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

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

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

We compared the validity of pancytopenia, the formol-gel test (FGT), the indirect fluorescence antibody test (IFAT), the direct agglutination test (DAT), and the rK39 dipstick test as diagnostic criteria for visceral leishmaniasis (VL) in Nepal. Between September 2000 and January 2002, 310 clinical suspects had a bone marrow aspirate, and if negative, a spleen aspirate smear examined for Leishmania donovani. Sensitivity and specificity of all tests were determined compared with parasitology and by latent class analysis (LCA). Compared with parasitology, the sensitivities of the other tests were as follows: pancytopenia = 16.3% (95% confidence interval [CI] = 11.3-22.5%), FGT = 39.9% (95% CI = 32.7-47.4%), IFAT = 28.4% (95% CI = 22.0-35.5%), DAT = 95.1% (95% CI = 90.8-97.7%), and the rK39 dipstick test = 87.4% (95% CI = 81.7-91.9%). Sensitivity estimates obtained by LCA were similar, but specificity estimates were substantially higher (DAT = 93.7% versus 77.8%; rK39 dipstick test = 93.1% versus 77.0%). The DAT or the rK39 dipstick test can replace parasitology as the basis of a decision to treat VL in Nepalese peripheral health services.

A comparative study of the effectiveness of diagnostic tests for visceral leishmaniasis.

Neuromyelitis optica (NMO) is a severe, debilitating human disease that predominantly features immunopathology in the optic nerves and the spinal cord. An IgG1 autoantibody (NMO-IgG) that binds aquaporin 4 (AQP4) has been identified in the sera of a significant number of NMO patients, as well as in patients with two related neurologic conditions, bilateral optic neuritis (ON), and longitudinal extensive transverse myelitis (LETM), that are generally considered to lie within the NMO spectrum of diseases. NMO-IgG is not the only autoantibody found in NMO patient sera, but the correlation of pathology in central nervous system (CNS) with tissues that normally express high levels of AQP4 suggests NMO-IgG might be pathogenic. If this is the case, it is important to identify and understand the mechanism(s) whereby an immune response is induced against AQP4. This review focuses on open questions about the "events" that need to be understood to determine if AQP4 and NMO-IgG are involved in the pathogenesis of NMO. These questions include: 1) How might AQP4-specific T and B cells be primed by either CNS AQP4 or peripheral pools of AQP4? 2) Do the different AQP4-expressing tissues and perhaps the membrane structural organization of AQP4 influence NMO-IgG binding efficacy and thus pathogenesis? 3) Does prior infection, genetic predisposition, or underlying immune dysregulation contribute to a confluence of events which lead to NMO in select individuals? A small animal model of NMO is essential to demonstrate whether AQP4 is indeed the incipient autoantigen capable of inducing NMO-IgG formation and NMO. If the NMO model is consistent with the human disease, it can be used to examine how changes in AQP4 expression and blood-brain barrier (BBB) integrity, both of which can be regulated by CNS inflammation, contribute to inductive events for anti-AQP4-specific immune response. In this review, we identify reagents and experimental questions that need to be developed and addressed to enhance our understanding of the pathogenesis of NMO. Finally, dysregulation of tolerance associated with autoimmune disease appears to have a role in NMO. Animal models would allow manipulation of hormone levels, B cell growth factors, and other elements known to increase the penetrance of autoimmune disease. Thus an AQP4 animal model would provide a means to manipulate events which are now associated with NMO and thus demonstrate what set of events or multiplicity of events can push the anti-AQP4 response to be pathogenic.

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Neuromyelitis optica pathogenesis and aquaporin 4

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

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.

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

INTRODUCTION The demonstration of Leishman-Donovan bodies (amastigotes) in spleen, bone-marrow or lymph node aspirates provides the definitive diagnosis of Kala-azar. These procedures have some limitationsI,2 because they are not always practicable in rural settings. Specific serological tests are complex, require trained manpower and a well equipped laboratory. People of low socio-economic group residing in the rural area are often the victims of Kala-azar. They are usually beyond the reach of well equipped laboratory facilities. In such circumstances the aldehyde test (AT) (Formol-Gel test), which is nonspecific, is simple to do and less costly. This communication assesses the role of this test in the diagnosis of Kala-azar in a part of the world where the diagnostic facilities are scarce.

Rafiqueuddin Ak

Papers

Copper sulphate poisoning

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

Aldehyde test (Formol-Gel test) in the diagnosis of kala-azar (visceral leishmaniasis).

Multiresistant typhoid fever in Bangladesh.

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