Why is bone health important in childhood?

Bones undergo changes throughout our lives, as old bone is broken down and new bone forms. But the most important time for building a strong skeleton is during childhood and adolescence. Bone strength depends on both the size of the bones and the amount of mineral they contain.

The greatest gains in bone size and mineral content occur in adolescence. At puberty, hormonal changes take place that start sexual maturity and speed up bone growth. Bones not only get longer and wider, they also get denser. People reach their peak bone mass, or maximum bone size and density, by their late teens or early twenties. As early as age 30, some bones begin to slowly lose mass.

The more bone mass we “Bank” in childhood and adolescence, the better we withstand the inevitable bone losses and the better protected we are from osteoporosis and bone fractures later in life.

What affects children’s bone health?

The genes we inherit, our hormones and our lifestyle all affect our peak bone mass. Genetic factors have the greatest influence on peak bone mass, but to reach his or her “genetic potential,” a child needs adequate levels of certain hormones along with healthy eating and exercise habits.

Growth hormone and the sex hormones estrogen and testosterone at puberty are essential for building bone mass in both boys and girls. Maintaining a healthy weight and getting enough vitamin D, calcium, protein, and physical activity are also key to bone health. Calcium is the main mineral in bone, and vitamin D helps the body absorb calcium. Weight-bearing exercise, such as running and jumping, helps build muscle and bone strength.

Adolescent girls need to be moderate in their approach to diet and exercise. Menstruation can stop in girls who exercise excessively or are extremely underweight (as in anorexia). Girls who never start their periods or stop menstruating often have low estrogen levels, which can harm their bone health.

Is your child getting enough vitamin D and calcium?

Vitamin D. Most of our vitamin D is produced when our skin is exposed to sunlight. Children get vitamin D from playing outdoors, but it’s hard to tell if they’re getting enough. Since few foods naturally contain vitamin D, most milk and infant formula are fortified (meaning vitamin D is added).

Infants, children, and adolescents need at least 400 IU (international units) of vitamin D each day. Children of all ages who do not get 400 IU a day from their diet should take a supplement, prescribed by their doctor.

Children and adolescents with dark skin, limited sun exposure, or certain chronic diseases are more likely to be deficient in vitamin D. A simple blood test can check for vitamin D deficiency.

Calcium. Pregnant and breastfeeding women need at least 1,000 mg of calcium each day, along with adequate vitamin D, to support their own and their babies’ bone health. The recommended daily calcium intake for children and adolescents varies by age:

0-6 months         210 milligrams (mg)

7- 12 months      270 mg

1-3 years            500 mg

4-8 years            800 mg

9-18 years          1,300 mg

What should you do with this information?

Set an example for your child by modeling good bone health habits. Keep calcium rich foods on hand and encourage physical activity. Talk about your child’s bone health whenever you consult your pediatrician. Ask if your child needs nutritional supplements or treatments for an underlying medical condition. If your child has a hormone related disorder that might threaten bone health, you should consult an Endocrinologist, a specialist in the field, about whether hormone treatment is needed.

]]> http://www.diabetesendocrinology.in/2010/02/19/bone-health/feed/ 0 http://www.diabetesendocrinology.in/2010/02/19/diabetes-and-driving/ http://www.diabetesendocrinology.in/2010/02/19/diabetes-and-driving/#comments Fri, 19 Feb 2010 05:08:45 +0000 admin http://www.diabetesendocrinology.in/?p=574

People with well-controlled diabetes are at greater risk for car crashes and other driving mishaps, according to two recent studies.

Diabetes patients strive for tight control of blood sugar, aspiring for glycosylated hemoglobin (hbA1c) levels of 6.5-7. However, the methods used to stay at these levels, including regular blood tests and treatment with insulin and drugs can cause episodes of hypoglycemia, leading patients to lose concentration or even consciousness.

One 2-year study in the Public Library of Science compared the Hba1c levels of 795 drivers with diabetes who had or hadn’t been in an accident. The researchers found that lower HbA1c levels were tied to a higher risk of a motor vehicle crash. Those in previous accidents had an average HbA1c level of 7.4, compared with 7.9 among those who had not. The authors claim that the increase risk of lower HbA1c might account for about one-third of the 57 accidents in the study.

