Medical Condition - Hyperparathyroidism
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Fore more details on the disease, Google search "hyperparathyroidism" and visit :
http://www.parathyroid.com/
In brief summary at the risk of oversimplification :
The parathyroids (4 of them, located around the thyroid gland) has the function of regulating the concentration of calcium in the blood. As some of you have studied, calcium is an important metabolite that participates in many vital biochemical processes everywhere in the human body, eg. nervous and muscular activity.
When calcium levels fall below normal, the parathyroids increase their secretion of the ParaThyroid Hormone (PTH), which causes calcium to leech out from bones (bones function as a store for calcium). When calcium levels are normal or above normal, the parathyroids should decrease their secretion of PTH.
In some individuals, the parathyroids, due to a variety of possible reasons (eg. tumour, hyperplasia, etc), secrete excessive amounts of PTH uncontrollably. As a result, excessive calcium is continuously leached from the bones, blood calcium level is abnormally high, and we have the following disastrous consequences and symptoms (only a few a listed below) :
Osteoporosis, weakened and brittle (more easily broken) bones, high blood pressure, headaches & migraines, nausea and vomitting, kidney stones (causing blood in urine), calcified kidneys, kidney failure, shortened life span and death.
Most individuals suffering from hyperparathyroidism (doctors estimate every 1 in 5000 people have this disease, but most) are not aware they have the disease, and live for 10-20 years (while the damage is being done) without knowing it, until they are crippled with pain from the kidney stones and kidney failure. Then, a variety of blood and urine tests will indicate their hyperparathyroid condition (there are two forms of the disease - primary hyperparathyroidism and secondary hyperparathyroidism).
Thus, hyperparathyroidism is one of the leading causes of kidney stones, kidney failure, as well as osteoporosis. The sad thing, is that for *many* people with these diseases, their doctors or hospitals may not do the right tests, and sometimes fail to identify hyperparathyroidism as the cause for their symptoms (because these same symptoms can have many different causes).
Currently, medical science has no way of healing the diseased parathyroid glands. The only option is surgery to remove the parathyroids. This is not without risks either - during the surgery the nearby vocal nerves may be damaged, leaving the person unable to speak (or only able to speak hoarsely) for the rest of his/her life. Another, perhaps worse, complication, is that all 4 of the parathyroids are either accidentally removed (usually only 1 of the 4 are problematic and responsible for the excessive secretion of PTH), or are accidentally killed during the surgery.
This (destruction or removal of healthy parathyroid glands, while accidental, is quite common during surgery) results in hypOparathyroidism, in which there is not enough (or sometimes nothing left at all!) healthy parathyroid tissue left to produce PTH, and the result is hypolcalcemia (abnormally low calcium levels in the blood), which causes a whole range of other (and equally delibitating) symptoms of its own.
Such victims have to inject themselves with PTH everyday, and take excessive amounts of calcium and vitamin D for the rest of their lives, and still suffer some of the symptoms.
The only other way, if one opts not to take the 'medical science path', is to explore alternative wholistic healing techniques, among the most helpful of course, would be the work of Aajonus Vonderplanitz. That of radical dietary change.
As you can see, neither path offers a 100% cure, and both paths present further difficulties for 100% successful execution.
I have not yet decided if I will go for the "medical science" route. Probably not, even if it means I'm gonna die of the diesease sometime. But I thought I wanted to let you guys know about this medical condition anyways, hence this post.
^_^ -
how about radioactive iodine?
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There are treatment strategies - not proven, for hyperparathyroidism depending on the type and stage of glandular enlargement.
For hyperPTH with glands that have enlarged and not become autonomous, newer drugs known as calcimimetics (mimics calcium)[trade-Sensipar] might be able to trick the gland in reducing the secretion of PTH.
When glandular activity is reduced, its size is also reduced.
Of course the gland has to be sensitive to these medications.(ie, still responsive to the feedback control of serum ionized calcium levels)
This strategy is currently being used in hyperPTH development in renal failure (kidney) patients.
I am not sure whether it is licensed for use in Singapore, but it is coming into routine use in the USA at this time.
The hard-core morbidity and mortality data is unavailable as yet but the ability to meet Kidney/Dialysis Outcomes Quality Initiative guidelines on the management of metabolic bone disease in end-stage renal failure patients (ESRD) are often not met (probably one of the hardest).
