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Hydatid disease is endemic in many parts of the world. The location is mostly hepatic (75%) and pulmonary (15%), and only 10% of the cysts occur in the rest of the body. It may develop in almost any part of the body. Although hydatidosis can be present in all parts of the human body, urinary tract involvement develops in only 2–4% of all cases, and isolated renal cysts are extremely rare. There are no specific clinical symptoms or signs that will reliably confirm the diagnosis of renal echinococcosis. In addition, there is no laboratory finding that is pathognomonic for hydatid disease except for hydatiduria. Routine blood tests are generally normal except for eosinophilia which is found in only 50% of the cases. Radiological studies have a more important place in the preoperative diagnosis of renal hydatic disease. However, there is no specific sign on plain radiography or intravenous urography, and ultrasound or computed tomography cannot always show a hydatidosis as a specific lesion. From these reasons, sometimes it is difficult to differentiate between a unilocular hydatid cyst without mural calcification and a simple renal cyst. So, despite its rarity, hydatid disease should be included in the differential diagnosis of cystic lesions in solid organs or other anatomic sites, especially in endemic countries. We present herein a patient with isolated renal hydatid cyst mimicking a simple cyst treated successfully with complete excision.

The presence of anti-gliadin antibodies (AGA) and their relationship with intestinal permeability and prevalence of undiagnosed coeliac disease (CD) in ankylosing spondylitis (AS) were investigated. Blood samples from 30 AS patients and 19 age- and sex-matched controls were analysed for human leucocyte antigen (HLA)-B27, AGA and endomysial antibodies (EMA). Immunoglobulin (Ig) A-type AGA and IgG-type EMA were determined by enzyme-linked immunosorbent assay. AGA-positive patients were examined by gastroduodenoscope and proximal small bowel mucosa biopsies were performed. Eleven (36.7%) AS patients were AGA positive (compared with none of the control subjects) and three (10.0%) of these AS patients were also EMA-positive. The presence of AGA was not associated with more severe AS. Mild-to-severe villous atrophy and hyperplasia of crypts with increased chronic inflammatory cells in the lamina propria, which is typical of CD, was only observed in one AGA/EMA positive AS patient; CD was subsequently diagnosed by histology. Although AGA positivity might contribute to the pathogenesis of AS by increasing intestinal permeability to micro-organisms or by modifying intestinal immune mechanisms, further work is required to clarify its role in AS.

We aimed to investigate the rate of MEFV, the gene mutated in familial Mediterranean fever, mutations in patients with myeloid neoplasm and to determine if known mutations of MEFV cause a tendency for myeloid neoplasms. The frequency of the five most common MEFV gene mutations (M694V, M680I, V726A, E148Q and M694I) was determined in 26 patients with myeloid neoplasm. We identified 1 homozygous (E148Q/E148Q), 1 compound heterozygous (M694V/E148Q) and 5 heterozygous MEFV gene mutations; none had their own and/or family history compatible with familial Mediterranean fever. The mean overall mutation rate was 0.269. We found a high frequency of carriers in patients with myelodysplastic syndrome (66.6%), polycythemia vera (33.3%) and acute myeloid leukemia (28.6%). However, there was no MEFV gene mutation in patients with chronic myeloid leukemia. In conclusion, this study reports for the first time a possibly high prevalence of MEFV gene mutations in patients with myeloid neoplasm, especially myelodysplastic syndrome, polycythemia vera and acute myeloid leukemia. Our findings could open new perspectives for MEFV gene mutations in myeloid neoplasms and its association with tumor promotion. Further research is needed to determine the actual role of MEFV gene mutations in these malignancies.