A 1-year study in Diabetes Care screened 452 drivers with type 1 diabetes for mishaps such as collisions, citations, and losing control, as ell as self-reported hypoglycemic episodes. More than half the drivers (52%) reported at least one hypoglycemia-related driving mishap, 32% reported two or more, and 5% reported six or more. Additionally, almost (41%) said they had experienced disruptive moderate hypoglycemia that impaired driving. Participants using pump therapy to manage their glucose were 35% more likely to record a hypoglycemia-related fender bender than those using insulin injections.

Both results suggest the need for laws that restrict driving in patients with diabetes. Countries that permit people with diabetes to drive (which is most) require that the drivers have no eyesight problems and can document their glycaemic control.

A new way to treat diabetes may be just around the corner. Several biotechnology companies are in hot pursuit of an oral form of insulin. So far, two options exits for patients with diabetes who require insulin – pumps or syringes, with other needle-free options remaining elusive. In 2007, Pfizer, Inc., withdrew Exubera, an inhaled insulin, saying it failed to find favor with doctors and patients.

The main hurdle with taking insulin by mouth is the challenge of avoiding digestive action that breaks it down.

Last month, Novo Nordisk started a phase 1 clinical trail in Germany with an oral insulin analog (NN1952). Novo is using Merrion Pharmaceuticals PIc’s GIPET technology to shield insulin from the digestive tract. The trial will investigate the safety and efficacy of NN1952 in healthy volunteers and people with type 1 or type 2 diabetes. The enrollment target is about 80, and results are anticipated in the first half of 2011.

Other biotechnology companies like Biocon Ltd as well are in the race to be the first out with an insulin pill. Oramed Pharmaceuticals is currently conducting phase 2B trials of its oral insulin capsule, ORMD-0801.

Oral Medicine in non-pill form are also in the works. Biodel is developing a sublingual oral insulin formulation called VIA tabTM that dissolves in minutes when placed under the tongue. Generex Biotechnology Corp. is forging ahead with an oral insulin spray, Oral-lynTM.

The last few decades has seen outstanding advancements in modern medicine in arresting & finding cures for many incurable maladies. But a cure for obesity has so far remained elusive. World over, doctors are increasingly worried about obesity. Recognized, since 1985, as a chronic disease, obesity is the second leading cause of preventable death, exceeded only by cigarette smoking. During the past 20 years, obesity among adults has increased significantly. 20% of the adult population consumes more than 80% of the visible dietary fat. Even by very conservative standards more than 5% of the adult population is overweight. The percentage of young people who are overweight has more than tripled since 1980. 30% of children and teens, from higher income groups are overweight.

Other than being aesthetically insensitive, the most important reason for being careful about this malady is its associated risk of heart disease. Cardiologists world over realize now is that excess weight over the middle – the proverbial apple, versus pear- increases the risk even more.

A man’s body is typically more “apple” shaped.
He tends to collect fat around his waist and
stomach area (beer belly). By contrast,
Women’s bodies are more “pear” shaped
as they tend to collect fat on their hips,
buttocks and thighs. People with “apple” body
shapes are more prone to develop diabetes
and heart disease than those with “pear” body shapes

Being obese or overweight increases the risk of many diseases & health conditions such as:

• High blood pressure
• High cholesterol
• Diabetes
• Heart Disease
• Stroke
• Gallbladder disease
• Osteo-arthritis
• Sleep apnoea (Snoring) & Respiratory problems
• Cancers (Endometrial, Breast & Colon)
• Polycystic ovarian disease, irregular periods & Infertility

1. BHATTACHARYYA A, Dash RJ. Plasma and Urine osmolarity in untreated thyroprivic hypothyroidism: Effect of Eltroxin therapy. J Asso Phy India 1994; 42(5): 366-368

2. Dash RJ, BHATTACHARYYA A. Thyroid hormones in diabetic ketoacidosis. J Asso Phy India 1993; 41:412

3. BHATTACHARYYA A, Wiles PG. Sexual dysfunction in diabetes mellitus Diabetes Annual, 1998; Chapter 12: pp 195-219.

4. BHATTACHARYYA A, Wiles PG. Thyroid crisis presenting as acute abdomen. J R Soc Med 1997; 90:681-682.

5. Sharma SC, BHATTACHARYYA A. Diabetes ketoacidosis in non-insulin dependent diabetes mellitus. J R Soc Med 1998; 91:34-35.

