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Re: Системный прогрессирующий остеопороз
Денис Елкин 11 Июнь 2003, 02:13
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Такими проблемами в Москве серьезно занимаются проф. Родионова Светлана Семеновна и Колондаев Александр Федорович. Работают в отделении костной патологии ЦИТО. Если узнаю, как можно связаться по E-mail, сообщу. Попытайтесь пока созвониться (тел. отделения 450-3729).
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Re: Системный прогрессирующий остеопороз
Отправитель: Александр Е. Клоков 14 Июнь 2003, 21:05
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Спасибо за внимание!
Сообщу пациенту. Изначально у него и родителей нет желания куда-либо ещё ехать на обследование: хлопотно (он лежачий больной) и денежно. Но теперь вроде как и не против.
Спасибо ещё раз.
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некроз головки правой тазобедренной кости
Отправитель: Елена 20 Март 2010, 18:40
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Могу я приехать на консультацию к доктору Родионовой Светлане Семеновне
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Re: Системный прогрессирующий остеопороз
А.В.Владзимирский 13 Июнь 2003, 11:50
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1) Морфофункциональное исследование щитовидной и паращитовидных желез, определение уровня кальция и щелочной фосфатазы в крови.
2) Лечение патологических переломов консервативным путем (закрытая репозиция, фиксация ортезами, ранняя нагрузка).
3) Препарат выбора v ?Миакальцик? для назального введения.
4) Эмпирическая терапия бифосфонатами (?IV Pamidronate?).
5) Prognosis pessima.
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Re: Системный прогрессирующий остеопороз
Отправитель: Александр Е. Клоков 14 Июнь 2003, 03:11
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> 1) Морфофункциональное исследование щитовидной и паращитовидных желез,
> определение уровня кальция и щелочной фосфатазы в крови.
Про УЗИ я уже написал, но напомню:
Очень давно, в 15-летнем возрасте (сейчас 23 года) делали УЗИ: Неоднородно уплотнена без очаговых изменений. Правая доля 17-13-42 мм, левая 14-9-41 мм, перешеек - 4 мм.
Более пациент УЗИ не делал, в том числе и любое другое физикальное исследование щитовидной железы.
Кальций сыворотки крови от 2,2 до 2,69 ммоль\л, фосфор - от 0,3 до 1,2 ммоль\л, щелочная фосфотаза от 1,46 до 5,12 ммоль\л. Последнее исследование в марте 2002 года. На днях будут свежие анализы.
> 2) Лечение патологических переломов консервативным путем (закрытая
> репозиция, фиксация ортезами, ранняя нагрузка).
Так и выполнялось. Спицы стоят вот уже почти год, консолидации нет.
> 3) Препарат выбора - "Миакальцик" для назального введения.
> 4) Эмпирическая терапия бифосфонатами ("IV Pamidronate").
А ничего более согласуемого с зарплатой бюджетных работников нет?
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Re: Системный прогрессирующий остеопороз
Отправитель: Alexander Chelnokov 14 Июнь 2003, 03:13
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А чего собственно консервативным? Это к остеопорозу от бездействия приведет еще больше. Уж если взялись лечить диафизарный перелом, то лучше бы его было хорошо сопоставить и фиксировать, идеально закрыто стержнем. Можно и
аппаратом, используя спицы с упорами, проводимые на разных уровнях. А на примере предплечья здесь - и вроде что-то делали, а в то же время и
сопоставления хорошего нет, и фиксация нестабильная, и из-за пучков спиц этих функция мышц нарушена... То бишь все условия для форомирования ложного сустава.
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Re: Системный прогрессирующий остеопороз
Abdelsalam Eid 14 Июнь 2003, 02:31
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You need to eliminate causes such as corticosteroid therapy, alcoholism, and then you should perform some investigations. Serum Ca , phosphate, Kidney function, serum PTH, sex hormone levels, urinary 24 hour excretion of Ca and phosphate. Then this may shed a light on the pathology and enable plans for treatment to be drawn.
Abdelsalam Eid, MCh(Ortho)(Zagazig), AFSA(Ortho)(Paris V)
Assistant Lecturer
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Re: Системный прогрессирующий остеопороз
Евгений Афанасьев 14 Июнь 2003, 02:48
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Диагноз не совсем ясен. Для уточнения необходимо
1. Одновременно взятые б\х крови (Са, фосфаты, калий, общ. белок, ЩФ, в-липопротеиды) и б\х мочи (Са, Na, К, Р, pH)
2. Согласен с коллегой, желательно узнать уровень кальцитонина, паратгормона в крови, если будет операция - обязательно резекция фрагмента для цитохимического исследования.
3. Есть ли у пациента боли? Важен подробный анамнез заболевания.
Попробую помочь.
