No abstract

Fasting during the lunar month of Ramadan is a religious obligation for all adult Moslems. Under certain circumstances, afewgroupsareexemptfromfastingsuchasbeing"sick" asjudgedbyanexperienceddoctor.Recentcollaboration between the International Islamic FiqhAcademy and The Islamic Organization for Medical Sciences produced a comprehensive guidance based on extensive review of the evidence of possible risk to diabetic patients if they observefasting.Thenewguidancecategorizedpeoplewith diabetesinto4groupsaccordingtotheirrisk.Group1and 2areexemptedfromfastingastheyhaveriskfromfasting. Theseincludedpatientswithpoorglycemiccontrolorwith complicationsandseriouscoexistingillnessesinadditionto type1patientsandpregnantwomenwithdiabetes.Patients in groups 3 and 4 are those with moderate to low risk of harmfromfasting.Theseareexemplifiedbyuncomplicated patientswithstablecontrolonoraldrugsnotassociatedwith excessriskofhypoglycemia.Thesegroupsofpatientshave no harm but may even benefit from fasting. Doctors and religious scholars have a joint responsibility to properly assess and advise patients to choose to fast or not to fast inlinewiththeserecommendations.Theadviceshouldbe givenwith no complacencywith the potentialhealth risks butwithgreatsensitivitytothepatientsreligiousfeelings.

Approaches to the management of Type 2 diabetes mellitus during Ramadan varied across regions. Episodes of hypoglycaemia and insulin therapy predicted risk of hypoglycaemia during Ramadan and identified individuals who required Ramadan-specific education.

In 1992, Cuneo et al. (1992) reviewed, in this journal, the consequences of growth (GH) deficiency during adult life and coined the term 'Growth hormone deficiency (GHD) syndrome in adults'. Limited information was available then on cardiovascular disease and risk factors in adults with hypopituitarism. More data have been published since on cardiovascular morbidity in symptom-free hypopituitary adults. Several groups have also published results on the effects of GH therapy on cardiac structure and function and on the cardiovascular risk factors.We shall review here the epidemiological and experimental data on cardiovascular morbidity and mortality in adult hypopituitarism. We shall also examine the prevalence of cardiovascular risk factors in this group of patients and their potential causes focusing on the possible role of GH deficiency and the effects of GH replacement. Cardiovascular disease in hypopituitarism

Growth hormone replacement therapy in adults for 6 months increased lean body mass, total body water and exercise tolerance, and decreased body fat. Growth hormone replacement for longer than 6 months maintains the advantageous effects seen in shorter-term studies and may have additional effects on body fat distribution, muscle strength and psychological well-being.

Objective-To assess cardiac structure and function in patients with treated hypopituitarism and to determine their relation to the degree of growth hormone deficiency and body composition pattern.Design-26 patients with treated hypopituitarism were studied by cross sectional and Doppler echocardiography and by exercise testing. The results were analysed and their relation to the degree of growth hormone deficiency and body composition determined.Setting-All tests were performed in the department of cardiology and the unit of metabolic medicine at a tertiary referral centre.Patients-Patients with hypopituitarism referred for endocrine assessment.Main outcome measures--Left ventricular mass, left ventricular diastolic function, and exercise capacity in patients with hypopituitarism and their relation to growth hormone deficiency.Results-Mean (SD) serum concentration of insulin-like growth factor 1 (IGE-1), a measure of growth hormone deficiency, was 82-4 (45)

The effects of replacement with biosynthetic human GH on carbohydrate tolerance and lipid metabolism were studied in 40 hypopituitary adults during a randomized double blind, placebo-controlled trial for 6 months, followed by a 12-month open trial. The daily GH dose was 0.04 +/- 0.01 IU/kg. Fasting plasma glucose, serum fructosamine, plasmid lipids, lipoproteins, and plasma C-peptide concentrations were measured, and an oral glucose tolerance test was performed every 6 months. There was no change in fasting triglyceride levels at any stage of the study. There was no significant change in fasting total or LDL cholesterol, total HDL cholesterol, high density lipoprotein2 (HDL2) cholesterol, HDL3 cholesterol, apoprotein-A1, or apoprotein-B during GH or placebo treatment in the placebo-controlled 6-months study. In the open phase of the trial, total and low density lipoprotein cholesterol showed a sustained downward trend during GH therapy. Compared to the pretreatment level, the HDL cholesterol concentration was significantly higher at 18 months. Cholesterol subfractions HDL2 and HDL3 and apoprotein-A1 and -B were not different from the pretreatment levels. The total/HDL cholesterol ratio decreased significantly at 12 and 18 months. During the controlled phase, fasting plasma glucose was similar during GH and placebo administration, but fasting insulin and C-peptide increased during GH therapy, but not during placebo treatment. The mean area under the curve (AUC) for glucose increased by a small, but significant, extent over the 6 months of GH treatment and was higher at 6 months than during placebo treatment. The AUC for insulin also increased during GH treatment. During the open trial, the fasting plasma glucose level increased at 6 and 12 months, and the fasting plasma insulin level increased at 6, 12, and 18 months of GH treatment. The plasma glucose AUC during the oral glucose tolerance test was significantly higher at 6 months, and the plasma insulin AUC was significantly higher at 6, 12, and 18 months of GH therapy. In conclusion, GH therapy has some metabolic effects that are considered beneficial and others that are less desirable.

Hypopituitary adults on conventional therapy have abnormal body composition with increased fat content, reduced body water content and reduced bone mineral mass.