6. BHATTACHARYYA A, Wiles PG. Diabetic ketoacidosis precipitated by thyrotoxicosis. Post Grad Med 1999;75:291-92.

7. BHATTACHARYYA A, Tymms DJ. Mitochondrial defects and endocrine dysfunction. Q J Med 1998; 91:375-376.

8. BHATTACHARYYA A, Tymms DJ. Mitochondrial defects and endocrine dysfunction. Q J Med 1998; 91:375-376.

9. BHATTACHARYYA A, Sharma SC. Autoimmune thrombocytopenic purpura in a splenectomised patient. Int J Clin Prac 1998;52(7):508-509

10. BHATTACHARYYA A, Tymms DJ. Heart failure with Fludrocortisone in Addison’s disease. J R Soc Med 1998; 91:433-434.

11. BHATTACHARYYA A, Chan KG, Tymms DJ. Fluctuating thyroid function in a young woman. Postgrad Med 1999;75:243-44.

12. BHATTACHARYYA A, Tymms DJ. Thyrotoxicosis and abdominal pain: atypical presentation in a middle aged man. Hosp Med 1999;60(4):303.

13. BHATTACHARYYA A, Tymms DJ. Life threatening hypoglycaemia in a patient with type 1 diabetes mellitus. Practical Diabetes Int 1999;16:90-92.

14. BHATTACHARYYA A, Wiles PG. Thyrotoxicosis in old age: a different clinical entity? Hosp Med 1999;60(2):115-118.

15. BHATTACHARYYA A, Tymms DJ, Naqvi N. Asymptomatic pituitary apoplexy following aortocoronary bypass surgery. Int J Clin Prac 1999;53:394-5.

16. BHATTACHARYYA A, Tymms DJ. Acute Adrenocortical crisis and an abnormal Electrocardiogram. Hosp Med 1999;60:908-909.

17. BHATTACHARYYA A, Patel MK, Tymms DJ. Adult coeliac disease with varied presentations. J R Soc Med 1999;92:286-289.

18. BHATTACHARYYA A, Greenham R, Tymms DJ. Autosomal dominant hypocalcaemia and renal damage with vitamin D. Br J Renal Med 1999;4:10-12.

19. BHATTACHARYYA A. Why has Ron been getting hypos for only the last two years? Practical Diabetes Int (Letter) 1999;16(2):61-62.

20. BHATTACHARYYA A, Vice PA. Insulin Lispro, Pregnancy and Retinopathy. Diabetes Care 1999;22:2101-2102.

21. BHATTACHARYYA A, Kaushal K, Dornan TL. Evolving ECG changes in a patient with Hyoerthyroidism. J R Soc Med 2000:93:589-90.

22. Bhavanani M, Lyod D, BHATTACHARYYA A, Marple J. Screening for genetic haemochromatosis in blood samples with raised alanine aminotransferase.Gut 2000;46:707-10.

23. BHATTACHARYYA A, Wiles PG. Aetiology and pathology of thyroid diseases. Hospital Pharmacist 2000; 7:6-13.

24. BHATTACHARYYA A, Buckler HM. Treatment of thyroid diseases. Hospital Pharmacist 2000;7:14-19.

25. BHATTACHARYYA A, Parthivan A, Tymms DJ. Radioiodine for hyperthyroidism: a patient satisfaction survey. Clin Endocrinol Oxf, 2000;52:795-7.

26. BHATTACHARYYA A, Vice PA. DIGAMI in a District General Hospital in the UK: Influence, Implementation and Outcome. Diabetes Today 2000;3:120-123

27. BHATTACHARYYA A, Tymms DJ. An unusual case of ruptured ectopic pregnancy. In J Clin Practice 2000;54:409-10.

28. Bhattacharyya S, BHATTACHARYYA A. Hyperthyroidism in an elderly patient. Postgrad Med J 2000:76;597-8.

29. BHATTACHARYYA A, Howell A, Lakhdar A. Hyperosmolar Nonketotic State in a Patient with Type 1 Diabetes Mellitus. Diabetes Today 2000;5:152-3.

30. BHATTACHARYYA A, Greenham R, Tymms DJ. The relationship between nephrocalcinosis, vitamin D therapy and renal failure in ADH – the debate continues: In reply. Br J Renal Med 2000;4:23.