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Re: Системный прогрессирующий остеопороз
Отправитель: Александр Е. Клоков 14 Июнь 2003, 21:02
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Спасибо за внимание!
1. Кальций сыворотки крови от 2,2 до 2,69 ммоль\л, фосфор - от 0,3 до 1,2
ммоль\л, щелочная фосфотаза от 1,46 до 5,12 ммоль\л. Последнее исследование
в марте 2002 года. На днях будут свежие анализы.
Сообщу при получении.
2. По поводу содержания гормонов, надеюсь скоро узнать, сообщу также. В плане оперативного лечения и гистологии - тут будет всё зависеть от желания пациента.
3. До 12 лет жалоб не предъявлял, занимался спортом (хоккей). Rg-обследования скелета не проводилось. Первый перелом в 10 летнем возрасте - перелом основной фаланги 1-го пальца правой кисти, консолидация в обычные сроки, однако на Rg отмечена "сетчетость" структуры диафизов, - остеопороз в лёгкой степени. Следующий перелом в 11 летнем возрасте 2-я пястная правой кисти, консолидация в обычные сроки, также отмечена остеопорозность тканей. С 12 летнего возраста стал отмечать умеренную боль и усталость в левой подколенной области. В дальнейшем, присоединилась быстрая утомляемость. Выраженного болевого синдрома не отмечал, затруднения в передвижениях и самообслуживании связывает с усталостью во всех конечностях и быстро наступающей общей утомляемостью. Деформация позвоночника по типу кифосколиоза и деформация крупных суставов отмечается с 15-16 летнего возраста. С 18 летнего возраста самостоятельно практически не передвигается. Патологические, несростающиеся переломы получены в 21 и 22 летнем возрасте. Сейчас пациенту 23 года.
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Re: Системный прогрессирующий остеопороз
Anatoly Yakushin 14 Июнь 2003, 03:08
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Извините, а щитовидную железу обследовали?
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Re: Системный прогрессирующий остеопороз
Отправитель: Александр Е. Клоков 14 Июнь 2003, 03:09
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Очень давно, в 15-летнем возрасте (сейчас 23 года) делали УЗИ: Неоднородно уплотнена без очаговых изменений. Правая доля 17-13-42 мм, левая 14-9-41 мм, перешеек - 4 мм.
Более пациент УЗИ не делал, в том числе и любое другое физикальное исследование щитовидной железы.
В 1995 году больной находился на обследовании в отделении эндокринологии РДКБ г. Москвы, диагноз: Генерализованный остеопороз, тяжёлая форма с грубыми деформациями скелета. Полиоссальная фиброзная дисплазия (?). С-м
гипофосфатемии неясного генеза(?), вторичный нервно-мышечный синдром. ВСД.
Функциональная кардиопатия.
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Re: Системный прогрессирующий остеопороз
Отправитель: Alexander Chelnokov 14 Июнь 2003, 03:30
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b> Очень давно, в 15-летнем возрасте (сейчас 23 года) делали УЗИ:
b> Неоднородно уплотнена без очаговых изменений. Правая доля 17-13-42 мм,
А функцию ее?
Вообще, по остеопорозу англоязычных материалов в сети много, вот, к примеру, статья по остеопорозу у мужчин (ювенильный - это, надо понимать, который разрешается после пубртатного периода?). Там же еще несколько обзоров на смежные темы
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PATHOGENESIS AND MANAGEMENT OF OSTEOPOROSIS IN MEN
R.M.Francis, MB ChB, FRCP,
Consultant Physician, Musculoskeletal Unit, Freeman Hospital, Newcastle upon Tyne, NE7 7DN, UK.
Summary
Although osteoporosis is widely considered to be a condition predominantly affecting women, it is now clear that osteoporotic fractures are not uncommon in men. Up to 20% of symptomatic vertebral fractures and 30% of hip fractures occur in men, causing substantial morbidity, excess mortality and health and social service expenditure. Bone density and therefore the risk of fracture at any age is determined by peak bone mass and the subsequent rate of bone loss. Peak bone mass in men is influenced by genetic factors, age at puberty and exercise and calcium intake during childhood, whereas causes of bone loss include declining sex steroid concentrations, physical inactivity, smoking, alcohol consumption and vitamin D deficiency. Over 50% of men presenting with symptomatic vertebral crush fractures have an underlying secondary cause of osteoporosis, such as hypogonadism, oral steroid therapy and alcohol abuse. Case-control studies of hip fractures
in men have shown an increased risk of fracture with disorders associated with secondary osteoporosis, such as thyroidectomy, gastric surgery and hypogonadism. There is also a greater risk of hip fracture with conditions related to an increased risk of falling, including hemiparesis, Parkinson's disease, dementia, vertigo, alcoholism and blindness. All men with osteoporosis should therefore be advised about measures to decrease bone loss and reduce the risk and impact of falls.
