Neuropsychiatric systemic lupus erythematosus (NPSLE) is a generic definition referring to a series of neurological and psychiatric symptoms directly related to systemic lupus erythematosus (SLE). NPSLE includes heterogeneous and rare neuropsychiatric (NP) manifestations involving both the central and peripheral nervous system. Due to the lack of a gold standard, the attribution of NP symptoms to SLE represents a clinical challenge that obligates the strict exclusion of any other potential cause. In the acute setting, management of these patients does not differ from other non-SLE subjects presenting with the same NP manifestation. Afterwards, an individualized therapeutic strategy, depending on the presenting manifestation and severity of symptoms, must be started. Clinical trials in NPSLE are scarce and most of the data are extracted from case series and case reports. High-dose glucocorticoids and intravenous cyclophosphamide remain the cornerstone for patients with severe symptoms that are thought to reflect inflammation or an underlying autoimmune process. Rituximab, intravenous immunoglobulins, or plasmapheresis may be used if response is not achieved. When patients present with mild to moderate NP manifestations, or when maintenance therapy is warranted, azathioprine and mycophenolate may be considered. When symptoms are thought to reflect a thrombotic underlying process, anticoagulation and antiplatelet agents are the mainstay of therapy, especially if antiphospholipid antibodies or antiphospholipid syndrome are present. Recent trials on SLE using new biologicals, based on newly understood SLE mechanisms, have shown promising results. Based on what we currently know about its pathogenesis, it is tempting to speculate how these new therapies may affect the management of NPSLE patients. This article provides a comprehensive and critical review of the literature on the epidemiology, pathophysiology, diagnosis, and management of NPSLE. We describe the most common pharmacological treatments used in NPSLE, based on both a literature search and our expert opinion. The extent to which new drugs in the advanced development of SLE, or the blockade of new targets, may impact future treatment of NPSLE will also be discussed.

/pdf/management-of-neuropsychiatric-systemic-lupus-erythematosus-2mzfbyjpwd.pdf

Management of Neuropsychiatric Systemic Lupus Erythematosus: Current Approaches and Future Perspectives

The modern medical literature implicates malaria, and particularly the potentially fatal form of cerebral malaria, with a risk of neurocognitive impairment. Yet historically, even milder forms of malaria were associated in the literature with a broad range of psychiatric effects, including disorders of personality, mood, memory, attention, thought, and behaviour. In this article, the history of psychiatric effects attributed to malaria and post-malaria syndromes is reviewed, and insights from the historical practice of malariotherapy in contributing to understanding of these effects are considered. This review concludes with a discussion of the potentially confounding role of the adverse effects of anti-malarial drugs, particularly of the quinoline class, in the unique attribution of certain psychiatric effects to malaria, and of the need for a critical reevaluation of the literature in light of emerging evidence of the chronic nature of these adverse drug effects.

/pdf/psychiatric-effects-of-malaria-and-anti-malarial-drugs-18bysonph9.pdf

Psychiatric effects of malaria and anti-malarial drugs: historical and modern perspectives.

Malaria remains a major cause of morbidity and mortality worldwide. The classic presentation of malaria with paroxysms of fever is seen only in 50%-70% of patients. Devel- opment of immunity, increasing resistance to antimalarial drugs, and indiscriminate use of antimalarial drugs have led to malaria presenting with unusual features. This review compiles a description of the various atypical manifestations of malaria.

/pdf/atypical-manifestations-of-malaria-3lhnx0n7ov.pdf

Atypical manifestations of malaria.

Susceptibility to quinoline antimalarial intoxication may reflect individual genetic and drug-induced variation in neuropharmacokinetics. In this report, we describe a case of chloroquine intoxication that appeared to be prolonged by subsequent use of multiple psychotropic medications. This case highlights important new considerations for the management of quinoline antimalarial intoxication.

/pdf/prolonged-neuropsychiatric-effects-following-management-of-4nv52h54tn.pdf

Prolonged neuropsychiatric effects following management of chloroquine intoxication with psychotropic polypharmacy.

The last couple of months have witnessed the world in a state of virtual standstill. The SARS-CoV-2 virus has overtaken the globe to economic and social lockdown. Many patients with COVID-19 have compromised immunity, especially in an aged population suffering from Parkinson 's disease (PD). Alteration in dopaminergic neurons and deficiency of dopamine in PD patients are the most common symptoms affecting 1% population above the age of 60 years. The compromised immune system and inflammatory manifestation in PD patients make them an easy target. The most common drugs under trial for COVID-19 are remdesivir, favipiravir, chloroquine and hydroxychloroquine, azithromycin along with adjunct drugs like amantadine with some monoclonal antibodies. Presently, clinically US FDA approved drugs in PD include Levodopa, catechol-O-methyl transferase (COMT) inhibitors, (Entacapone and Tolcapone), dopamine agonists (Bromocriptine, Ropinirole, Pramipexole, and Rotigotine), monoamine oxidase B (MAO-B) inhibitors (Selegiline and Rasagiline), amantadine and antimuscarinic drugs. The drugs have established mechanisms of action on PD patients with known pharmacodynamics and pharmacokinetic properties along with dose and adverse effects. Conclusion and relevance of this review focus on the drugs that can be tried on PD patients with SAR CoV-2 infection, in particular, amantadine that has been approved by all the developed countries as a common drug possessing both antiviral properties by downregulation of CTSL, lysosomal pathway disturbance and change in pH necessary to uncoat the viral proteins and anti- Parkinson properties. To deal with the significant prognostic adverse effect of SARS-CoV-2 on PD, the present-day treatment options, clinical presentation and various mechanisms are the need of the hour.