31. BHATTACHARYYA A. The aetiology and pathology of type 2 diabetes. Hospital Pharmacist 2001;8(1):5-9.

32. BHATTACHARYYA A. Severe hyperkalaemia, impaired renal function and diabetes mellitus. Diabetes Today 2001;4:18-9.

33. BHATTACHARYYA A. Treatment of type 2 diabetes. Hospital Pharmacist 2001;8(1):10-16.

34. BHATTACHARYYA A, Webb F. Needle in Foot. Practical Diabetes Int 2001;18:133.

35. BHATTACHARYYA A, Macdonald J, Lakhdar AA. Acute Adrenocortical crisis: Three different presentations. Int J Clin Prac 2001;55:141-4.

36. BHATTACHARYYA A, JD Wright, PA Vice. Obstetric difficulties due to Graves’ disease. Postgrad Med J 2002;77:661,669-70.`

37. BHATTACHARYYA A, Brown S, Hughes SM, Vice PA. Pregnancy outcome using Insulin Lispro and regular Insulin in one clinician led antenatal clinic in the UK. Q J Med 2001;94:255-60.

38. BHATTACHARYYA A, Tymms DJ, Bhavnani M. Serious interaction of Digoxin and Warfarin. British Journal of Cardiology 2004;9(9): 356-7.

39. BHATTACHARYYA A, Kaushal K, Dornan TL. Glucose control in patients admitted to the Hospital for reasons other than Diabetes. Diabet Med 2002;19:4-7.

40. BHATTACHARYYA A, Christodoulides C, Kaushal K, New JP, Young RJ. In-patient management of diabetes mellitus and patient satisfaction. Diabet Med 2002;19;412-6.

41. BHATTACHARYYA A, New JP, Buckler H. Hungry Bone Syndrome – Revisited. J R Coll Physicians Edinb 2002;32:83-6.

42. Deepak PJ, Sunitha K, Jagdish N, Sanjukta K, BHATTACHARYYA A. Inpatient management of Diabetes: Suevey in a tertiary care centre. Postgrad Med J 2003;79:585-7.

43. BHATTACHARYYA A, Dornan D. Diabetes in Hospital. Clinical Medicine 2004;4:314-7.

44. Kaushal K, BHATTACHARYYA A, Verghese B, Davis JRE. Adequacy of information delivered to patients during consultation for thyrotoxicosis. Clin Endocrinol (Oxf) 61;778-9: 2004.

45. BHATTACHARYYA A, Kaushal K, Tymms DJ, Davis JRE. Setroid withdrawal syndrome after successful treatment of Cushing’s disease: a reminder. European Jn Endocrinol 2005;153:207-10.

National

1. BHATTACHARYYA A. Glycaemic control in hospitalised patients with or without known Diabetes Mellitus. Endocrine Newsletter Feb. 2002.

2. A BHATTACHARYYA, Vineet Nayar. Glucose control in Hospital: Time for an aggressive approach. National Medical Jn of India 2002;15:208-9.

3. Sunitha K, Kavitha M, Sampath K, BHATTACHARYYA A. A young girl with lower limb weakness. Karnataka Journal of Medical Sciences 2003;02(03):26-7.

4. 48. Ramkrishna B, Deepak PJ, BHATTACHARYYA A. Management of Diabetes in Hospitalized Patients. Asian Jn Diabetol 2003;5:20-8.

5. Pillai P, Bhattacharyya A. Beta-cell Preservation in Type 2 Diabetes Mellitus. Asian J Diabetol 2004;6(1):21-6.

6. Prahlad P, Elveyna E, BHATTACHARYYA A. Thyrotoxic periodic paralysis: A series of three cases. Karnatake Jn Medical Science 2004;3:14-6.

7. Jagdish N, Elveyna E, BHATTACHARYYA A. Feeling not too well with an unusual thyroid function test. Ind Jn Thyroid Research 2005 (in press).

8. Jagdish N, BHATTACHARYYA A. Abdominal Pain in Thyrotoxicosis. Indian Jn Clin Prac 15(3);37-47:2004.

9. Hypercalcaemia in Everyday Practice. Elveyna E, Prahlad P, Bhat V, BHATTACHARYYA A. Indian Jn Clin Practice 2005;15(8): 55-63.

