Cobalamin deficiency may cause cognitive deficits and even dementia. In Alzheimer's disease, the most frequent cause of dementia in elderly persons, low serum levels of vitamin B12, may be misleading. The aim of this work was to characterize the cognitive pattern of B12 deficiency and to compare it with that of Alzheimer's disease. Nineteen patients with low levels of vitamin B12 were neuropsychologically evaluated before treatment and a year later. Results were compared with those of 10 healthy control subjects. Final results suggest that there is a different pattern in both diseases. Twelve elderly patients with dementia improved with treatment. Seven elderly demented patients did not improve; they deteriorated after 1 year although their levels of cobalamin were normal. Analysis of the initial evaluation showed that the 2 groups of patients had a different neuropsychological profile. The group that improved had initially more psychotic problems and more deficits in concentration, visuospatial performance, and executive functions. They did not show language problems and ideomotor apraxia, which were present in the second group. Their memory pattern was also different. These findings suggest that cobalamin deficiency may cause a reversible dementia in elderly patients. This dementia may be differentiated from that of Alzheimer's disease by a thorough neuropsychological evaluation.

Minor salivary gland biopsy is a potentially simple procedure with high diagnostic value used primarily in the diagnosis of Sjögren's syndrome. We summarise our experience performing a simplified biopsy procedure, which is modified to allow its use by rheumatologists and other non-surgical physicians in an outpatient setting.

No abstract

A diagnostic delay of several years in primary Sjögren's syndrome is common, even in patients who present with sicca symptoms. It is much more likely in cases with prominent symptomatic extraglandular involvement. We report on three such patients who presented as Coomb's positive haemolytic anaemia, systemic symptoms with agranulocytosis and gingival bleeding due to immune thrombocytopenia, to alert clinicians to the fact that primary Sjögren's syndrome may present as clinically significant immune-mediated cytopenia in the absence of sicca symptoms. Sjögren's syndrome, a common autoimmune disorder, should be considered in the differential diagnosis of apparently 'idiopathic' cytopenias and actively sought by directed history, Schirmer test and autoantibody screening.

The case: A 52-year-old woman was admitted with painful swelling in her left thigh. She had a 12-year history of type 2 diabetes mellitus and hypertension, and she was a smoker (40 pack-year smoking history). At her last examination, her HbA 1C level was 7.7%, her serum total cholesterol level was 8.65 (normal < 5.17) mmol/L and her triglyceride level was 3.77 (normal < 2.26) mmol/L. She had diabetic retinopathy and microalbuminuria, and she had a myocardial infarction 12 years earlier. Two months before admission, the patient underwent a left femoropopliteal bypass for peripheral vascular disease. Her medications at the time of admission included acetylsalicylic acid, enalapril, metformin, glibenclamide and simvastatin.On admission, the patient complained of continuous severe pain in her anterior thigh that had developed gradually. The pain was not reduced by nonsteroidal antiinflammatory drugs taken orally. She reported that the pain was very intense, and that it was present at rest but became worse with movement. The pain had increased over the 4 weeks before presentation. She denied any trauma, fever or chills. The patient had lost 4 kg, and she was unable to walk because of the pain.A physical examination showed a firm swelling in the anterior part of her thigh. An area that measured 10 × 5 cm was hard and felt warm, and there was mild erythema and tenderness. The patient's muscle strength and motion were markedly limited by pain.Her acute phase reactants were elevated: her erythrocyte sedimentation rate was 153 (normal 0-30) mm/h, and her C-reactive protein level was 115 (normal 0.2-3.0) mg/L. She was anemic (hemoglobin 6.2 mmol/L) and had mild leukocytosis (11.2 [normal 3.8-9.8 . The results of liver function tests were normal. Doppler ultrasonography showed no abscess or deep vein thrombosis. Her femoropopliteal bypass graft and larger arteries were patent. Magnetic resonance imaging showed increased signal intensity on T 2 -weighted images of her left quadricep, with diffuse subcutaneous and fat edema. There was extensive swelling of the quadriceps vastus medialis and rectus with intermuscular edema (Figure 1, Figure 2). Despite 3 weeks of bed rest, opiates, enoxaparin and clopidogrel, there was only a slight clinical improvement. However, her Creactive protein level gradually decreased. An open muscle biopsy was performed to rule out a tumour. Instead, diabetic muscle infarction was confirmed (Figure 3). One week after the biopsy, there was significant worsening of her pain and severe edema of