Metabolic disorders

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Chapter 37 Metabolic disorders

Pineal Gland

Synthesizes melatonin, which – because of its position in the third ventricle – is secreted directly into the cerebrospinal fluid (CSF), from where it finally ends up in the blood. Melatonin affects reproductive development and daily physiology.

Pituitary Gland

The ‘master gland’ of the body; possesses two lobes:

• Anterior (adenohypophysis): is attached but not directly connected to the hypothalamus.

• Posterior (neurohypophysis): directly connected to the hypothalamus via neural tissue. Does not produce its own hormones but stores and releases hormones when they are required.

Anterior Pituitary Gland

The anterior pituitary gland secretes:

• Growth hormone (GH): stimulates growth of bones, muscles, etc. by stimulating protein synthesis.

• Follicle-stimulating hormone (FSH).

• Prolactin (PL): stimulates the development of female breast glandular tissue during pregnancy and milk production after birth.

• Luteinizing hormone (LH).

• Thyroid-stimulating hormone (TSH): stimulates secretion of thyroid gland.

• Adrenocorticotrophic hormone (ACTH): stimulates secretion of adrenal glands.

• Endorphins.

The anterior pituitary gland responds to:

• Growth-hormone-releasing hormone (GHRH): causes the release of growth hormone (GH), which controls growth.

• Thyrotropin-releasing hormone (TRH): causes the release of thyroid-stimulating hormone (TSH) and prolactin (PL).

• Corticotrophin-releasing hormone (CRH): causes the release of adrenocorticotrophic hormone (ACTH), which controls blood pressure.

• Dopamine (DA): inhibits release of prolactin under normal conditions.

• Gonadotrophin-releasing hormone (GnRH): causes release of FSH and LH, which control pregnancy.

Posterior Pituitary Gland

The posterior pituitary gland secretes:

• Oxytocin: involved in childbirth.

• Antidiuretic hormone (ADH): affects blood pressure, water and concentration of salts in the nephron (see Chapter 26 ‘Cardiovascular disorders’, p. 193).

Treatment of Pituitary Disorders

It is evident from the above that any patient with a pituitary condition of any kind will probably be under orthodox medical care. This can be complex and the patient is carefully monitored. However, it is worth being aware of the condition of diabetes insipidus, which is caused by a reduction in ADH. The patient will urinate excessively. The difference between this and diabetes mellitus is the normal blood sugar levels.

A careful case history should enable a practitioner to identify the medication the patient is on and consult a formulary for the actions of the drug and any side effects. Note that severe trauma to the head can be responsible for pituitary dysfunction.

Thyroid Gland (see Chapter 41 ‘scientific tests’ Table 41.1, p. 340, Table 41.2, p. 341)

Dysfunction of this gland is commonly encountered in clinical practice.

The thyroid is a double-lobed endocrine gland situated in the neck. It produces the hormones thyroxine (T4) and triiodothyronine (T3). These hormones are responsible for:

• regulating metabolic rate generally

• affecting growth.

Iodine is necessary for the production of both hormones. Disorders of the thyroid include:

• Hyperthyroidism: overactive thyroid

• Hypothyroidism: underactive thyroid.

Thyroid-releasing hormone is released by the hypothalamus, via the pituitary gland (see above); occasionally the pituitary is at fault.

Parathyroid Gland

Calcium Regulation in the Body

• The amount of calcium in the blood and fluid has to be tightly controlled. There is always some loss of calcium from the body, (100–240 mg in the urine and between 45 and 100 mg in the faeces) but this is not a problem if it is being replaced.

• The parathyroid glands detect when the calcium concentration in the blood decreases and secrete parathyroid hormone (PTH). PTH stimulates the conversion of inactive vitamin D to active calcitriol.

• Calcitriol increases the absorption of calcium from the small intestine.

• The PTH and calcitriol stimulate the release of calcium from bone by activating osteoclasts (responsible for bone resorption) and increase the absorption of calcium in the kidneys.

• An increase in the concentration of the calcium in the blood above normal levels will switch off the production of PTH. The kidneys will then begin to excrete excess calcium in the urine.

Although this system maintains good control of calcium in the body, it does so at the expense of the calcium in the bone.