Targeting COVID-19 in Parkinson's patients: Drugs repurposed.

To the Editor: Drug reaction with eosinophilia and systemic symptoms (DRESSs), also called drug-induced hypersensitivity syndrome, is a life-threatening adverse drug reaction with mortality rates of up to 10%–20%.1 The clinical presentation includes mucocutaneous rash, fever, lymphadenopathy, hematologic abnormalities such as eosinophilia and atypical lymphocytes, and multiple organ dysfunction, including liver, kidneys, heart, and lungs.1 Although fever and rash are the most common presentations, the defining characteristic of the syndrome is organ dysfunction. It usually presents 2–8 weeks after the introduction of the causative agent and symptoms may persist for a longer period of time, despite discontinuing the offending drug. Most commonly associated medications are aromatic antiepileptics.2,3 Others include sulfonamides/sulfones, nonsteroidal anti-inflammatory agents, angiotensinogen-converting enzyme inhibitors, and antidepressants. The precise incidence of DRESS is yet to be determined; an estimate is 1/1000 to 1/10,000 new users of antiepileptic therapy may present with this hypersensitivity reaction.4,5 The patient is a 29-year-old woman with a history of chronic pancreatitis and gastric bypass surgery, who initially presented with lower extremity swelling in the setting of hypoalbuminemia and protein-calorie malnutrition. She was started on a high calorie/protein diet and was discharged on furosemide andmultivitamin tablets. Three weeks after discharge, she noticed peri-oral rash, which extended to lower extremities, groin, and trunk. On presentation she had multiple areas of erythema and crusting over body, with small tense vesicles of legs and bilateral lower extremity edema. Blood work showed elevated liver enzymes, elevated International normalized ratio, low vitamin D, macrocytic anemia, and elevated eosinophils. She underwent skin biopsy of the left forearm, which showed spongiotic epidermis with paucicellular intraepidermal vesicle/bullae with scattered eosinophils and neutrophils. Rare necrotic keratinocytes sites were identified within the epidermis. The Naranjo algorithm score was 5 that indicated probable adverse dug reaction to furosemide, and no other offending agents were identified. She was diagnosed with DRESS syndrome secondary to furosemide and was started on oral prednisone therapy in view of liver dysfunction. The rash and liver function improved with oral steroid therapy. Hospital course was complicated by sudden drop in hemoglobin. No source of bleeding was identified. Hemolysis workup came back positive with elevated Lactate Dehydrogenase, low haptoglobin, elevated reticulocyte count, and positive C3 and poly antibody Coombs tests (negative Immunoglobulin G Coombs test). She was diagnosed with autoimmune hemolytic anemia refractory to oral prednisone therapy and received 1 dose of intravenous immunoglobulin therapy. She also received 1 unit of packed red blood cells. Her hemoglobin remained stable, without any further drop. She was discharged on oral prednisone therapy and completed prednisone taper over the next 12 weeks as an outpatient. No recurrence of hemolytic episodes is seen in 6 months outpatient follow-up. DRESS syndrome is a severe delayed type hypersensitivity (type IV hypersensitivity) reaction with a prolonged latency period of 3–8 weeks. The clinical course of the syndrome varies widely. Early in the course it may present with prodromal symptoms (fever, pruritus, dysphagia, or lymphadenopathy) and a mucocutaneous rash.1 Internal organ involvement is the characteristic feature of DRESS syndrome, and the most commonly involved organs are the liver, kidneys, heart, and lungs. Although fever and rash are the most common presenting features, liver damage may develop before the onset of a rash in up to 10% of patients.6 Hematologic abnormalities, including eosinophilia and atypical lymphocytosis may be seen on initial presentation. The most commonly associated drugs are aromatic anticonvulsants (carbamazepine, phenytoin, and phenobarbital). Although cross-sensitivity as high as 75% has been reported among the aromatic anticonvulsants, carbamazepine remains the most widely reported agent.7 There are only a few case reports of DRESS syndrome in association with loop diuretics (furosemide and torsemide). American Journal of Therapeutics 0, 1–3 (2020)

Furosemide-Associated Drug Reaction With Eosinophilia and Systemic Symptoms.

Chloroquine is a commonly prescribed antimalarial drug that is widely used for the presumptive treatment of malaria in India. It has rarely been reported to cause psychosis, and to the best of our knowledge, recurrent psychosis due to chloroquine use has been reported only once, in 1996. We are reporting the second case of chloroquine-induced recurrent psychosis. We also discuss some of the possible neurobiological mechanisms leading to this neurotoxic adverse effect and our recommendations for future use of this drug.

Chloroquine-induced recurrent psychosis.

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Furosemide-Associated Drug Reaction With Eosinophilia and Systemic Symptoms.

Chloroquine-induced recurrent psychosis.