Are CRH & NGF as psychoneuroimmune regulators in women with polycystic ovary syndrome?

PURPOSE: Polycystic ovary syndrome (PCOS) affects quality of life and can worsen anxiety and depression either due to the features of PCOS or due to the diagnosis of a chronic disease. Corticotrophin-releasing hormone (CRH) and nerves growth factor (NGF) are the modulator for the actions of the sympathetic nervous and immune systems. METHODS: In total, 171 women divided into two groups: study and control groups. Serum CRH, NGF, and interleukins: IL-1α. IL-1ß, 17A, and TNFα were determined by ELISA Kits in both groups. RESULTS: The results showed that IL-1α (p < 0.001) and ß (p = 0.017) significantly increased in PCO group. CRH, NGF, and IL-17α in serum of patients with PCO significantly lower than the control group (p < 0.001). The results of this study indicate: (1) destruction of three cytokines pattern, (2) Reduction of CRH, NGF, and IL-17α in serum of PCO patients can be under the direct influence of the sympathetic nervous system (SAS), and (3) reduction of CRH and NGFα can be reason of psych/emotional distress in women with PCOS. CONCLUSIONS: The results of this study confirm (1) low-grade chronic inflammation in PCOS. This impaired cytokine pattern can play a major role in the immune-pathogenesis of PCOS; (2) hyponeurotrophinemia and reduction of CRH in women with PCOS could reflect deficit of neuronal stress-adaptation in these patients.

No apparent mineralocorticoid receptor defect in a series of sporadic cases of pseudohypoaldosteronism.

Pseudohypoaldosteronism (PHA) is characterized by congenital resistance of the kidney and/or other mineralocorticoid target tissues to aldosterone, resulting in excessive salt wasting. Although the mineralocorticoid receptor (MR) was suggested as a potential locus of the defect in this disease, no such abnormality was found in 3 recently reported cases, one of whom belongs to this series of 5 patients. Molecular studies of the MR complementary DNA and gene in this series of sporadic cases of pseudohypoaldosteronism are reported. Four of these patients had multiple mineralocorticoid target tissue resistance, whereas 1 had transient isolated resistance in the kidney. A nonconservative homozygous mutation (C944-->T944, Ala241-->Val241) was identified in the complementary DNA of 4 of the patients but was also found in 62 of 100 normal alleles. One of these 4 patients had an additional conservative heterozygous mutation (A760-->G760, Ileu180-->Val180), which was also present in 11 of 100 normal alleles. None of the patients had any abnormalities in the first untranslated exon and 0.9 kilobases of the 5'-regulatory region of the MR gene, which were fully sequenced and compared with the normal sequence. It is concluded that the mutations identified in 4 of these 5 patients with PHA are polymorphisms, which on their own have no apparent pathophysiological significance. It is hypothesized that the defect causing PHA might be in a post-MR step of aldosterone action or in an unsuspected nonclassic receptor for this hormone.

Rheumatic valvulitis and constrictive pericarditis. Report of case.

A 13-year-old girl was admitted with congestive heart failure, edema, ascites, and jaundice. There was an apical pansystolic murmur of mitral insufficiency and marked cardiomegaly. Her venous pressure was elevated. Despite medical treatment her condition deteriorated, hepatic and renal failure as well as disseminated intravascular coagulation ensued, leading to her death. At post mortem she was found to have rheumatic mitral valvulitis and constrictive pericarditis. The pathologic picture of pericarditis was nonspecific, but in presence of a positive skin test for tuberculosis the latter is considered to be the most likely cause of the pericarditis, nevertheless, rheumatic etiology of pericarditis in this case cannot be excluded. The presence of rheumatic heart disease and cardiomegaly may have led to the exacerbation of symptoms and signs of constrictive pericarditis and severe right heart failure.