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A complex case of Multiple Endocrine Neoplasia type 1 with Metastatic Parathyroid Carcinoma

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Kalavalapalli S., Talapatra I., Connell I.
Open Medicine
|
2010
|
vol. 5
|
issue 1
53-58
EN
We describe below a patient with Multiple Endocrine Neoplasia type 1 (MEN type 1) who presented with features of Primary Hyperparathyroidism. However, the actual diagnosis of Parathyroid Carcinoma was delayed until metastases to the lung were discovered. She was also found to have Pituitary Macro adenoma with Silent Acromegaly, with no clinical features whatsoever. She underwent transphenoidal hypophysectomy with postoperative radiotherapy. However, the disease process remained biochemically active necessitating commencement of somatostatin analogues. There is also a tumour at the head of the pancreas which at present is non functional with normal gut hormone profile and normal 24 hour urinary 5-hydroxyl indole acetic acid (5-HIAA) excretion assay. Our case highlights the pitfalls in diagnosing the parathyroid carcinoma due to lack of initial proper histological features. The diagnosis of parathyroid carcinoma was based on histologically confirmed metastases to the lungs. We also discuss below the entity called Silent Acromegaly where patients have biochemically and/or histologically confirmed growth Hormone (GH) excess with no clinical features suggesting Acromegaly. We discuss the benefits of somatostatin analogues in indirectly controlling the rest of the tumours in MEN1 and hypothesise the same for metastatic parathyroid carcinoma. Metastatic parathyroid carcinoma with multiple endocrine neoplasia type 1 is extremely rare. Our case highlights the complexities of managing MEN1 with metastatic parathyroid carcinoma and the dilemmas in dealing with the various aspects of the care.
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Successful discontinuation of insulin treatment after gestational diabetes is shown to be a case of MODY due to a glucokinase mutation

88%
Talapatra I., Kalavalapalli S., Robinson J., Ellard S., Tymms D.
Open Medicine
|
2008
|
vol. 3
|
issue 2
225-228
EN
We describe a woman who first presented with gestational diabetes at 26 weeks gestation and was managed with insulin. Following delivery of a healthy baby she had an abnormal OGTT (oral glucose tolerance test) 6 weeks post partum and was managed with diet. In her second pregnancy she was diagnosed with gestational diabetes at 10 weeks and required insulin. Following delivery she was again managed on diet alone. Four years later, during her third pregnancy, she was managed with insulin from the outset. She remained on insulin post partum and for several years. Later her two younger children, aged 11 years and 7 years, were found to have GCK mutation causing MODY (Maturity Onset Diabetes Of the Young) subtype glucokinase. Following this she underwent molecular genetic testing and was also shown to have the GCK mutation. She was gradually taken off insulin and is now managed on diet alone with excellent glycaemic control. Her two children are under regular follow up care and on no medication for diabetes.
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