Systematic review of the clinical effectiveness of neuromodulation in the treatment of faecal incontinence.

BACKGROUND: Over the past 18 years neuromodulation therapies have gained support as treatments for faecal incontinence (FI); sacral nerve stimulation (SNS) is the most established of these. A systematic review was performed of current evidence regarding the clinical effectiveness of neuromodulation treatments for FI. METHODS: The review adhered to the PRISMA framework. A comprehensive search of the literature included PubMed, MEDLINE, Embase and Evidence-Based Medicine Reviews. Methodological quality assessment and data extraction were completed in a systematic fashion. RESULTS: For SNS, 321 citations were identified initially, of which 61 studies were eligible for inclusion. Of studies on other neuromodulation techniques, 11 were eligible for review: seven on percutaneous tibial nerve stimulation (PTNS) and four on transcutaneous tibial nerve stimulation (TTNS). On intention-to-treat, the median (range) success rates for SNS were 63 (33-66), 58 (52-81) and 54 (50-58) per cent in the short, medium and long terms respectively. The success rate for PTNS was 59 per cent at the longest reported follow-up of 12 months. SNS, PTNS and TTNS techniques also resulted in improvements in Cleveland Clinic Incontinence Score and quality-of-life measures. Despite significant use of neuromodulation in treatment of FI, there is still no consensus on outcome reporting in terms of measures used, aetiologies assessed, length of follow-up or assessment standards. CONCLUSION: Emerging data for SNS suggest maintenance of its initial therapeutic effect into the long term. The clinical effectiveness of PTNS is comparable to that of SNS at 12 months, although there is no evidence to support its continued effectiveness after this period. PTNS may be a useful treatment before SNS. The clinical effectiveness of TTNS is still uncertain owing to the paucity of available evidence. A consensus to standardize the use of outcome measures is recommended in order that further reports can be compared meaningfully.

Chronic arsenic toxicity in Bangladesh and West Bengal, India--a review and commentary.

Fifty districts of Bangladesh and 9 districts in West Bengal, India have arsenic levels in groundwater above the World Health Organization's maximum permissible limit of 50 microg/L. The area and population of 50 districts of Bangladesh and 9 districts in West Bengal are 118,849 km2 and 104.9 million and 38,865 km2 and 42.7 million, respectively. Our current data show arsenic levels above 50 microg/ L in 2000 villages, 178 police stations of 50 affected districts in Bangladesh and 2600 villages, 74 police stations/blocks of 9 affected districts in West Bengal. We have so far analyzed 34,000 and 101,934 hand tube-well water samples from Bangladesh and West Bengal respectively by FI-HG-AAS of which 56% and 52%, respectively, contained arsenic above 10 microg/L and 37% and 25% arsenic above 50 microg/L. In our preliminary study 18,000 persons in Bangladesh and 86,000 persons in West Bengal were clinically examined in arsenic-affected districts. Of them, 3695 (20.6% including 6.11% children) in Bangladesh and 8500 (9.8% including 1.7% children) in West Bengal had arsenical dermatological features. Symptoms of chronic arsenic toxicity developed insidiously after 6 months to 2 years or more of exposure. The time of onset depends on the concentration of arsenic in the drinking water, volume of intake, and the health and nutritional status of individuals. Major dermatological signs are diffuse or spotted melanosis, leucomelanosis, and keratosis. Chronic arsenicosis is a multisystem disorder. Apart from generalized weakness, appetite and weight loss, and anemia, our patients had symptoms relating to involvement of the lungs, gastrointestinal system, liver, spleen, genitourinary system, hemopoietic system, eyes, nervous system, and cardiovascular system. We found evidence of arsenic neuropathy in 37.3% (154 of 413 cases) in one group and 86.8% (33 of 38 cases) in another. Most of these cases had mild and predominantly sensory neuropathy. Central nervous system involvement was evident with and without neuropathy. Electrodiagnostic studies proved helpful for the diagnosis of neurological involvement. Advanced neglected cases with many years of exposure presented with cancer of skin and of the lung, liver, kidney, and bladder. The diagnosis of subclinical arsenicosis was made in 83%, 93%, and 95% of hair, nail and urine samples, respectively, in Bangladesh; and 57%, 83%, and 89% of hair, nail, and urine samples, respectively in West Bengal. Approximately 90% of children below 11 years of age living in the affected areas show hair and nail arsenic above the normal level. Children appear to have a higher body burden than adults despite fewer dermatological manifestations. Limited trials of 4 arsenic chelators in the treatment of chronic arsenic toxicity in West Bengal over the last 2 decades do not provide any clinical, biochemical, or histopathological benefit except for the accompanying preliminary report of clinical benefit with dimercaptopropanesulfonate therapy. Extensive efforts are needed in both countries to combat the arsenic crisis including control of tube-wells, watershed management with effective use of the prodigious supplies of surface water, traditional water management, public awareness programs, and education concerning the apparent benefits of optimal nutrition.

Chromosomal aberrations induced by cobaltous chloride in mice in vivo.

The effects of cobaltous chloride in inducing chromosomal aberrations were observed on laboratory bred mice in vivo after single oral administration of different fractions (1/10, 1/20, 1/40) of the lethal toxic dose of the salt. Bone marrow cells were flushed out and processed for chromosome studies following colchicine, hypotonic, giemsa, air drying procedure. The parameters screened were chromosomal aberrations, with and without gaps and break per cell. Slides were screened after the expiry of 6, 12, 18, and 24 h. Statistical analysis indicated the clastogenic effects of the salt. The degree of chromosome damage was directly related to the concentration, and also to the period after administration. The different stages of the cell cycle were affected.

Cytotoxic effects of cobalt chloride on mouse bone marrow cells in vivo.

Various dilutions (1/10, 1/20, 1/40) of the lethal toxic dose of cobalt chloride, a non-carcinogenic salt, were found to be clastogenic to bone marrow cells of mice when administered orally in vivo. The clastogenic effects, mainly chromosome breaks, increased significantly with increasing concentration. The frequency of cell division was affected only by higher concentrations of the salt.

Iron in sickle cell disease.

Iron deficiency anaemia was detected in 23% of cases with homozygous sickle cell disease. The aetiology of iron deficiency was similar to the other population in the community. High serum ferritin level was detected in 15.4% of the cases and was well correlated to the number of transfusions. Tissue haemosiderosis was not detected in any case. Patients with heterozygous sickle cell had either normal or low serum ferritin levels.