Interestingly, the efficiency of absorption of calcium from a supplement is inversely proportional to the total amount of calcium ingested. The cells of the gut wall have a maximum capacity for how much calcium they can pass across from the lumen to the capillaries.

Vitamin D is required for optimal calcium absorption.

Figure 37.1 Demonstrating the interrelationship between calcium and vitamin D and calcium metabolism.

Interaction of Food Substances with Calcium

See Chapter 13 ‘Vitamins and minerals’ (p. 96).

Osteoporosis

Bone continually remodels itself. This occurs due to action of the osteoclasts, which dissolve and reabsorb bone, and the osteoblasts, which synthesize new bone to replace that reabsorbed.

Osteoporosis can occur when the rate of bone resorption is greater than its formation. Although osteoporosis is thought to be a postmenopausal problem it is possible even in children. Osteoporosis is caused by more than one factor. Risk factors are:

• Female sex.

• Oestrogen deficiency.

• Metabolic disease such as hyperthyroidism.

• Certain medication such as corticosteroids and anticonvulsants.

There is also an element of genetic and lifestyle factors.

• Assessment of Osteoporosis or Osteopaenia

• Full blood counts and hormone levels are checked for underlying causes.

• Alkaline phophatase levels (see Chapter 41 ‘Scientific tests’, p. 335) are usually raised.

• Single and dual X-ray absorptiometry (DXA) and digital X-ray radiogrammetry (DXR): these procedures assess the mineral content of the entire skeleton. DXA is considered to be the gold standard for diagnosis of bone density reduction, particularly in the hip area. DXR is a newer and simpler technique using a standard radiograph of the hand.

• Treatment

Conservative Treatment

• Weight-bearing exercise has been showed to help osteoporotic patients but the exercise has to be high-impact based.

• Vitamin D and calcium supplementation (see Chapter 13 ‘Vitamins and minerals’, pp. 95 and 107) have been shown to be beneficial.

Orthodox Medication

Bisphosphonates

These attach to bone tissue and are ingested by and kill the osteoclasts (the bones cell that break down bone tissue). This slows bone resorption but not bone forming. So, over a period of time, the bone density should increase.

Bisphosphonates have to be taken on an empty stomach and with at least 8 fluid ounces of water. The patient then needs to remain upright for at least 1 hour to be sure that the bisphosphonate has passed out of the oesophagus.

Hormone Replacement Treatment (HRT)

This is no longer considered a primary means of treating osteoporosis as it has been shown to increase the risk of breast cancer.

Selective Oestrogen (Estrogen) Receptor Modulator (SERM)

• Reduces bone loss and vertebral fracture but might increase the risk of blood clots and can exacerbate hot flushes.

• Does appear to be linked with a decrease in the risk of breast cancer.

Adrenal Glands

Responsible for the ‘fight or flight response’. The adrenals secrete:

• corticosteroids (see Chapter 30 ‘Inflammation and immune system’, p. 230).

• catecholamines (see Chapter 31 ‘The nervous system’, p. 240).

Cushing Syndrome

Although this can be caused by a tumour in the pituitary or adrenal glands, the more common reason seen in complementary practice is the long-term usage of steroids, e.g. prednisolone, to reduce inflammation in arthritic conditions, or asthma.

Thymus Gland

• Involved in the immune system.

• Produces T lymphocytes.

Reproductive Hormones

See Chapter 38 ‘Reproductive hormones’ (p. 299).

Pancreas

Treatment of Type 2 Diabetes

The pancreatic islet cells are still functioning.

• Conservative Treatment

• Dietary control: the intake of simple sugars is reduced and that of more complex carbohydrates is increased (see Chapter 9 ‘Carbohydrates’, p. 68).

• Orthodox Medication

Sulphonylureas: Gliclazide

• Augments insulin secretion and therefore some beta cell activity is required.

• Has a short half-life (see Chapter 17 ‘Metabolism’, p. 129) and therefore reduces the possibility of hypoglycaemia.

• Not suitable in pregnancy.

Adverse Effects

• Gastric disturbances.

• Constipation.

Polycystic Ovarian Syndrome

The cause is not properly understood.

• Diagnostic Blood Tests

• LH elevated.

• LH : FSH ratio increased; FSH is normal.

• Raised levels of prolactin in the blood.

• Thyroid function tests.

