Giant Cell Arteritis Presenting as Multiple Ischaemic Strokes: A Successful case of Endovascular Treatment.

Giant cell arteritis (GCA) may manifest with aggressive intracranial stenosis resistant to medical therapy, and patients may develop refractory neurologic deficits and cerebral infarcts, making GCA a life-threatening condition. We report the case of a 68-year-old woman recently diagnosed with GCA, medicated with prednisolone 60 mg daily. Two weeks later, the patient was admitted to our Stroke Unit after a sudden episode of global aphasia. Magnetic resonance angiography showed two recent ischaemic lesions, besides an erythrocyte sedimentation rate of 17 mm/hour. A cerebral angiography revealed bilateral stenosis and dilation in the petrous, cavernous and supraclinoid segments of internal carotid arteries (ICA). The patient was started on intravenous methylprednisolone pulses (250 mg daily for five days). Computed tomography (CT) angiography and Doppler ultrasound showed severe vascular disease affecting multiple territories, without significant intracranial involvement. The hypothesis of GCA with extracranial vasculitic involvement was considered as the aetiology of ischaemic cerebral infarctions in multiple territories and, given the severity of the disease, it was decided to add tocilizumab. Despite this, the patient evolved with significant worsening neurological deficits and a CT scan confirmed the presence of new vascular events. Endovascular treatment (EVT) with balloon angioplasty was conducted on both ICAs, with improved calibre and downstream filling. After that, the patient presented sustained clinical improvement, without recurrence of any ischaemic events at the one-year follow-up. This clinical case stands out for the importance of EVT as an effective therapy in patients with medically refractory GCA with symptomatic intracranial stenosis, improving their prognosis. LEARNING POINTS: Giant cell arteritis may manifest with aggressive and symptomatic intracranial arterial stenoses.Endovascular treatment is an effective intervention to prevent ischaemic complications in intracranial giant cell arteritis.

One Size Does Not Fit All: Medication Reconciliation and Review at the Hospital at Home.

Mistakes in the medication process are frequent and a common cause of morbidity and mortality. Medication reconciliation (MRec) and medication review (MRev) are the processes of creating the most accurate medication list and adapting it to optimize the effectiveness of medicines and minimize adverse effects. This is crucial in all stages of medical care, especially at discharge. The present study aims to evaluate and describe the process of MRec and MRev, with a focus on deprescribing, that we conduct at the Hospital at Home. We performed a retrospective cohort study including adult patients admitted at our Hospital at Home from 1 November 2022 to 30 April 2023. MRec and MRev were applied during hospitalization, according to patients' characteristics and clinical evolution, and then communicated to patients upon discharge. Our study involved 125 patients, with an average age of 67.6±18.0 years, and half of them had polypharmacy. We discovered discrepancies in 43.2% of patient's medication and did deprescribing in one-third of them. In the deprescribing group, patients were significantly older (mean age, 76.1 versus 66.4 years; p=0.044). It is imperative to create mechanisms to identify patients at a greater risk of adverse drug events and to minimize the burden of care and harms associated with treatments. The Hospital at Home could be an opportunity, although further research is essential.

Fat Embolism: A Rare Complication of Bone Biopsy.

We report a woman who was admitted to the hospital with a sudden onset of extensive maculopapular erythematous rash involving the trunk and extremities, six weeks after initiating antihypertensive medication. She had atypical lymphocytosis with Gumprecht shadows, elevated liver enzymes, and acute kidney injury. The diagnosis of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome secondary to antihypertensive drugs was suspected and the antihypertensive drugs were suspended. A hypothesis of lymphoproliferative disease was also considered, and consequently, a myelogram and bone biopsy of the iliac crest were performed. After the procedure, the patient developed acute hypoxemia. After the exclusion of pulmonary thromboembolism by CT angiography, we assumed a presumptive diagnosis of iatrogenic fat embolism syndrome (FES) associated with bone biopsy. The patient deteriorated with worsening hypoxemia and ultimately died. This case represented a diagnostic challenge and highlighted iatrogenesis's undesirable and potentially fatal effects. Careful consideration of the risk-benefit ratio of all medical procedures is paramount in daily medical practice and knowledge of the possible risks is necessary for their early recognition and therapeutic approach.

Gabapentin-Induced Cutaneous Leukocytoclastic Vasculitis: A Case Report.

Leukocytoclastic vasculitis (LCV) is a type of small vessel vasculitis, characterized by a perivascular neutrophilic inflammatory infiltrate with fibrinoid necrosis and fragmentation of nuclei ("leukocytoclasia"). Although up to half of the cases of LCV are idiopathic, infections and drugs are the most common secondary triggers for this condition. We present the case of an 88-year-old woman who developed an erythematous maculopapular rash on both thighs three days after starting gabapentin for neuropathic leg pain, without other associated symptoms. Skin biopsy was compatible with cutaneous vasculitis with a leukocytoclastic pattern. The skin lesions resolved within about 10 days after discontinuing gabapentin, supporting the diagnosis. To our knowledge, there are only four published cases of LCV secondary to gabapentin. This case highlights the importance of being alert for diagnosing drug-related cutaneous manifestations, even if the drug is used in our daily practice and vasculitis is not a common side effect, since discontinuing the suspected agent is crucial to resolve skin lesions and to avoid more serious complications.

Metamizole-Induced Type I Kounis Syndrome.

Kounis syndrome (KS) is defined as acute coronary syndrome (ACS) triggered by mast cell and platelet activation in the setting of allergic or anaphylactic insults. KS is a unique and complex cause of ACS and many cases may be missed due to its highly variable clinical manifestations. In this report, we present a case of KS type I triggered by metamizole in the absence of a previous history of allergy to this drug. Following the administration of metamizole, the patient developed generalized acute urticaria, chest pain and diaphoresis. Electrocardiography (ECG) showed ST-segment elevation suggestive of myocardial infarction complicated by ventricular tachycardia. No coronary disease was observed on coronary angiography. The cardiac manifestations of KS may be life-threatening, and so it is important to appropriately recognize and treat this condition. LEARNING POINTS: Kounis syndrome (KS) diagnosis requires a high index of suspicion and should be considered in patients who present with acute coronary syndrome (ACS) soon after the administration of a new medication or possible allergic stimulus.Treatment should be administered carefully, since some drugs used to treat the cardiac manifestations of KS can worsen the allergic reaction.The prognosis is generally good with appropriate treatment, but some complications may occur, such as malignant arrhythmia.

Gitelman Syndrome: A Rare Case of Hypokalaemia and a Novel Mutation.

Gitelman syndrome (GS) is a hereditary renal tubulopathy caused by mutations in the SLC12A3 gene which encodes the thiazide-sensitive apical sodium-chloride cotransporter. GS is characterized by hypokalaemia, hypomagnesaemia and metabolic alkalosis. Treatment is based on potassium and magnesium replacement ad eternum. We present the case of a young man with palpitations and persistent hypokalaemia, who was diagnosed with GS. Genetic testing revealed 2 mutations in the gene SLC12A3 of combined heterozygosity, both considered pathological. Interestingly, 1 of these mutations was not yet described in the literature or in the reviewed databases. We also discuss the clinical approach and the specificities of managing this rare hereditary renal tubulopathy.. LEARNING POINTS: Gitelman syndrome is a rare cause of persistent hypokalaemia.A definitive diagnosis is determined by the identification of mutations in the SLC12A3 gene.Management consists of chronic potassium and magnesium supplementation aimed at symptom control.