10. Elveyna E, Sangeetha V, BHATTACHARYYA A. Approach to thyroid disease: A summary for Primary Care Physician. Thyroid Research and Practice 2005;2:25-30.

11. Sabeer TK, Rashmi MN, Elveyna E, Prahlad P, Praveen K, BHATTACHARYYA A. Management of diabetes in patients undergoing CABG- How good are we? Asian Journal of Diabetes 2005 (In print)

12. Sabeer TK, BHATTACHARYYA A, Jagan P. Diabetes in hospital. Why important? Indian Journal of Clinical Practice 2005 (In print)

13. Sabeer TK, BHATTACHARYYA A, Jagan P. Diabetes in hospital. Why diabetes control in hospital destabilize? Indian Journal of Clinical Practice 2005 (In print)

14. Sabeer TK, BHATTACHARYYA A, Latha MS. Diabetes in hospital. Assessment. Indian Journal of Clinical Practice2005 (In print)

15. Sabeer TK, BHATTACHARYYA A, Latha MS. Diabetes in hospital. Principles of management. Indian Journal of Clinical Practice 2005 (In print)

16. Sabeer TK, BHATTACHARYYA A. Diabetes in hospital. Insulin regimens and special situations. Indian Journal of Clinical Practice 2005 (In print)

17. Sabeer TK, BHATTACHARYYA A. Diabetes in hospital. Discharge planning. Indian Journal of Clinical Practic 2005 (In print)

18. Naveen A, Sabeer TK, BHATTACHARYYA A. Hot nodule – Always toxic? Indian thyroid society journal 2005 (In print)

19. Sabeer TK, BHATTACHARYYA A. Beta cell preservation in Type 2 Diabetes mellitus. Practical? Care for Diabetes 2005 (In print)

Patient Information Booklet

1. S Bhattacharyya, A BHATTACHARYYA. A Journey with Thyroid Problems: Handbook for people with or without Thyroid Disease. First Edition (English and Kannada), Bangalore, 2002.

2. S Bhattacharyya, A BHATTACHARYYA. Do It Yourself: The Journey with Diabetes. First Edition, Bangalore 2002 (English and Kannada).

3. S Bhattacharyya, A BHATTACHARYYA. Do It Yourself: The Journey with Diabetes. Second Edition, Bangalore 2005 (English, Kannada, Bengali, Hindi).

4. S Bhattacharyya, A BHATTACHARYYA. A Journey with Thyroid Problems: Handbook for people with or without Thyroid Disease. Second Edition, Bangalore, 2005 (English, Kannada, Bengali, Hindi).

1. Fibronectin in BAL fluid and plasma in Tuberculosis – World Conference of Lung Health, IUATLD, Italy, 1990.

2. Autosomal dominant hypocalcaemia: treatment with vitamin D can cause renal damage even at low normal serum calcium levels. Clinical case meeting (Society of Endocrinilogy) at Royal College of Physician(London), Feb.1998.

3. A novel complication of treatment of Addison’s disease. RCP postgraduate meeting in Diabetes and Endocrinology, Manchester, May,1998.

4. A young woman with fluctuating hypo- and hyperthyroidism. North West Endocrine Society meeting, Manchester, Dec,1998.

5. Addison’s disease and its varied presentation. Lancashire canter for medical studies, Preston, Feb. 1999.

6. Graves’ disease in pregnancy complicated by sensitivity reaction to both Carbimazole and Propylthiouracil. Society for Endocrinology conference, Bournemouth, Apr.1999.

7. Prevalence of genetic Haemochromatosis in patients with raised Alanine Aminotransferase. Northwest Association of Physician meeting (Manchester Medical Society presntation), Preston, Apr.1999.

8. Radioiodine for hyperthyroidism: A patient satisfaction survey. North West Endocrine Society meeting, Liverpool, may, 1999.

9. Obstetric difficulties due to thyroid disease. Clinical Practice day, Society for Endocrinology, Manchester, Oct, 1999.