• Fasting glucose and oral glucose tolerance test to reveal any insulin-resistant diabetes.

• Fasting lipid levels.

• Testosterone and oestriol may be elevated. Very high levels of testosterone might be due to a tumour.

• Treatment

Usually according to symptoms:

• Diet and exercise: weight loss may help general symptoms and insulin resistance.

• Type 2 diabetes medication: see above.

• Clomifen: to induce ovulation.

• Anti-androgens: to counter hirsutism.

Other Metabolic Conditions

Metabolic Syndrome X

• Central obesity: excessive fat tissue in the abdominal region.

• Insulin resistance.

• Dyslipidaemia: high levels of triglycerides and low levels of high-density lipoproteins.

• Hypertension.

• Abnormal levels of blood-clotting factors (high fibrinogen or plasminogen activator inhibitors in the blood).

• Low levels of high-density lipoprotein and high levels of low-density lipoprotein cholesterol and triglyceride, ultimately encouraging plaque formation in artery walls (see Chapter 41 ‘Scientific tests’, p. 340).

• Proinflammatory state: elevated high-sensitivity C-reactive protein in blood (see Chapter 41 ‘Scientific tests’, p. 334).

• Reasons for Predisposition to Metabolic Syndrome X

• May be genetic: members of the same family are more likely to develop the condition.

• Treatment

• Exercise and diet can reverse insulin resistance.

If exercise does not work:

• Lipid-lowering drugs: e.g. statins (see Chapter 27 ‘Problems with lipid metabolism’, p. 207)

• Aspirin: to prevent blood clotting.

• Hypertensive drugs if blood pressure is high (see Chapter 26 ‘Cardiovascular disorders’, p. 195).

• Diabetic medication: if blood sugar levels are high.

Gout

Purines are excreted by soluble uric acid, but uric acid and urates are only just water soluble. This becomes a problem when the urine becomes particularly acidic (high meat intake, particularly red meat full of purines and pyrimidines; see Chapter 18 ‘Drug excretion’, p. 134). High levels of uric acid in the blood (uraemia) can result in uric acid crystals in the joints, most frequently the first metatarsophalangeal joint. The attacks are acute and very painful. Repeated attacks lead to tissue damage and arthritic malformations.

• Treatment

1) Reducing the immune response to uric acid deposits.

2) Reduce the inflammation.

3. Reduce uric acid synthesis.

4) Increase renal excretion of uric acid.

1) Reducing the immune response to uric acid deposits:

• glucocorticoids

• non-steroidal anti-inflammatories (NSAIDs; see Chapter 30 ‘Inflammation and the immune system’, p. 231):

Indomethacin is commonly used.

Colchicine

Thought to inhibit cell division of neutrophils. How colchicine works is not yet properly understood. However, it is thought to: (1) reduce lactic acid production by leucocytes, which results in a decrease in uric acid deposition; (2) reduce phagocytosis. This combined effect reduces the body’s response to inflammation, thus allowing the inflammation to subside.

Adverse Effects of Colchicine

• Abdominal pain.

2) Reduce Inflammation

• Glucocorticoids.

• Cherries: the flavonoids in cherries can act as an anti-inflammatory, and also increase the renal filtration of urate (fitting into the fourth category of gout treatment), while decreasing its reabsorption (Jacob et al 2003).

3) Reduce Uric Acid Synthesis

Allopurinol is a competitive inhibitor (see Chapter 19 ‘Pharmacodynamics: how drugs elicit a physiological effect’, p. 138) and attaches so securely to the enzyme-binding site that the normal substrate cannot attach itself and take part in the necessary reaction. This reduces the production of uric acid, leaving more soluble products in the blood, which are likely to deposit as crystals in the joints. It is used between attacks. There are few adverse effects.

4) Increase Renal Excretion of Uric Acid

• Probenecid: increases the excretion of urate. Few side effects but on withdrawal of drug there might be fever, a general feeling of being unwell, muscle pain and skin rash.

• Sulfinpyrazone: more powerful than probenecid but has antiplatelet effects and so is used with caution in patients on antiplatelet or anticoagulation drugs. Gastrointestinal disturbances sometimes occur. Avoid in patients with peptic ulcers.

• Cherries (see above): reduce inflammation.

