Muscles In patients with hypothyroidism, disordered muscle function often is the predominating feature of the clinical syndrome. Generalized muscular hypertrophy, accompanied by easy fatigue and slowness of movements, occurs in some myxoedematous children or adults. It has been referred to as the Kocher– Debré– Sémélaigne syndrome in children and as Hoffmann’s syndrome in adults. These patients do not have the classic electromyography findings of myotonia. The myopathy of hypothyroidism in some patients is associated with weakness even though the muscles are hypertrophied. The typical patient presents with firm large well- developed muscles, like those of an athlete. The entire musculature is affected to some extent, but the most obvious enlargement is in the arms and legs.

Muscle symptoms such as myalgia, muscle weakness, stiffness, cramps, and easy fatigability are very prevalent in hypothyroid patients. The symptoms are aggravated by exposure to cold. They are also prominent during the rapid onset of hypothyroidism after surgery or 131 I treatment. Impairment of mitochondrial oxidative metabolism provides a biochemical substrate for these complaints.

Reflex contraction and relaxation time is prolonged, mainly because of the intrinsic alterations in muscle contractility. Nerve con duction time may also be prolonged. Delayed reflex relaxation is characteristic and has been developed into a diagnostic test of thy roid function. The rate- limiting step in muscle relaxation is the re uptake of calcium by the sarcoplasmic reticulum. In skeletal muscle, this process is dependent on the content of Ca2+- ATPase. Recent studies have indicated that Ca2+- ATPase activity of the fast twitch variety (SERCA1) is markedly reduced in hypothyroidism with impairment of calcium reuptake as a consequence. This occurs at a transcriptional level, since thyroid hormone response elements have been identified in the 5′ flanking region of the SERCA1 Ca2+- ATPase gene. The reduction in Ca2+- ATPase would explain the delayed relaxation of the deep tendon reflexes. On histopathological examination the muscles appear pale and swollen. The muscle fibres may show swelling, loss of normal striation, and mucinous deposits.

Skeletal System: Calcium and Phosphorus Metabolism

In the adult skeleton, thyroid hormone deficiency decreases recruitment, maturation, and activity of bone cells, leading to decreased re modelling, which is especially reflected in the impaired function of the osteoclasts. Bone mass may be normal or slightly increased; however hypothyroid patients show a two- to threefold increased risk fracture. In some patients, fracture may occur before bone mass reaches levels compatible with osteoporosis, reflecting an impairment of bone quality. Recent data suggest that high TSH levels may be linked to the risk of osteoporotic fractures only in young and middle- aged men, while in postmenopausal women, the long term risk of hip and other osteoporotic fractures is strongly related to the cumulative duration of LT4 overtreatment.

Urinary excretion of calcium is decreased as is the glomerular filtration rate, whereas faecal excretion of calcium and both urinary and faecal excretion of phosphorus are variable. The concentrations of calcium and phosphorus in serum are usually normal, but calcium may be slightly elevated. Serum alkaline phosphatase levels are often decreased, as are serum osteocalcin levels. Because the levels of parathyroid hormone are often slightly increased, some degree of resistance to its action may be present. Serum concentrations of 1,25- dihydroxycholecalciferol are also increased.

Joints

At the clinical level, patients with hypothyroidism often complain of articular and muscular pain and stiffness of the extremities. These symptoms may suggest rheumatoid arthritis or also polymyalgia rheumatica or primary myositis. Patients may exhibit joint effusions involving the knees and small joints of the hands and feet. In 5– 10% of patients with carpal tunnel syndrome, primary hypothyroidism may be the cause due to the accumulation of the hygroscopic glycosaminoglycan in the interstitial space with compression of the median nerve.

Changes in Kidney Function

Clinically significant disturbances of kidney function, and hence of water and electrolyte metabolism, are uncommon in hypothyroidism. Renal blood flow and glomerular filtration rate can be reduced. Because of the moderate extent of these reductions and the hypothyroidism- induced decreased metabolism, renal failure does not usually occur. Factors contributing to the decrease in renal blood flow are a decrease in cardiac output, a decrease in plasma volume, and a narrowing of renal blood vessels through enlargement of endothelial and mesangial cells and thickening of the glomerular basement membrane.

Laboratory examinations may reveal a slight increase of serum creatinine and uric acid. Urine flow is reduced, and delay in the excretion of a water load may result in reversal of the normal diurnal pattern of urine excretion. The delay in water excretion ap pears to be due to decreased volume delivery to the distal diluting segment of the nephron resulting from diminished renal perfusion and inappropriate secretion of vasopressin. Since urinary hydroxycorticoid excretion is decreased, the adrenals might be re sponsible for delayed water excretion. Other evidence suggests that the tissue supply of adrenal cortical hormones is usually normal in myxoedema. The ability to concentrate urine may be slightlyim paired. Occasionally, minimal proteinuria is seen. This condition could be due to congestive heart failure or to the increased capillary transudation of protein typical of hypothyroidism.

The total body sodium content is increased. The excessive sodium is presumably bound to extracellular mucopolysaccharides. In spite of reduced renal blood flow and blood volume, the sodium retention is probably not a reflection of altered renal function. In fact, salt loads are usually excreted readily and serum sodium concentrations tend to be low, in contrast to other clinical situations as sociated with sodium retention, such as congestive heart failure. No consistent changes in plasma potassium levels have been reported. Total magnesium levels may be elevated and the bound fraction and urinary excretion are reduced. Plasma homocysteine concentrations are increased in hypothyroidism, related to lower folate levels and a lower creatinine clearance in thyroid hormone deficiency.

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Organ System Manifestations of Hypothyroidism: Cerebral and neurological Changes

Organ System Manifestations of Hypothyroidism: Respiratory Changes

Organ System Manifestations of Hypothyroidism: Cardiovascular Changes

Organ System Manifestations of Hypothyroidism : Cutaneous Manifestations and Changes in the Connective Tissues

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