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Riyadh, Saudi Arabia

Almalki M.H.,Endocrine and Metabolism Center | Almalki M.H.,King Saud bin Abdulaziz University for Health Sciences | Alshahrani F.,King Saud bin Abdulaziz University for Health Sciences
Frontiers in Endocrinology | Year: 2016

The Muslim population is about 1.5 billion worldwide. Based on a global diabetes prevalence of 4.6%, it is estimated that there are about 50 million Muslims with diabetes around the world who observe fasting during the month of Ramadan each year. Ramadan, one of the five pillars of Islam, and which takes place during the ninth month of the Islamic calendar, involves fasting from sunrise to sunset. During the fast, Muslims are required to refrain from eating food, drinking, using medications, and smoking from dawn until after sunset, with no restrictions on food or fluid intake between sunset and dawn. Islam exempts people from the duty of fasting if they are sick, or if fasting may affect their health, as fasting for patients with diabetes carries a risk of an assortment of complications, including hypoglycemia, postprandial hyperglycemia, and metabolic complications, associated with dehydration. Nevertheless, a large number of people with diabetes who still choose to fast during Ramadan despite the advice of their doctor, and the permission received from religious authorities thus create medical challenges for themselves and their health-care providers. It is thus important for patients with diabetes who wish to fast during Ramadan to make the necessary preparations to engage in fasting as safely as possible. This review presents a guide to the care of diabetic patients during Ramadan to help them fast safely if they wish to do so. © 2016 Almalki and Alshahrani. Source

Ansari M.S.,Endocrine and Metabolism Center | Almalki M.H.,Endocrine and Metabolism Center | Almalki M.H.,King Saud bin Abdulaziz University for Health Sciences
Frontiers in Endocrinology | Year: 2016

Secondary pituitary enlargement due to primary hypothyroidism is not a common manifestation. The loss of thyroxin feedback inhibition in primary hypothyroidism causes overproduction of thyrotropin-releasing-hormone (TRH), which results in secondary pituitary enlargement. TRH has a weak stimulatory effect on the lactotroph cells of the pituitary, so a mild to moderate increase in prolactin (PRL) levels is expected. We report the case of a 67-year-old female who presented with a large pituitary mass and a very high level of TSH in association with a significant rise in PRL level. In this case, diagnosing a sellar mass was challenging; it was difficult to distinguish between pituitary prolactinoma and primary hypothyroidism with secondary pituitary hyperplasia. Thyroid hormone replacement proved that this patient's hyperprolactinemia was due to hyperplasia of the pituitary gland. As such, making the correct diagnosis and initiating thyroid hormone therapy can prevent unnecessary treatment with dopamine agonists. © 2016 Ansari and Almalki. Source

Alhuzaim O.N.,Endocrine and Metabolism Center | Aljohani N.,Endocrine and Metabolism Center | Aljohani N.,King Saud bin Abdulaziz University for Health Sciences
Clinical Medicine Insights: Case Reports | Year: 2014

Objective: Besides its classical role in calcium and bone homeostasis, vitamin D is considered a potent immunomodulator that can affect the patho-genesis of several autoimmune diseases. Our aim is to evaluate the effect of vitamin D correction to a patient with new onset Graves' disease (GD) with an underlying vitamin D deficiency. Method: We describe the effect of vitamin D3 on untreated Graves' disease with vitamin D deficiency. Results: A healthy Saudi woman in her 40s sought consultation with a three-month history of palpitation. She denied any history of heat intolerance, weight loss, menstrual irregularity or sweating. She has a history of chronic muscle aches and pains. Physical examination revealed a mild diffusely enlarged and non-tender thyroid gland with no bruit. She had no signs of Graves' ophthalmopathy. In laboratory examinations, the initial thyroid function test, which was done in an outside hospital, revealed a TSH, 0.01 mIU/L; FT4, 22.5 pmol/L and FT3, 6.5 pmol/L. Vitamin D 25-OH level was done in our hospital and showed a result of 26.0 nmol/L with a TSH, 0.013 mIU/L; FT4, 16.7 pmol/L; and FT3, 3.8 pmol/L. TSH receptor antibody was positive. TC-99 m thyroid scintigraphy demonstrated an enlarged thyroid gland with increased radiotracer trapping and heterogeneous distribution. Te patient was given only oral cholecalciferol 4000 IU per day since November 2012 (prescribed by an outside hospital) then from May 2013 onwards she was given 50,000 IU per month. Follow-up laboratory exams revealed improved vitamin D levels as well as TSH and FT4. She eventually improved both clinically and biochemically with a satisfactory outcome. Conclusion: Vitamin D deficiency may exacerbate the onset and/or development of GD and correction of the deficiency may be able to reverse it. However, further prospective clinical studies will be needed to define the role of vitamin D treatment in GD. © the authors, publisher and licensee libertas academica limited. Source