Other studies by related physicians in these area (endocrinology) will hopefully clarify the potential uses of this medication in the control of hyperPTH in other clinical situations.
Anyway was there a specific reason for starting this thread in "talk-cock" forum?
That much I know for now.
P.S. Radio-iodine is typically employed for hyperthyroid gland (thyreos for shield) which is the gland that is shield like in appearance and sits on your windpipe (trachea). The thyroid gland concentrates iodine which is used in the production of its hormone, thyroxine. In patients with over-activity of this gland, radio-active iodine may restore an euthyroid state (normal), although it should be cautioned that in many individuals, they will end up being hypothyroid later in life and require thyroid supplementation. Also, thyroxine regulates the general metabolic activity state of the body. -
Osteoporosis, weakened and brittle (more easily broken) bones, high blood pressure, headaches & migraines, nausea and vomitting, kidney stones (causing blood in urine), calcified kidneys, kidney failure, shortened life span and death.
Not certain where the threadstarter got this piece of information from but he appears to have confused osteoporosis, which is the loss in amount of normal bone particularly in women following menopause, from osteomalacia as a result of excess parathyroid hormone function.
Not sure why he/she thinks he has hyperparathyroidism either...
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You sure is osteoporosis?
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Anybody heard that this disease can lead to mental illness?
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Yes, of course...standard teaching to medical students captured in the mneumonic bones (bone pain), stones, groans (kidney stones and pain), moans (psychiatric manifestations).Originally posted by casino_king:Anybody heard that this disease can lead to mental illness? -
tml i go collect my report..
haix..
dont knw wat ill will i have.. -
Originally posted by oxford mushroom:
Your well meaning intention to share is appreciated, thanks. But in this particular aspect, the confusion is not mine, but yours.
Not certain where the threadstarter got this piece of information from but he appears to have confused osteoporosis, which is the loss in amount of normal bone particularly in women following menopause, from osteomalacia as a result of excess parathyroid hormone function.
Osteoporosis refers to a diseased condition of the bone, not exclusive to women following menopause. In osteoporosis, bone is broken down faster than it is re-formed. In osteomalacia, the two activities are balanced, but the bone that is formed does not become dense and properly mineralized. Hyperparathyroidism has various forms and degrees, and both osteoporosis and osteomalacia are possible symptoms.
But thanks for wanting to share your understanding on the entire matter, as well as for your offering helpful suggestions or therapies (eg. possible drugs for treatment). Are you a medical student or practicing doctor? Where are you currently studying or practicing? -
I am a specialist medical doctor and have experience with the diagnosis of osteoporosis, renal osteodystrophy and osteitis fibrosa cystica in primary hyperparathyroidism. Your information and understanding on osteoporosis and osteomalacia in the context of hyperparathyroidism is erroneous. There is plenty of good material on the web. You might like to read up a little before making comments:Originally posted by UltimaOnline:Your well meaning intention to share is appreciated, thanks. But in this particular aspect, the confusion is not mine, but yours.
Osteoporosis refers to a diseased condition of the bone, not exclusive to women following menopause. In osteoporosis, bone is broken down faster than it is re-formed. In osteomalacia, the two activities are balanced, but the bone that is formed does not become dense and properly mineralized. Hyperparathyroidism has various forms and degrees, and both osteoporosis and osteomalacia are possible symptoms.
But thanks for wanting to share your understanding on the entire matter, as well as for your offering helpful suggestions or therapies (eg. possible drugs for treatment). Are you a medical student or practicing doctor? Where are you currently studying or practicing?
http://www.emedicine.com/radio/topic500.htm
http://www.emedicine.com/radio/topic355.htm
http://www.emedicine.com/radio/topic503.htm -
Your point is taken. May I again say I sincerely appreciate and thank you for your willingness to share your expertise, information and suggestions on this area, Doctor.
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Sure or not? While no doubt osteoporosis is not exclusive to women, the bone is not broken down faster than it is reformed.Originally posted by UltimaOnline:Osteoporosis refers to a diseased condition of the bone, not exclusive to women following menopause. In osteoporosis, bone is broken down faster than it is re-formed. In osteomalacia, the two activities are balanced, but the bone that is formed does not become dense and properly mineralized. Hyperparathyroidism has various forms and degrees, and both osteoporosis and osteomalacia are possible symptoms.
