Study on the association between the polymorphism of MCP-1 rs1024611 and the genetic susceptibility of type 2 diabetes with sepsis.

Monocyte chemoattractant protein-1 (MCP-1) rs1024611 (-2518 A > G) polymorphism are associated with inflammatory diseases. In this study, we investigate the relationship between MCP-1 rs1024611 polymorphism and genetic susceptibility of type 2 diabetes mellitus (T2DM) with sepsis. Two hundred eighty-five patients with T2DM are divided into the diabetes with sepsis group (combined group, 113 cases) and the diabetes group (172 cases). Blood samples and corresponding clinical data were collected. MCP-1 rs1024611 polymorphism in blood samples was detected by pyrosequencing. Meanwhile, the expressions of MCP-1, tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1ß, and IL-6 in blood samples were detected by real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The relationship between different genotypes of MCP-1 rs1024611 polymorphic locus and T2DM with sepsis was analyzed by combining with the clinical data of the patients. The frequencies of rs1024611 AG/GG genotypes and G allele in T2DM with sepsis group were significantly higher than those in T2DM patients without sepsis (P = .004 for AG/GG vs AA genotypes; P = .037 for G allele vs A allele). Subgroup analysis showed that the rs1024611 G allele frequency in the septic shock group was significantly higher than the general sepsis group (P = .02). The expressions of MCP-1 and TNF-α in GG genotypes in T2DM with sepsis group were significantly higher than AA or GA genotypes (P < .05). This study preliminarily showed that the rs1024611 A > G polymorphism within the promoter region of MCP-1 gene can upregulate the expression of MCP-1 gene and proinflammatory cytokine TNF-α, which ultimately contributed to the predisposition and progression of T2DM with sepsis.

Be aware of the effects of glucocorticoids on SIADH: A case report.

RATIONALE: Hyponatremia is one of the most common electrolyte disorders in clinic. Due to the complicated etiology and the nonspecific clinical manifestations, the diagnosis of hyponatremia is a complicated process. A variety of clinical disorders can cause inappropriately increased antidiuretic hormone (ADH) secretion, leading to inappropriate water retention and consequent hyponatremia. The most common cause of hyponatremia in hospital inpatients is syndrome of inappropriate antidiuretic (SIADH). The action of glucocorticoid against pituitary posterior lobe can reduce the secretion of ADH. However, the effect of hormone on diuretic hormone during treatment has been less reported. PATIENT CONCERNS AND DIAGNOSIS: The patient in this case report was misdiagnosed as anterior pituitary hypofunction because of the long-term glucocorticoid therapy was effective in this patient, and the patient was finally diagnosed as SIADH after reassessment. The patient is a 76-year-old male with long-term symptomatic hyponatremia after traumatic brain injury (TBI). The patient has been consistently diagnosed as anterior pituitary hypofunction. Based on the diagnosis, glucocorticoid replacement therapy was administered. The serum sodium of the patient gradually increased to normal level after hydrocortisone intravenous injection but dropped again after switch to hydrocortisone oral administration. Through examination and analysis of the patient status during the five-time hospitalization, syndrome of inappropriate antidiuretic hormone (SIADH) was considered. INTERVENTIONS: Water intake limitation and oral furosemide and antisterone were administered after glucocorticoid therapy was stopped. OUTCOME: The serum sodium level of the patient gradually increased and maintained within normal range based on his clinical follow-up. LESSONS: For hyponatremia with effective glucocorticoid treatment, SIADH should still be excluded.