10. Glucose tolerance test and drug induced Diabetes. International Diabetes update, Bangalore, Nov.2001.

11. Early Insulin therapy in type 2 Diabetes Mellitus. Workshop NNDU Singapore 2004.

National

1. Lipid alternation in Primary Hypothyroidism with effect on treatment -Endocrine Society of India Conference, Chandigarh, 1991

2. Plasma and urine osmolarity in Primary hypothyroidism Endocrine Society of India Conference, Bombay, India, 1993

3. Beta cell preservation in type 2 Diabetes Mellitus. ESICON 2002, Calcutta, Dec 2002.

4. Hospital management of Daibetes Meliitus. Madurai, April, 2002.

5. Syndrome X and complications of Diabetes Mellitus. Nagpur, February, 2003.

6. Prandial glucose regulation. Regional Diabetes Update, Kochin, 2003

7. Diabetes Management in Hospital setting , PGIMER, Chandigarh, Sep 2004

Regional

1. Pregnancy and thyroid dysfunction. Bangalore Society of Obstetrics and Gynaecology, Dec. 2001.

2. Postprandial Glucose Control. Which, When, How, Why? Karnataka chapter APICON, 2002, Hubli.

3. Newer oral agents in the treatment of type 2 Diabetes Mellitus, Ranbaxy Diabetes update, Bangalore, Sept. 2001.

4. Proponent for debate “HRT is a must for all postmenopausal women, unless contraindicated” KAPICON 2003, Mysore.

5. Opponent for debate “Early Insulin therapy in type 2 Diabetes” KIMC, Mangalore, Dec 2003.

6. Proponent for debate – Secretagogues vs Insulin in treatenmnt of early type 2 Diabetes. RSSDI 2004.

7. Hospital management of Diabetes Mellitus – API meeting Bellary, Aug 2004.

8. In patient manage,ment of Diabetes – Quotyam Diabetes Club meet – 2005

Patient Education

1. Diabetes and Diet, Diabetes Club, Bangalore 2002.

2. Diabetes for the elderly – Rotary Club, Indiranagar 2004.

3. Osteoporosis – Infosys, Bangalore 2004.

4. Diabetic complication – Diabetes Club, Bangalore 2004

]]> http://www.diabetesendocrinology.in/2009/06/11/orations/feed/ 0 http://www.diabetesendocrinology.in/2009/06/11/research-activities/ http://www.diabetesendocrinology.in/2009/06/11/research-activities/#comments Thu, 11 Jun 2009 09:08:43 +0000 admin http://www.diabetesendocrinology.in/?p=522 1. Collaborative Atorvastatin in Diabetes Mellitus, North Manchester General Hospital – Co-Investigator – 1996

2. Cross-over comparison of Viagra TM and Placebo for the treatment of pain in diabetic polyneuropathy in adult males A 1481016 , Hope Hospital, Manchester – Co-Investigator – 2000

3. A double blind comparison of Viagra and placebo: 148-1040 Study in Diabetic Foot Ulcers – Hope Hospital, Manchester – Co-Investigator – 2000

4. Glimepiride vs Metformin in children with type 2 Diabetes as monotherapy in Paediatric subjects with type 2 Diabetes Mellitus: A single blind comparison study. HOE490/4038. 2003-4. – Pr Investigator, Manipal Hospital, Bangalore.

5. Glycon Registry: Open labelled trial to see efficacy on glycaemic control, lipids with injection Glargine once daily in patients with type 1 and 2 Diabetes mellitus. 2003-4 Pr Investigator, Manipal Hospital, Bangalore.

6. An open labelled randomised, three treatment, three period, three sequence cross-over, relative bio-availability study of two formulations of Testosterone with one formulation of Restendol in hypogonadal subjects under fed condition. Pr Investigator Lotus Lab, 2004

7. A multicentric 12-week comparative study of twice-daily Novomix 30 + Pioglitazone versus Sulphonylurea + Pioglitazone. 2004, Pr Investigator, Manipal Hospital, Bangalore.

]]> http://www.diabetesendocrinology.in/2009/06/11/research-activities/feed/ 0 http://www.diabetesendocrinology.in/2009/05/28/underactive-adrenal-or-hypocortisolism/ http://www.diabetesendocrinology.in/2009/05/28/underactive-adrenal-or-hypocortisolism/#comments Thu, 28 May 2009 09:37:32 +0000 admin http://www.diabetesendocrinology.in/?p=482 What are the causes of Low cortisol hormone??

The disease of low cortisol production can arise either because of destruction of adrenal gland itself (Addison’s disease or primary hypocortisolism) or due to malfunction of pituitary or hypothalamus (secondary hypocortisolism). Common causes of secondary adrenal insufficiency are tumors of the pituitary, head injury, radiotherapy and long standing steroid medication suppressing the axis.

