Diabetes Secondary to Endocrine Disorders and PCOS
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This book contains five sections, each consisting of several papers. The section headings are: Biochemistry and Physiology of GH and Growth Factors, Pathology of Acromegaly, Clinical Endocrinology of Acromegaly, Nonsurgical Therapy of Acromegaly, and Surgical Therapy of Acromegaly.
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During the past decade the importance of medical therapy, especially treatment with somatostatin analogues has increased significantly in patients with active acromegaly.Authors analyzed the outcome of somatostatin analogue treatment in acromegalic patients evaluated and followed up at the 2nd Department of Medicine, Faculty of Medicine, Semmelweis University, during the past 10 years.Changes in serum growth hormone (GH) and insulin-like growth factor-1 (IGF-1) concentration, as well as morphologic changes of pituitary adenomas followed by MRI scans were evaluated and compared in 32 acromegalic patients (26 women, 6 men) during long-term somatostatin analogue treatment (mean+/-SE, 3.1+/-0.3 years, range, 1-7 years). Primary somatostatin analogue treatment was applied in 10 patients (7 women and 3 men), whereas 15 patients (14 women and 1 man) had pituitary surgery and 7 patients (5 women and 2 men) underwent both pituitary surgery and irradiation therapy prior to somatostatin analogue treatment.After a 3-month treatment with somatostatin analogues, both serum GH and IGF-1 levels decreased significantly and they remained around the same decreased levels throughout the treatment period. Serum GH decreased from 15.7+/-4.9 to 5.5+/-1.4 ng/ml, and serum IGF-1, expressed as a percentage of the upper limit of age- and sex-adjusted reference value, decreased from 204+/-14% to 135+/-12% at the end of treatment. The efficacy of somatostatin analogue treatment was not influenced by surgical or surgical and irradiation therapies which were applied prior to medical treatment. At the end of treatment 36.7% of patients had safe serum GH (<2.5 ng/ml), while serum IGF-1 returned below the upper limit of age- and sex-adjusted reference range in 41.4% of patients. Pituitary MRI showed regression of the adenoma in 46% of patients, and none of the patients had progression of the pituitary adenoma.Somatostatin analogues are effective therapeutic options for acromegalic patients when primary surgical treatment cannot be performed due to complications and associated disorders, or in patients whose acromegaly remains active after pituitary surgery or after pituitary surgery and irradiation.
Somatostatin Analogue
Medical treatment
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Summary Objective The estimated prevalence of acromegaly is 40–125 per million. The diagnosis of acromegaly is often delayed due to deficits in recognizing the signs of the disease. It is not known how many subjects with increased IGF‐1 levels have acromegaly. We aimed to assess the prevalence of acromegaly in primary care by screening for elevated IGF‐1 levels. Design A cross‐sectional, epidemiological study (the DETECT study). Patients A total of 6773 unselected adult primary care patients were included. Measurements We measured IGF‐1 in all patients and recommended further endocrine evaluation in all patients with elevated IGF‐1 levels (> 2 age‐dependent SDS). Results Of 125 patients with elevated IGF‐1 levels, 76 patients had indeterminate results and acromegaly could be excluded in 42 patients. One patient had known florid acromegaly. Two patients had newly diagnosed acromegaly and pituitary adenomas. Four patients had biochemical acromegaly but refused further diagnostics. This corresponds to a prevalence of 1034 per million patients. Conclusions Our study shows a high prevalence of undiagnosed acromegaly in primary care. These results imply that acromegaly is underdiagnosed and stress the importance of detecting acromegaly.
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Acromegaly is a rare disease, caused by growth hormone (GH) hypersecretion and secondarily elevated insulin-like growth hormone 1 (IGF-1) level. Nearly all patients with acromegaly suffer from somatotroph pituitary adenoma. The main goal of treatment is to normalise both GH and IGF-1 levels, which reduces symptoms, complications and mortality. Transsphenoidal selective adenomectomy performed by an experienced neurosurgeon is the first-line therapy of choice. Therapy with somatostatin analogues (SSA) is used as a neoadjuvant treatment prior to surgery and in a persistent disease following the surgery. The long-acting somatostatin analogues reduce serum GH/IGF-1 levels and tumour volume. In this clinical review, mechanisms and role of 1st and 2nd generation somatostatin analogues in the treatment of patients with acromegaly are presented, with particular emphasis on the effects on somatotroph pituitary adenoma volume reduction.
Transsphenoidal surgery
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Ketogenesis
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We present a case of acromegaly with normal growth hormone levels. The patient had markedly elevated IGF-1 and a pituitary microadenoma. He refused all modalities of treatment, and over a span of 30 years the signs and symptoms of acromegaly progressed. This case illustrates the shortcomings of growth hormone–based parameters in the diagnosis of acromegaly and the clinical importance of prolonged elevation of IGF-1. The literature on the diagnostic criteria for acromegaly and on cases of acromegaly without a significant growth hormone elevation is reviewed.
Pegvisomant
Treatment modality
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Somatostatin was infused for 6 h into seven normal subjects with and without a replacement dose of glucagon. The addition of glucagon to somatostatin resulted in a 30-40% rise in plasma glucagon, whereas plasma insulin declined by 40-50% in both treatment groups. Plasma glucose and glucose production initially increased 2-fold with glucagon replacement, and subsequently declined by 2-3 h to levels comparable to those observed with somatostatin alone. After 6 h plasma glucose and glucose kinetics were no different whether or not glucagon was present. The rise in blood ketones after somatostatin was not exaggerated by glucagon replacement. We conclude that glucagon lack is not a modifying factor in the late hyperglycemic and hyperketonemic response to prolonged infusions of somatostatin.
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SUMMARY Cerebrospinal fluid (CSF) and plasma levels of somatostatin have been measured in patients with active acromegaly and the results compared to those obtained in patients with non‐endocrine diseases. Plasma levels have also been studied in acromegalics given oral glucose. The mean CSF somatostatin level in twenty patients without endocrine disease was 76 pg/ml (range 46–112) which did not diner significantly from that found in eight acromegalics (mean 87 pg/ml, range 48–160). Plasma somatostatin in twenty‐two acromegalic patients on no medical treatment was 43 pg/ml (range 9–113), not significantly different from values in a normal control population. There were no differences in the somatostatin levels of non‐diabetic acromegalics. After oral glucose, there was a rise in circulating somatostatin in eleven out of twelve acromegalic patients, and this rise did not differ from that seen in normal subjects. It is probable that altered somatostatin secretion is neither the cause nor the result of acromegaly; however it is possible that local changes in somatostatin concentration which are not reflected in peripheral plasma or CSF levels may occur near the site of its production.
Pituitary disease
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