Bilateral massive adrenal haemorrhage revealing coeliac disease

Sir, We describe a case of coeliac disease that remained undiagnosedfor many years and induced a hypocoagulant state and bilateraladrenal haemorrhage. This is the first reported case of bilateraladrenal haemorrhage in a patient with this disorder. A 43-year-old woman presented with sub-acute back pain requiringmorphine. She did not smoke, drink alcohol, or take medicationsor     

Bilateral massive adrenal haemorrhage complicating anaphylactic shock: A case report

A case of bilateral adrenal haemorrhage complicating anaphylactic shock is reported. Hypovolemic shock related to peritoneal haemorrhage was the main feature leading to laparotomy. Ultrasonographic examination was not contributive, but CT scan easily documented the adrenal haemorrhage and must be considered a valuable diagnostic tool when adrenal haemorrhage is suspected.     

Bilateral adrenal haemorrhage and acute adrenal insufficiency in a blunt abdominal trauma: a case-report and literature review.

Blunt abdominal trauma is frequently associated with adrenal haemorrhage, and is preferentially diagnosed by computed tomography scan. Lesions are mostly unilateral and asymptomatic and are therefore frequently overlooked. Bilateral haemorrhage, however, has a high mortality rate as a result of acute adrenal insufficiency. We report on a 30-year-old polytraumatic patient who developed cardiocirculatory arrest when all lesions were surgically controlled and stable and without evidence of a primary cardiac problem. Autopsy revealed bilateral adrenal haemorrhage, leading to the diagnosis of acute adrenal insufficiency as the cause of death. We conclude that adrenal haemorrhage should be looked for in every polytrauma patient, and that although it is a rare occurrence, acute adrenal insufficiency caused by bilateral adrenal haemorrhage should be considered in every patient with unexplained cardiocirculatory failure. Such patients may benefit from the prompt administration of corticosteroid replacement, which can be life saving.     

Bilateral giant adrenal myelolipomas

Adrenal myelolipomas are rare benign tumors that comprise mature adipose cells and hematopoietic elements. They are usually found incidentally at autopsy and on imaging. Most cases are isolated and small. Although they are not hormonally active, there is very rarely an association with functional adrenal disorders such as Cushing syndrome and congenital adrenal hyperplasia. It is believed that in these patients high corticotropin levels contribute to the pathogenesis of these neoplasms. We report the imaging appearances of bilateral giant adrenal myelolipomas in a patient known to have congenital adrenal hyperplasia. To our knowledge, these are the largest bilateral adrenal myelolipomas reported in association with congential adrenal hyperplasia. A distinct change in their appearances after a period of steroid treatment is described for the first time.     

Migraine and coeliac disease

The pathophysiology of migraine remains unclear. To incriminate a comorbid factor is always hypothetical, even if suppression of this factor appears to prevent the migrainous attacks. In our patient, treatment of coeliac disease coincided with total disappearance of severe migraine attacks. Moreover, the coeliac disease was first revealed during the evaluation of a migraine with aura.     

Heparin-induced thrombocytopaenia complicated by bilateral adrenal haemorrhage

Acute adrenal insufficiency due to bilateral adrenal haemorrhage is an important clinical diagnosis and its association with heparin-induced thrombocytopaenia is infrequent. We report on a patient in whom life threatening acute adrenal insufficiency occurred consequent to such an association. The clinical manifestations simulated septic shock, highlighting the need to consider specifically acute adrenal insufficiency in such settings, and institute therapy promptly prior to obtaining results of confirmatory tests.     

Genetics of coeliac disease

Coeliac disease is one of the most common gastrointestinal disorders. The clinical features of the disease are protean, possibly due to heterogeneity. A familial basis for coeliac disease is well recognized, and although a strong HLA association is seen, this cannot entirely account for the increased risk seen in relatives of affected cases. A gene (or genes) at an HLA-unlinked locus also participates in causing coeliac disease and is likely to be a stronger determinant of disease susceptibility than the HLA locus. Such a gene (or genes) could theoretically act either additively or multiplicatively in conjunction with HLA. However, the familial risks seen in siblings and monozygotic twins are most parsimonious with a multiplicative model. Without evidence for a particular HLA-unlinked gene, and because no genetic model can be reliably ascribed to the non-HLA-linked locus, identifying causative non-linked HLA genes is likely to be through a genome-wide linkage search using non-parametric methods.      

