Chlorpyrifos is an organophosphate compound recognized as causing acute toxicity. However, organophosphate-induced delayed polyneuropathy (OPIDP), although rare, has also been described. We describe an unusual presentation of OPIDP with flaccid quadriplegia progressing to a locked-in-like syndrome, 30 days after a 60-year-old man voluntarily ingested chlorpyrifos. In the absence of specific treatment, the patient only recovered partial motor responses and the ability to communicate. The authors present this report in order to highlight a form of OPIDP which can hinder diagnosis due to its atypia and the delay in the onset of symptoms from initial contact with the toxicant. LEARNING POINTS• Organophosphate-induced delayed polyneuropathy (OPIDP) is a late presentation which is often overlooked despite causing significant morbidity.• OPIDP can present in several forms, hindering the final diagnosis and consuming resources. KEYWORDSOrganophosphate poisoning, delayed neuropathy, quadriplegia BACKGROUND Organophosphates are known for their muscarinic and nicotinic toxicity occurring within minutes to hours after exposure
Anti-signal recognition particle (SRP) myopathy is a rare idiopathic inflammatory myositis that usually affects middle-aged women and is characterized by rapidly progressive proximal and symmetrical muscle weakness, elevated creatine kinase levels, severe necrotizing immune-mediated myopathy, presence of anti-SRP autoantibodies and poor response to steroid therapy. We report the case of a previously independent geriatric patient presenting with slow onset of proximal paraparesis, myalgia and severe gait impairment. Steroid and azathioprine treatment resulted in laboratory improvement and pain relief, but poor muscle strengthening. The atypical presentation delayed the correct diagnosis. LEARNING POINTS• Anti-signal recognition particle (SRP) myopathy is a rare idiopathic inflammatory myositis which can occur in the elderly.• Atypical onset of the disease can hamper the diagnosis.• SRP myopathy should be considered in the differential diagnosis of similar entities.
The association between mesenteric panniculitis and Sjögren’s syndrome, although rare, is starting to be recognized. Usually, mesenteric panniculitis is symptomatic, presenting with either general or gastrointestinal symptoms. Sjögren’s syndrome is an autoimmune disease that typically affects secretory glands, but may have serious systemic involvement. We report the case of a 77-year-old patient in whom accidental discovery of asymptomatic mesenteric panniculitis on computed tomography led to the diagnosis of Sjögren’s syndrome with several systemic manifestations. LEARNING POINTS Mesenteric panniculitis is a rare condition, sometimes associated with autoimmune diseases, which can make the differential diagnosis with more frequent systemic diseases difficult. There is no specific treatment for mesenteric panniculitis, but it is agreed that only symptomatic patients should be treated. Although Sjögren’s syndrome typically presents with xerostomia and xerophthalmia (dry eyes and mouth syndrome, DEMS), it should always be kept in mind that systemic manifestations can occur, especially in more severe cases.
Antibiotics are known to cause adverse reactions, but multiple organ involvement associated with nonspecific symptoms can lead to a delay in diagnosis. A definitive correlation between each toxin and its effects is difficult to establish due to concomitant potential toxins in the circulation. This article highlights an uncommon case of concomitant nitrofurantoin-induced autoimmune hepatitis and lung fibrosis that fulfills the definitive clinical criteria for diagnosis, presenting histological, imagiological, and immunological evidence of nitrofurantoin-induced toxicity. It occurred in a 68-year-old woman with extended nitrofurantoin intake for urinary tract infection prophylaxis who presented with progressive exercise dyspnea and jaundice. Similar published cases are also reviewed in this article.
Creutzfeldt-Jakob disease (CJD) is a rare, incurable and fatal condition that can only be confirmed through neuropathological investigation, such as brain biopsy or post-mortem study. However, a probable diagnosis can be made using clinical criteria. CJD manifests as rapidly progressive dementia with myoclonus and to a lesser extent visual impairment and cerebellar and pyramidal/extrapyramidal signs. We report the case of a previously independent adult male that met all the clinical criteria. Taken together, the investigation results suggested probable CJD.
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