 to 1.48 +/- 0.45) or concanavalin A-induced suppressor cell function (from 44 +/- 9% to 47 +/- 13%). Thus, colchicine non-selectively decreased the circulating helper/inducer and suppressor/cytotoxic T cells.     

Nutritional status and diarrhoeal pathogen in hospitalized children in Bangladesh

We studied the relationship between nutritional status and infection due to specific enteropathogens in young children with diarrhoea. Overall, 26% of the children were severely underweight, 27% were severely wasted and 19% were severely stunted. Children with Shigellae and V. cholerae O1 were significantly more severely underweight, wasted and stunted than those with rotavirus diarrhoea ( p < 0:0001). Our results indicate that an effective nutrition programme for young children might have greater impact on diarrhoeal illness caused by Shigella and V. cholerae than by rotavirus diarrhoea.