Deliberate self-harm is a major problem in the developing world, responsible for around 600 000 deaths in 1990. The toxicity of available poisons and paucity of medical services ensure that mortality from self-poisoning is far greater in the tropics than in the industrialized world. Few data are available on the poisons most commonly used for self-harm in different parts of the world. This paper reviews the literature on poisoning, to identify the important poisons used for self-harm in these regions. Pesticides are the most important poison throughout the tropics, being both common and associated with a high mortality rate. In some regions, particular pesticides have become the most popular method of self-harm, gaining a notoriety amongst both health-care workers and public. Self-poisoning with medicines such as benzodiazepines and antidepressants is common in urban areas, but associated with few deaths. The antimalarial chloroquine appears the most significant medicine, self-poisoning being common in both Africa and the Pacific region, and often fatal. Paracetamol (acetaminophen) is used in many countries but in few has it reached the popularity typical of the UK. Domestic and industrial chemicals are responsible for significant numbers of deaths and long-term disabilities world-wide. Self-poisoning with plant parts, although uncommon globally, is locally popular in some regions. Few of these poisons have specific antidotes. This emphasizes the importance of determining whether interventions aimed at reducing poison absorption actually produce a clinical benefit, reducing death and complication rates. Future research to improve medical management and find effective ways of reducing the incidence of self-harm, together with more widespread provision of interventions proven to be effective, could rapidly reduce the number of deaths from self-poisoning in the developing world.

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Patterns and problems of deliberate self‐poisoning in the developing world

A b s t r ac t P<0.001); and in patients receiving amphotericin B, as compared with those receiving paromomycin, nephrotoxicity (4% vs. 0, P<0.001), fevers (57% vs. 3%), rigors (24% vs. 0, P<0.001), and vomiting (10% vs. <1%, P<0.001). Conclusions Paromomycin was shown to be noninferior to amphotericin B for the treatment of visceral leishmaniasis in India. (ClinicalTrials.gov number, NCT00216346.)

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Injectable paromomycin for Visceral leishmaniasis in India.

Antibodies to aquaporin-4 (also known as AQP4-Ab or NMO-IgG) are sensitive and highly specific serum markers of autoimmune neuromyelitis optica (NMO). Second-generation recombinant diagnostic assays can detect AQP4-Ab in >or=80% of patients with NMO, and a role for AQP4-Ab in the pathophysiology of this condition was corroborated by a series of in vitro studies that demonstrated disruption of the blood-brain barrier, impairment of glutamate homeostasis and induction of necrotic cell death by AQP4-Ab-positive serum. Additional evidence for such a role has emerged from clinical observations, including the demonstration of a correlation between serum levels of AQP4-Ab and disease activity. The finding of NMO-like CNS lesions and clinical disease following passive transfer of AQP4-Ab-positive serum in several independent animal studies provided definitive proof for a pathogenic role of AQP4-Ab in vivo. Together, these findings provide a strong rationale for the use of therapies targeted against B cells or antibodies in the treatment of NMO. In this Review, we summarize the latest evidence in support of a direct involvement of AQP4-Ab in the immunopathogenesis of NMO, and critically appraise the diagnostic tests currently available for the detection of this serum reactivity.

AQP4 antibodies in neuromyelitis optica: diagnostic and pathogenetic relevance

Kala-azar has re-emerged from near eradication. The annual estimate for the incidence and prevalence of kala-azar cases worldwide is 0.5 million and 2.5 million, respectively. Of these, 90% of the confirmed cases occur in India, Nepal, Bangladesh and Sudan. In India, it is a serious problem in Bihar, West Bengal and eastern Uttar Pradesh where there is under-reporting of kala-azar and post kala-azar dermal leishmaniasis in women and children 0-9 years of age. Untreated cases of kala-azar are associated with up to 90% mortality, which with treatment reduces to 15% and is 3.4% even in specialized hospitals. It is also associated with up to 20% subclinical infection. Spraying of DDT helped control kala-azar; however, there are reports of the vector Phlebotomus argentipes developing resistance. Also lymphadenopathy, a major presenting feature in India raises the possibility of a new vector or a variant of the disease. The widespread co-existence of malaria and kala-azar in Bihar may lead to a difficulty in diagnosis and inappropriate treatment. In addition, reports of the organism developing resistance to sodium antimony gluconate--the main drug for treatment--would make its eradication difficult. Clinical trials in India have reported encouraging results with amphotericin B (recommended as a third-line drug by the National Malaria Eradication Programme). Phase III Trials with a first-generation vaccine (killed Leishmania organism mixed with a low concentration of BCG as an adjuvant) have also yielded promising results. Preliminary studies using autoclaved Leishmania major mixed with BCG have been successful in preventing infection with Leishmania donovani. Until a safe and effective vaccine is developed, a combination of sandfly control, detection and treatment of patients and prevention of drug resistance is the best approach for controlling kala-azar.

