Vitamin B12 deficiency is a common finding in medical practice. It is easily treated with supplementation and typically has a favourable prognosis. In rare circumstances, it can hide a severe disease that should be promptly addressed. We report the case of an acute myeloid leukaemia presenting as an initially predictable B12 deficiency in a vegetarian patient with chronic gastritis. The supplementation rapidly corrected the deficit and the accompanying cytopenias. However, in the following month the cell counts fell once again, leading to the suspicion that other aetiology could be lying beneath the surface. Maintaining a normal peripheral blood smear, the bone marrow biopsy showed myeloblasts and extensive fibrosis compatible with the diagnosis of acute myeloid leukaemia. The neoplasm justified the vitamin deficit by excessive cellular turnover, a vicious cycle only uncovered after supplementation and that ultimately led to the patient’s death.

Uveo-meningeal syndromes are any disorder characterized by the involvement of the uvea and the meninges. They can have multiple causes, including infectious, autoimmune and malignant diseases. We report the case of a patient with a 10-year-old diagnosis of myelodysplastic syndrome that had been stable. He presented with new onset uveitis, ataxia, diplopia and fluctuating consciousness level, without any obvious cause revealed by brain imaging or blood chemistries. An extensive aetiological search showed no obvious cause. Initially, the patient improved spontaneously and was discharged. However, 2 months later, he deteriorated once again, this time with disperse adenomegalies that were not present previously. The bone marrow biopsy showed a high number of blasts, which affirmed the progression of the previously known myelodysplastic syndrome. The lymph nodes were not biopsied due to very low life expectancy, making the procedure futile. A presumptive diagnosis of uveo-meningitis caused by paraneoplastic syndrome was made. The patient died a few months later.

Objective:Vasculitides are a group of rare, systemic diseases that induce inflammatory reactions in blood vessels, causing a reduction of blood flow and ischemia. In the kidney, luminal narrowing reduces blood flow and activates the renin-angiotensin-aldosterone system, causing renovascular hypertension.Design and method:Clinical case report.Results:A 47-year-old male with previous intestinal tuberculosis and hypertension diagnosed two years prior (blood pressure around 220/110 mmHg) was referred to our Hypertension Clinic. He reported self-limited episodes of lumbar pain, tender erythematous nodules in the shins and arthralgias. His mean office blood pressure was 203/118 mmHg, confirmed in home blood pressure monitoring, without medication. He had left ventricular concentric hypertrophy and chronic kidney disease (eGFR 66 mL/min/1.73m2) with albuminuria (561 mg/24 h). Verapamil and clonidine were prescribed to search for secondary hypertension but he missed the following appointment. A few months later he was admitted to the Intensive Care Unit due to a hypertensive emergency, with acute kidney failure and a large peri-renal hematoma. A CT scan and an angiography showed bilateral renal scarring, intrarenal pseudoaneurysms and small irregularities in the renal arteries. The immunologic panel was negative. A PET scan showed a slight enhancement of the aorta walls and common carotid arteries and the diagnosis of large-vessel vasculitis was established. He was discharged with high-dose corticosteroids and lisinopril and returned to our Hypertension Clinic. His blood pressure remained uncontrolled despite full-dose amlodipine, chlorthalidone and nebivolol; lisinopril was stopped due to worsening kidney function. Due to doubts on the diagnosis, the CT scan was repeated, now showing also irregularities in the common hepatic artery and mesenteric artery, suggesting a medium-vessel vasculitis, namely polyarteritis nodosa, and cyclophosphamide was started. His blood pressure is now controlled with lisinopril 2.5 mg, amlodipine 10 mg bid, furosemide 40 mg bid, nebivolol 5 mg and clonidine 0,15 mg tid and his kidney function is stable.Conclusions:Renovascular hypertension is responsible for less than 1% of all cases of hypertension and, when present, it is usually caused by atherosclerotic disease or fibromuscular dysplasia. However, in more infrequent cases, an inflammatory systemic disease may be present and must be considered.