The primary adrenal deficiency, also called Addison’s disease, is the result of infective or inflammatory or infiltrative processes involving the adrenal glands. The most common is the autoimmune destruction of the glands. This is followed by less commoner conditions like metastasis, amyloidosis, tuberculosis, opportunistic infection in AIDS/HIV, infarction, haemorrhage, adrenomyeloneuropathy, congenital adrenal hyperplasia etc.

What are the clinical features of Addison’s disease?

Symptoms are non-specific. Common presentations are loss of weight, loss of appetite, tiredness, hyper-pigmentation of the skin, dizziness and low BP, nausea, vomiting, decreased axillary and pubic hair and reduced libido in women. It could be associated with vitiligo i.e. patchy whitening of the skin. Blood test may show low sodium, high potassium, elevated urea, low hemoglobin.

What other problems could be associated with this?

This disease could be a part a cluster of autoimmune diseases called autoimmune polyglandular syndrome where other than low cortisol there is low level of thyroid, parathyroid and sex hormones. Type 1 diabetes could also be a part of it.

How do we confirm this?

There are several ways to confirm this problem. Low blood sodium, high blood potassium with elevated urea indirectly point to low cortisol. Finding low blood cortisol, which fails to increase after injection of synacthen is diagnostic of Addison’s disease. This test is called short synacthen test. Other tests that the doctor may want is adrenal CT scan

What is the treatment?

This problem of low cortisol is corrected by administration of the hormones in the tablet form. The most natural replacement is through tablet hydrocortisone, however prednisolone can be used for economic reason. The other hormone aldosterone is replaced by giving tablet fludrocortisone. The initiation of hydrocortisone requires monitoring. This monitoring can be done by observing for several parameters like weight, BP, blood sodium and potassium levels, blood cortisol levels in the form of cortisol day curve. One has to get admitted for a day for the last test. One more important thing to note is that this hydrocortisone tablet should be taken at particular time of the day i.e. on waking, at midday and at 5 pm. Compliance is very important here.

How to manage during an intercurrent illness?

The requirements of cortisol go up when a patient of cortisol deficiency undergoes a surgery or develops a severe illness like pneumonia. For moderate elective procedures or investigations e.g. Endoscopy or angiography, patients should receive a single dose of 100mg hydrocortisone before the procedure. For major surgery patient should take 20mg hydrocortisone orally or 100mg intrmuscular injection before surgery, and receive 100mg intrmuscular injection every sixth hourly for the first three days and then rapidly go back to pre surgery level. In case of pneumonia patients should receive 50-100mg intrmuscular injection every sixth hourly until completely cured.

Does management differ during pregnancy?

No. One can continue the same dose during the pregnancy. If the hyper emesis gravidarum i.e. the condition of excess vomiting in the first three months, ensues then intramuscular injection may be required. During labor 100mg of hydrocortisone is given by intramuscular injection every sixth hourly.

What are the implications of long-term steroid administration?

The steroid medications like prednisolone, betamethasone or dexamethasone are given for various medical conditions like asthma, rheumatoid arthritis and many connective tissue disorders like SLE for longer periods to achieve remission. If any of these are given for more than 3 weeks or if prednisolone or its equivalent is given at 40mg/day or more for less than 3 weeks or a short term therapy (< 3weeks) is given within one year of cessation of long term therapy (>3 weeks) or is given as a evening dose then the body fails produce its own cortisone when external therapy is withdrawn. Therefore in such situations the steroids should be withdrawn slowly. After the remission has been achieved these drugs are reduced to a dose of 7.5mg of prednisolone or equivalent per day and then further reduction is carried out more gradually over months. Ideal would be to start on hydrocortisone tablet and to do a test called short synacthen test to know whether the body has regained its capacity to produce cortisol on its own before finally stopping the drug.

]]> http://www.diabetesendocrinology.in/2009/05/28/underactive-adrenal-or-hypocortisolism/feed/ 0 http://www.diabetesendocrinology.in/2009/05/28/steroid-medications/ http://www.diabetesendocrinology.in/2009/05/28/steroid-medications/#comments Thu, 28 May 2009 09:33:05 +0000 admin http://www.diabetesendocrinology.in/?p=480 1) What is steroid?