Epidemiology of visceral leishmaniasis in India.

The differential diagnosis of acute inflammatory transverse myelitis (ATM) is broad. Therefore, physicians must be aware of the many potential etiologies for acute myelopathy, and should pursue an ordered, efficient, and cost-effective approach to the diagnosis based on the patient's clinical history, examination, and magnetic resonance imaging (MRI) findings. Clinical, immunological, and radiological findings of non-compressive myelopathies are reviewed, as are how these findings can be used to distinguish between demyelinating, infectious, other inflammatory, vascular, neoplastic, and paraneoplastic etiologies. We also review predictors of further episodes of ATM in patients with demyelinating disorders. We discuss the diagnostic clues and pitfalls of the not uncommon clinical scenario of a presumed "myelopathy with normal MRI." Finally, we suggest an algorithm for the diagnosis and management of acute myelopathies.

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An approach to the diagnosis of acute transverse myelitis

A number of cases of copper sulphate poisoning from the southern region of Bangladesh are presented. There was a high mortality (24.9%) in comparison to other forms of poisoning. Hepatotoxicity, acute renal failure and gastrointestinal bleeding were the main complications. This degree of copper sulphate poisoning in one particular area is cause for alarm.

Copper sulphate poisoning

Twenty-seven out of five hundred and fifty three patients hospitalized for visceral leishmaniasis (Kala-azar) died during treatment with sodium antimony gluconate. Data from these patients were evaluated to find out the cause of death. Eight patients had associated diseases such as pulmonary tuberculosis (3), severe malnutrition (1), acute gastroenteritis (1), spleenic infarction (1), acute renal failure (1) and atrial septal defect (1) which could be attributed to death. Twelve patients developed spontaneous haemorrhages from nose, gums and gastrointestinal tract and died, despite of adequate supportive measures. Seven other patients who were improving slowly with antimony therapy died unexpectedly. Though, cause of death could be explained in some patients with associated disease conditions, it could not be explained in others as significant clinical manifestations, haematological, biochemical and electrocardiographic alterations were not evident prior to death. Our impression is that mortality in Kala-azar patients during standard antimonial therapy is more related to the drug rather than the disease process.

Deaths in visceral leishmaniasis (Kala-azar) during treatment.

was extensor and the left was equivocal. There was hypoathesia on the left side of the body from the level of C4 downwards. Posterior column sensation was intact. He developed retention of urine on the day of admission. The haemoglobin concentration was 115 g/I: the total white blood count (WBC) 7.3 x 109/1; platelet 249x 1()'l/I; and urine examination normal. The monos pot and brucella agglutination test were negative. Computed tomography (CT) of the brain was normal. The cerebrospinal fluid (CSF) was clear, with a protein concentration of 815 mg/I; glucose 4 mmol/I (plasma glucose was 6.2 mmol/I); red cells 65 x 106/1; and WBC 38 x 106/1 with 90070 lymphocytes. The CSF protein electrophoresis showed no oligoclonal band. Blood urea serum creatinine and liver enzymes were normal. The parents refused myelography. A CT scan of the spinal cord without myelogram showed no cord compression. Serological tests for common viruses, including cytomegalovirus and Epstein-Barr virus, were negative in blood and CSF. Visual and auditory evoked response values were normal. Electromyogram and nerve conduction studies revealed no evidence of peripheral neuropathy. The patient was treated with dexamithasone for 6 weeks. He required a urinary catheter for the first 2 weeks. Eventually he made a complete recovery without neurological sequelae. Our final diagnosis was post vaccination BrownSequard syndrome affecting the cervical cord.

Ahasan Ha

Papers

Copper sulphate poisoning

Deaths in visceral leishmaniasis (Kala-azar) during treatment.

Neuromyelitis optica (Devic's disease) following chicken pox.

Multiresistant typhoid fever in Bangladesh.

Neuroparalytic complications after anti-rabies vaccine (inactivated nervous tissue vaccine)