Tubercular meningitis is a devastating presentation of extra pulmonary tuberculosis, with fatality in each case without treatment. A 39 years male, a regular consumer of alcohol and a known case of major depressive disorder, presented with the alleged history of using an electric heater in a closed room, and presented to emergency with unconsciousness and cardiac arrest. As his neurological status didn’t improve over 72 hrs, a magnetic resonance imaging brain was done which was non-conclusive. Electroencephalogram revealed diffuse right fronto-parietal seizure activity ceasing with midazolam injection, hence levetiracetam was started. Lumbar puncture revealed increased adenosine deaminase and nil white blood cells. Repeat lumbar puncture showed lymphocytic–predominant pleocytosis, elevated protein and low glucose. The patient was started on anti-tubercular therapy and an injection of dexamethasone was added. Repeat electroencephalogram didn’t show any seizure-like activity. It is important to be aware of variety of presentations of tubercular meningitis. Delay in treatment leads to irreversible neurological damage and even death.

Azathioprine (AZA) is commonly used as immunosuppressive therapy for autoimmune diseases, including systemic lupus erythematosus (SLE). Myelosuppression is a common side effect of AZA. Here we report a case of severe myelosuppression following AZA therapy in a 15-year-old girl despite a normal thiopurine methyltransferase (TPMT) level. She had been receiving AZA for SLE and presented with neutropenic fever and pancytopenia. AZA was stopped. After stopping AZA, her blood counts steadily improved. When TPMT genotyping results were normal, AZA was reintroduced. Pancytopenia reappeared after starting AZA, despite normal TPMT genotype. AZA was replaced with mycophenolate mofetil which consequently resulted in improvement of blood counts. It is essential to understand the temporal relationship between AZA use and pancytopenia onset in patients with normal TPMT activity. This case illustrates that regular monitoring of blood cell counts should be routine practice after starting AZA regardless of TPMT activity.azathioprine, systemic lupus erythematosus, thiopurine methyltransferase Key points• Azathioprine-induced myelosuppression can occur in patients with normal thiopurine methyltransferase (TPMT) activity. • Total cell counts should be evaluated on a frequent basis after initiating azathioprine even in patients with normal TMPT activity.

Isoniazid is an anti-tuberculosis medication that is extensively used for treatment and prevention of tuberculosis. Acute isoniazid poisoning is characterized by a clinical triad of recurrent seizures, raised anion gap metabolic acidosis and coma. The seizures are unresponsive to standard anticonvulsant drugs, instead requiring pyridoxine administered in a dose equal to the amount of isoniazid consumed. Due to the high incidence of tuberculosis in low-income countries like Nepal, isoniazid intoxication should be considered in any patient who present with such unresponsive seizures and coma. We report a case of a 31 years old woman from Nepal, who intentionally ingested 12 grams of isoniazid and presented with generalized tonic-clonic seizures. She was successfully managed with 10 grams of pyridoxine along with other supportive management, including sodium bicarbonate for metabolic acidosis and mechanical ventilation. Doctors working in low-income countries, like Nepal, where tuberculosis is endemic, should be well acquainted with presentations and management of isoniazid intoxication.

Paraquat (1, 1′-dimethyl-4,4′-bipyridinium) is a commonly used herbicide that is highly toxic when ingested. Ingestion of toxic doses of paraquat has serious complications on the lungs, gastrointestinal tract, kidney, liver, and other organs. Due to its inherent toxicity and the lack of a specific antidote, it has a high case fatality rate. Despite being restricted to commercially licensed users in Nepal, it is a common herbicide causing both intentional and accidental poisoning. Although there have been numerous anecdotal cases of paraquat poisoning in Nepal, no reports have been published in the literature. . We report a case of a 30-year old female, who developed gastrointestinal symptoms like vomiting, diarrhoea and odynophagia, renal and liver injury after accidental ingestion of 10ml of 20% paraquat. Symptoms and organ involvement subsided with timely and appropriate supportive management.