Atypical Presentation of Adrenocortical Insufficiency with Anorexia and Jaundice.

BACKGROUND Adrenal insufficiency is mainly due to insufficient adrenal corticosteroid hormones secretion by the adrenal cortex, which leads to clinical manifestations such as weakness, weight loss, hyperpigmentation, hypotension, and vomiting. However, the clinical manifestations of adrenocortical insufficiency may be atypical: anorexia, ascites, impaired liver function, and alacrima have been reported. Jaundice and anorexia presenting together in the same patient as the main symptoms are rare. CASE REPORT We present a rare case of a 65-year-old woman diagnosed as having adrenocortical insufficiency with chief complaints of anorexia and jaundice. The patient had a history of hiatus hernia and gastroesophageal reflux disease, which can easily lead to a misdiagnosis in clinical practice, which is what happened with this patient at the beginning in our hospital and in the other hospitals that treated her previously. Hiatus hernia was considered the mostly likely cause of her vomiting, and a laparotomy was done to repair the hernia at the local hospital. However, there was no improvement. After regular glucocorticoid replacement, the patient's symptoms all soon disappeared. CONCLUSIONS Adrenal insufficiency can atypically present as anorexia and jaundice. In order to avoid misdiagnosis, physicians should pay attention to these atypical symptoms.

Angiotensin-converting enzyme polymorphism affects outcome of local Chinese with acute lung injury.

INTRODUCTION: Acute Lung Injury (ALI) with genetic predisposition is fatal. Relationship between angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphism and the prognosis of local Chinese patients with ALI was investigated; meanwhile, the mechanisms involved were explored. METHODS: 101 ALI patients, 408 non-ALI patients and 236 healthy blood donors were enrolled. ACE I/D polymorphism was detected by polymerase chain reaction, then ACE genotype (II, ID, DD) and allele (I, D) frequencies were compared. Clinical data of ALI patients was calculated. Also, peripheral blood mononuclear cells (PBMC) were isolated from healthy volunteers with different ACE genotypes. Lipopolysaccharide (LPS)-induced ACE gene mRNA expression and ACE activity was measured. RESULTS: There was no significant difference in the frequencies of the genotypes and alleles. Acute Physiology and Chronic Health Evaluation (APACHE) II score was higher in DD subgroup than in II subgroup (19.7 ± 8.7 and 15.6 ± 6.2; P < 0.05). The 28-day mortality was significantly different (17.4%, 26.8%, and 64.3% for II, ID, and DD; P = 0.013). DD genotype was the independent prognostic factor for 28-day outcome. Furthermore, LPS-induced ACE mRNA expression and ACE activity from PBMC in DD genotype subgroup were both significantly higher than those in the other two subgroups. CONCLUSIONS: ACE I/D polymorphism is a prognostic factor for ALI. Patients with the DD genotype have higher mortality of ALI. Polymorphism influences the expression of ACE gene in LPS-stimulated PBMC, DD genotype leads to higher level of mRNA and enzyme activity. It may be one of the mechanisms involved.