Epidemiological survey of coeliac disease and inflammatory bowel disease in first-degree relatives of coeliac patients

One hundred and sixty-two of 182 patients with coeliac disease provided satisfactory details of family size and the prevalence of coeliac disease and inflammatory bowel disease among their first-degree relatives. Patients ranged in age from 11 months to 79 years with a mean age of 41 (+/- 23) years. Twenty patients had at least one first-degree relative with coeliac disease: a total of 25 of 861 relatives were affected (prevalence = 2904/100,000) compared with an expected 0.9 cases (prevalence = 100/100,000; p less than 0.001). Six relatives had inflammatory bowel disease (prevalence = 697/100,000) compared with an expected 1.3 cases (prevalence = 150/100,000; p less than 0.001). Five of these had ulcerative colitis, and one had Crohn's disease. The relative risk of ulcerative colitis is, therefore, five times greater for first-degree relatives of people with coeliac disease than for the general population (95 per cent confidence interval, 4.7-7.2). There is a clear association between coeliac disease and ulcerative colitis, which may point to factors involved in the aetiology of colitis.     

Recent advances in coeliac disease

Coeliac disease, or gluten-sensitive enteropathy, affects 1 in 100-200 people in the UK. The condition, which is exacerbated by wheat, rye, barley and possibly oats, can be treated with a gluten-free diet in which these cereals are omitted. Serological screening, particularly of high-risk groups, with both IgA and IgG based systems can be used to identify cases. Diagnosis depends on the use of a small intestinal biopsy, which reveals the classical changes of loss of the normal villous architecture. Evidence suggests that gluten-sensitive T cells are involved in the pathogenesis of the disease. Use of in vitro systems has suggested an immunodominant epitope within wheat gliadin, which has been shown to exacerbate the condition in vivo. This information can be used to devise strategies to develop immuno-modulatory peptides and cereals with the baking and nutritional qualities of wheat, rye and barley, but which do not exacerbate the condition.     

双侧肾上腺巨大囊肿1例

患者,女,24岁,自觉腹胀4个月,体检发现腹部膨隆.患者血皮质醇、醛固酮、儿茶酚胺检查均正常.超声显示:肝肾间及脾肾间各有18 cm×15 cm×15 cm及12 cm×9 cm×8 cm无回声液性暗区,边界清晰,被膜完整,内透声好,其内未见明显血流信号.超声提示:腹腔多发囊肿.进一步CT检查:肝脏右叶后方与右肾间见类圆形囊性病变,边缘有少量条形钙化;胰尾后方与左肾之间见类圆形囊性病变;两者内部密度均匀,平扫CT值约17～19 HU,增强无明显强化;周围脏器受压移位(图1).     

Bilateral cystic lymphangioma of the adrenal gland

We report the case of a 22-year-old woman with a large, bilateral lymphangiomatous cyst originating from the adrenal glands. Since she was having persistent pain and the diagnosis was uncertain, we did surgery.     

双侧肾上腺巨大囊肿1例

患者女,41岁.发现上腹部肿物1年.查体:右季肋部隆起,可触及一直径约10 cm肿物,质软,表面光滑,边界清,无压痛.CT:右侧腹部见一巨大囊实性病灶,自膈下至左肾下级水平,最大截面约17 cm×19 cm,肝脏明显受压变薄,下腔静脉及胰腺受压向左前方移位,右肾受压向下移位.病灶与周围组织分界清,其前壁见点状钙化,下前壁见结节状影,增强扫描囊壁及结节明显强化,内液密度无强化.     

New diagnostic findings in coeliac disease

Coeliac disease, a life-long gluten-sensitive disorder, characterized by malabsorption, villous atrophy and crypt hyperplasia, is well recognized. However, the disease is evidently underdiagnosed, and the classic forms constitute only the tip of the 'coeliac iceberg'. Patients with coeliac disease can have subtle symptoms, if any. Diagnostic difficulties may further emerge when minor mucosal changes are found. In coeliac screening and case-finding a novel test, the antitissue transglutaminase test, has proven promising with a sensitivity and specificity of over 95 %. Genetic and immunohistological research has taken a great leap forward. Coeliac disease is strongly associated with HLA-DQ2, coded by the DQA1*0501 and DQB1*02 alleles, or the DQ8 (DQA1*03, DQB1*0302 alleles). The disease is rare in patients who do not share these alleles, a circumstance which can be utilized in diagnostics. An increase in small bowel intraepithelial lymphocytes especially gammadelta+ T-cell receptor-bearing cells is typical, albeit not pathognomonic, for coeliac disease. Combining new symptoms, humoral immunity, genetics and immunohistological staining can today offer a greater diagnostic scope for coeliac disease, especially in cases where clinical presentation and small bowel biopsy findings remain doubtful.