Hyperhomocysteinaemia

A high level of circulating total homocysteine (tHcy) is an independent risk factor for vascular diseases:

• Homocysteine is an amino acid, but not one that is part of the metabolism or structure of the body, as it is an intermediary product. It is synthesized from methionine.

• Homocysteine is effectively at the centre of two pathways, one that requires folate and vitamin B12, the other that requires vitamin B6. Deficiencies in these vitamins are therefore likely to leave a high level of homocysteine in the body.

• It is possible that homocysteine encourages the formation of superoxide radicals (see Chapter 7 ‘Free radicals’, p. 44) in the blood. These damage the blood vessels wall and, once damaged, plaques can form (Chapter 27 ‘Problems with lipid metabolism’, p. 204).

• Homocysteine has prothrombotic effects and enhances the activities of factor XII and factor V (see Figure 28.1, p. 212).

• Predisposing Factors

• Sex: men have a tendency for high levels of homocysteine.

• Genetic: there are also genetic differences, as can be see with race.

• Exacerbating Factors

• Heavy coffee consumption (approximately eight cups a day) combined with smoking has been associated with high levels of homocysteine.

• Treatment

Plasma homocysteine levels can be lowered by taking folic acid along with vitamin B12, which works synergistically. The higher the level, the greater the drop with this type of supplementation.

Wilson’s Disease

• Recessively inherited disorder of copper metabolism.

• Causes the body to retain copper: the liver of a person with Wilson’s disease does not release copper into bile as it should.

• Copper is absorbed from food and builds up in the liver, damaging the liver tissue: this damage eventually releases the copper directly into the bloodstream, resulting in copper being carried throughout the body.

• The copper build-up leads to damage in the kidneys, brain and eyes.

• If not treated, Wilson’s disease can cause severe brain damage, liver failure and death.

• Wilson’s disease is hereditary: symptoms usually appear between the ages of 6 and 20 years, but can begin as late as age 40.

• Signs and Symptoms

• Presents as liver disease in children and adults.

• Kayser–Fleischer ring present as a greenish brown or gold ring on the cornea in 90% of symptomatic patients.

• Reduced serum copper and ceruloplasmin concentrations (see Chapter 41 ‘Scientific tests’, p. 340).

Early Signs and Symptoms

Asymmetrical tremor at rest or with movement. In older patients, Wilson’s disease can be mistaken for Parkinson’s disease.

Later Signs and Symptoms

• Arthritis with osteopenia.

• Spasticity.

• Dystonia: extended muscle contraction in a group of muscles.

• A small percentage may have psychological problems.

• Nephrocalcinoisis: excessive deposition of calcium in kidneys.

• Cardiomyopathy: damage of heart muscle.

• Increased concentration of copper in the brain and viscera: therefore neurological (e.g. epileptic seizures) and hepatic symptoms (possible cirrhosis).

• Initial Diagnostic Screening Tests

Blood Test

• Ceruloplasmin (copper-containing protein) levels: low (less than 20 mg/dL).

Urine Test

• If ceruloplasmin levels are low then urine is collected over a period of 24 hours.

• Normal levels of urinary copper are between 10 to 30 μg/24 hours.

• Treatment

• Patients are advised to abstain from alcohol to avoid damaging the liver further.

• Potentially hepatotoxic drugs are avoided.

• Avoidance of foods high in copper: dietary copper is kept below 2 mg a day (see Chapter 13 ‘Vitamins and minerals’, p. 98).

• Zinc supplementation to interfere with absorption of copper.

• Chelating agent – penicillamine – forms a complex with the copper, thereby removing it from the body’s metabolism. Readily absorbed from the gastrointestinal tract and quickly excreted in urine. Other chelating agents are available if there is lack of tolerance to penicillamine, e.g. trientine. However, this drug creates problems in patients with an iron deficiency.

• Patient has to undergo frequent urinalysis and complete blood counts.

Adverse Effects of Penicillamine

• Nausea and vomiting.

• Nephrotic syndrome: large amounts of protein leak into urine.

• Arthropathy: swelling or dysfunction of joints.

• Optic neuropathy.

• Various blood disorders.

Reference

Jacob RA, Spinozzie GM, Simon VA, et al. Consumption of cherries lowers plasma urate in healthy women. Journal of Nutrition. 2003;;133(6):1826-1829.

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