Hakami O.,Endocrine and Metabolism Center | Ahmad M.M.,Endocrine and Metabolism Center | Al Johani N.,Endocrine and Metabolism Center | Al Johani N.,King Abdulaziz University | Al Johani N.,King Saud University
Clinical Medicine Insights: Case Reports | Year: 2016

Thyrotoxic periodic paralysis (TPP) is a potentially lethal complication of hyperthyroidism characterized by recurrent muscle weakness and hypokalemia. It has been commonly reported in non-Asian populations. Four cases were reported in Saudis so far, and one had a life-threatening arrhythmia. We describe an additional case of a 28-year-old apparently healthy Saudi male patient, who presented with acute paraparesis associated with hypokalemia (K: 2.0 mmol/L), complicated by ventricular tachycardia and cardiac arrest. He was successfully resuscitated and his hypokalemia was cor-rected. A diagnosis of Graves’ disease associated with TPP was made. He was initially treated with carbimazole and β-blockers and then given a definitive therapy with radioactive iodine, which showed a good response. This case highlights the importance of early recognition and prompt treatment of TPP as a differential diagnosis for muscle weakness. A brief review of TPP and associated arrhythmia is included. © the authors, publisher and licensee Libertas Academica Limited. Source

Alhuzaim O.N.,Endocrine and Metabolism Center | Almohareb O.M.,Endocrine and Metabolism Center | Sherbeeni S.M.,Endocrine and Metabolism Center
Clinical Medicine Insights: Case Reports | Year: 2015

Objective: Carbonic anhydrase (CA) II deficiency is a rare autosomal recessive disorder caused by mutation in the CA II gene that leads to osteopet-rosis, renal tubular acidosis (RTA), and cerebral calcification. Our aim is to present a patient with the classic triad of CA II deficiency syndrome to enhance the awareness about this rare syndrome. Methods: We describe the clinical and radiological findings of a Saudi woman patient with CA II deficiency syndrome. Results: A Saudi woman in her 20s presented to our hospital for evaluation of increased bone density. She was known to have delayed developmental milestone with growth retardation and poor scholastic performance. She had multiple fragile fractures started at the age of 15 involving the lower extremi-ties. A physical examination revealed dysmorphic features and intellectual disability with intelligence quotient (IQ) of 36. The initial blood workup showed a picture of distal RTA with hypokalemia, and the radiological imaging confirmed the presence of osteopetrosis and multiple kidney stones. The com-bination of osteopetrosis with RTA raised the possibility of CA II deficiency. Therefore, computed tomography (CT) of the brain was done and showed intracranial calcification involving the basal ganglia. She was started on potassium chloride and sodium bicarbonate. In addition, she underwent right-sided percutaneous nephrolithotripsy. Her DNA analysis came to show a sequence variant c.232+1G.A, which was detected in both of the CA II genes (homozygous). Conclusion: Early recognition of the disease is a key, as an early appropriate treatment institution is essential in order to prevent further complications. © the authors, publisher and licensee Libertas Academica Limited. Source

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