Steroid is name of a hormone that comes form Adrenal glands mainly. There are different types of steroids in our body; they serve various types of metabolic function. Some of the steroids are life-saving, meaning without them we can not survive. Some of them suppress inflammation. Other steroids come form Testes and Ovaries; they are called sex-steroids. In addition to controlling metabolism they are important in sexual function.

2) What are their uses?

These drugs are used for various medical conditions in which the inflammatory response has to be controlled. In diseases like asthma these are given by tablet, injection or through inhaler. In certain other medical conditions like rheumatoid arthritis, SLE and other connective tissue disorders these are very helpful. These are the life saving medications in situations like adrenal insufficiency and severe allergic reactions.

3) What are different types of steroids?

There are different types of steroids. They are mainly classified on the basis of their potency. While hydrocortisone, commonly called as hysone or histone, is least potent; dexamethasone, commonly known as dexona, is the most potent. However most commonly used steroid is prednisolone which is intermediate in potency.

4) Are their any side effects to these drugs?

If one uses these drugs in excess then they create a variety of problems. The most dramatic of all is the Cushing’s syndrome in which patient manifests with florid signs of steroid excess. These drugs can cause increase in blood sugar leading to diabetes, increase BP, weaken the bones (osteoporosis), muscle weakness, ulcer in the tummy, raised pressure in the eyes (glaucoma), increased chance of infections etc. However if used judicially then they help in combating many ailments effectively. Also if a person is taking a steroid drug for a long time then it must be reduced slowly otherwise patient may develop crisis which could be life threatening.

5) Is there any difference between these steroids and steroids used by sports persons for performance enhancement?

Yes, there is a lot of difference between them. They are called anabolic-androgenic steroids. These are basically male sex related hormones; anabolic means body building and androgenic means masculine characteristics. In sports their use is illegal. They are used in the belief that they increase the muscle strength and hence performance. Although it may be true in short term they are deleterious to health if used on a long term basis.

6) What are the problems of its long term use?

In both men and women they can cause liver and kidney cancer, jaundice, increased blood pressure, bad cholesterol, mood swings etc. In men testicles may shrink, sperm production and fertility decreases, baldness increases. They are at increased risk of developing prostate cancer. The women develop excessive facial hair, male pattern bald ness, menstrual disturbances, and changes in genetalia. If children abuse these drugs then their overall growth will be stunted.

The patients suffering from this disorder may have following picture. They can have a round face, a buffalo hump (collection of fat in the back just below the neck), weakness of muscles resulting in difficulty in getting up from the sitting position, weakness of bone (osteoporosis) resulting in easy fractures, menstrual disturbances, thinning of the skin, raised blood pressure and high blood sugar. Many experience mood disturbances like depression. Loss of sexual drive can be another problem. Many become susceptible to infections.

When a person has clinical features suggestive of Cushing’s syndrome the clinician looks for evidence of increased cortisol production. He would order for measurement of blood cortisol at 8 am and midnight. If they are high then a tablet called dexamethasone will be given at 11pm and your blood will be tested next morning at 8 am for cortisol level. In normal persons there will be low level of cortisol in the next morning but if it is high then the suspicion of Cushing’s syndrome is strong. From here he proceeds to find out if this excess is coming from adrenals or from ACTH excess. Estimation of ACTH value, which is done only at a few centers in India, helps solve this problem. While in the former ACTH is undetectable in the latter it is high. If ACTH is found to be high then it could be of either pituitary source or of an ectopic source. A MRI scan of the pituitary or CT scan of abdomen or chest can reveal the culprit.

If the cause is in the pituitary then a surgery called Trans sphenoidal surgery is done to remove the tumor from the pituitary. It may be followed by radiotherapy in case of failure of surgery. If it is located in the adrenal then either one or both glands are removed. We have two options here. One is an open surgery second one is laparoscopic surgery. In the latter the advantage is that a small cut is needed and recovery is faster. However it is useful only if size is less than six cms. If it is more than six cms then probability that it could be cancerous lesion are high, whence open surgery is preferable. In either case one has to be on replacement of the hormones in appropriate dose later. If it is an ectopic source then an attempt is made to remove the source. But in case it is not possible then certain drugs like ketoconazole or metyrapone are given to suppress the cortisol production.