"Osteoporosis is defined either by the presence of a fragility fracture or a bone mineral density (BMD) measurement which falls below a threshold level arbitrarily set at 2.5 S.D. below the mean peak bone mass of young adults."
http://www.moh.gov.sg/cmaweb/attachments/publication/osteo_pdf.pdf -
pst. osteoporosis IS cos bone resorption is faster than bone deposition... that's why its fragile mah...Originally posted by ndmmxiaomayi:Sure or not? While no doubt osteoporosis is not exclusive to women, the bone is not broken down faster than it is reformed.
"Osteoporosis is defined either by the presence of a fragility fracture or a bone mineral density (BMD) measurement which falls below a threshold level arbitrarily set at 2.5 S.D. below the mean peak bone mass of young adults."
http://www.moh.gov.sg/cmaweb/attachments/publication/osteo_pdf.pdf -
Humpty-Dumpty told Alice, "When I use a word, I want to mean exactly what I mean...no more and no less.." Problems do arise when people (doctors included) mean different things when they use the same word.Originally posted by starblue:pst. osteoporosis IS cos bone resorption is faster than bone deposition... that's why its fragile mah...
Osteoporosis comes from the Greek workd osteo for bone and porus for porous. Osteoporosis refers to a reduction in bone density and hence its structural stability, but the composition is normal. There is little or no biochemical disturbance of calcium and other minerals in the blood (although we do advise taking in more calcium to try to slow down the bone loss). Under the microscope, you see normal bone trabeculae but they are thinner than normal. And yes, SB, you get osteoporosis when the net balance between bone formation and bone degradation is tilted towards bone loss. That happens in menopause, in women lacking estrogen due to surgical removal of the ovaries, in people taking steroids long term and also in those who have not been using their bones eg. bed bound patients.
Osteomalacia comes from the Greek word osteo for bone and malacia for softness. It was originally applied to the bones in patients with rickets (Vitamin D deficiency) where the bone is poorly mineralised due to the lack of calcium. Under the microscope, the bone lacks the calcium that is normally deposited on top of the bone matrix. The composition of the bone is abnormal, 'becomes softer' and often children with this condition grow up bow-legged because the bones are not able to sustain the weight of the body.
Endocrine (hormonal) abnormalities affect proper bone formation. Parathyroid hormone (and its counterpart, calcitonin) are important for regulating the body calcium level. The major store of calcium in the body is in the bones. So if you need more calcium in the blood, parathyroid hormone will mobilize the calcium from the bone (at the expense of destroying some bone).
In primary hyperparathyroidism, a tumour, usually a benign tumour of the parathyroid gland (adenoma) or excessive growth of the parathyroid gland (hyperplasia) and rarely a malignant tumour (a parathyroid carcinoma) produces excessive parathyroid hormone. This excess hormone leads to excessive mobilization of calcium from the bone by activating specialized cells called osteoclasts which 'eat up' the bone and release calcium to the blood. Under the microscope, the bone is initially mineralized as for normal bone but the bony trabeculae have big holes or empty pouches in them where the osteoclasts have been eating away at them. That's why the bone disease in this condition is also called 'osteitis fibrosa cystica' (Greek kysto- a pouch). Although the mechanism is quite different from rickets, you can expect the bone to lose its structural integrity and so some people used the term osteomalacia (bone softening) to refer to it as well. But you will appreciate the disease is quite different from rickets or osteoporosis.
Sometime there can be excessive parathyroid hormone produced even when there is no tumour or excessive growth of the gland. In persons with kidney failure, the calcium level drops because the kidney cannot produce active Vitamin D. The low calcium level triggers excessive parathyroid hormone production which is what is known as secondary hyperparathyroidism. The effect of the excess parathyroid hormone on the bones is similar. However, although the bone disease is the same, in this context, the term renal osteodystrophy is often used (Greek. dys- for defective, trophe from the Greek word trephein, to nourish).
Yet a third scenario exists. If the renal failure is been around for a long time and there has been continued stimulation of parathyroid hormone production, the overly stimulated parathyroid gland can grow very big and sometimes even sprout a benign tumour. As a result, there will be hyperparathyroidism even if you treat the renal failure and correct the vitamin D deficiency. That condition is known as tertiary hyperparathyroidism.