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CASE REPORT

Adrenal Insufficiency Due to Isolated Adrenocorticotropin Deficiency Complicated by Autosomal Recessive Polycystic Kidney Disease

, M.D., Ph.D., , , &
Pages 485-492 | Published online: 26 Aug 2009

Figures & data

Table 1. Day profile of fasting plasma levels of glucose, insulin, and ratio of insulin to glucose

Figure 1. Response of plasma concentrations of cortisol and aldosterone to 250 µg of synthetic adrenocorticotropin (ACTH) injection. The response of plasma cortisol to ACTH injection is subnormal compared with normal response. The response of plasma aldosterone concentration is normal.

Figure 1. Response of plasma concentrations of cortisol and aldosterone to 250 µg of synthetic adrenocorticotropin (ACTH) injection. The response of plasma cortisol to ACTH injection is subnormal compared with normal response. The response of plasma aldosterone concentration is normal.

Figure 2. Response of plasma adrenocorticotropin (ACTH) concentration to 1 µg/kg of human corticotropin releasing hormone (CRH) injection. Response of plasma ACTH to CRH is blunted compared with normal response.

Figure 2. Response of plasma adrenocorticotropin (ACTH) concentration to 1 µg/kg of human corticotropin releasing hormone (CRH) injection. Response of plasma ACTH to CRH is blunted compared with normal response.

Figure 3. Gel filtration of plasma from our patient on a Sephadex G-75 column. The elusion profile of plasma sample from our patient chromatographed on a Sephadex G-75 column showed two peaks of (1-39)-ACTH and β-lipotropin, with no evidence of high molecular weight form of ACTH.

Figure 3. Gel filtration of plasma from our patient on a Sephadex G-75 column. The elusion profile of plasma sample from our patient chromatographed on a Sephadex G-75 column showed two peaks of (1-39)-ACTH and β-lipotropin, with no evidence of high molecular weight form of ACTH.

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