Secondary osteoporosis should also be identified and treated where possible, as this may reverse the osteoporotic process and increase bone density. There is as yet no well established treatment for male osteoporosis, but therapeutic options include testosterone replacement in men with hypogonadism, bisphosphonates in men with idiopathic osteoporosis and calcium and vitamin D supplementation in frail, elderly men with the condition.
Introduction
Osteoporosis is characterised by a reduction in bone density associated with skeletal fragility and an increased risk of fracture after minimal trauma. Although osteoporosis is widely considered to be a condition predominantly affecting women, it is now clear that osteoporotic fractures are not uncommon in men. Up to 20% of symptomatic vertebral fractures and 30% of hip fractures occur in men, causing substantial morbidity, excess mortality and health and social service expenditure [1].
Epidemiology of Fractures in Men
There is a bimodal distribution of fracture incidence with age, with peaks in youth and old age. Fractures in young people generally follow significant trauma and are more common in men than women. Fracture incidence rises rapidly in women above the age of 45 years, whereas the increase occurs at a later age in men, such that the fracture rate in elderly women is twice that of men of the same age. The most common osteoporotic fractures are those of the forearm, vertebral body and hip.
Although the incidence of forearm fractures increases in women in middle age, there is little change with advancing age in
men [2].
The lifetime risk of symptomatic fracture for a 50 year old white man in the UK has been estimated to be 2% for the forearm, 2% for the vertebra, and 3% for the hip, whereas the corresponding figures for a 50 year old woman are 13%, 11%, and 14%, respectively [2]. The European Vertebral Osteoporosis Study shows an overall prevalence of radiological vertebral
deformity of 12% in both men and women, but the relationship between prevalence and age is less steep in men [3]. There is substantial geographical variation in the prevalence of vertebral deformity in men across Europe (8 to 20%), with the highest rates in Scandinavian countries [3]. There is also marked variation in the incidence of hip fractures in men and
women across Europe, with lower rates in Mediterranean countries [4]. This study showed a larger difference in hip fracture incidence between countries than between sexes, suggesting the importance of genetic, environmental and lifestyle factors [4].
The number of men presenting with osteoporotic fractures is rising, because of the demographic trend towards an ageing
population and a doubling of the age specific incidence of fractures over the past three decades [5-7]. The increase in
age-specific incidence has been demonstrated for fractures of the forearm, vertebral body, humerus and hip [6,7]. The
reasons for this remain uncertain, but may include the survival of more frail individuals and secular changes in smoking,
alcohol consumption, diet and physical activity [8]. Even if the age-specific incidence of fractures is no longer rising
[9], the demographic trends make a rise in the number of men presenting with osteoporotic fractures inevitable [5].
Osteoporotic fractures are associated with substantial morbidity in men and women. Men with symptomatic vertebral fractures
may complain of back pain, loss of height and kyphosis, but also have significantly less energy, poorer sleep, more
emotional problems and impaired mobility compared with age-matched control subjects [10]. There is also considerable
morbidity after hip fracture in men, with only 21% living independently in the community a year later, whereas 26% receive
home care and 53% live in an institution [11].
There is increased mortality after vertebral crush fracture of about 18% at five years, but mortality does not rise steeply
in the first year after fracture, suggesting that the excess mortality is due to coexisting conditions associated with
osteoporosis rather than the fracture itself [12]. In contrast, much of the 17% excess mortality after hip fracture occurs
in the first year, suggesting a more direct relationship to the fracture and subsequent surgery [12]. A number of studies
show a higher mortality after hip fracture in men than women, but the reason for this remains unclear [13,14]. The annual
cost of osteoporotic fractures in the UK has recently been estimated at ?942 million, of which 23% is due to fractures in
men [15].
Pathogenesis of Osteoporosis and Fractures in Men
The risk of fracture is determined by a number of factors, including bone mass, bone turnover, trabecular connectivity,
skeletal geometry and the frequency and severity of trauma applied to the skeleton. Bone mass at any age is determined by
the peak bone mass, the age at which bone loss starts and the rate at which it proceeds. By the age of 18 years, 95-99% of
the ultimate peak bone mass has been attained [16]. Although the peak bone mass is higher in men than women, bone density at
maturity is similar in both sexes [16]. The adolescent rise in bone mass occurs at a younger age in females, because of
their earlier onset of puberty [16]. Genetic factors account for up to 80% of the variance in peak bone mass in men and
women [17,18]. Men with a family history of osteoporosis have a lower than expected bone mineral density (BMD) and an
increased risk of vertebral fractures [10,19], although the major genetic factors determining bone density and fracture risk
in men remain uncertain. A recent study suggests that COL1A1 Sp1 polymorphism is associated with an increased risk of
vertebral fracture in men and women, but this appears to be partly independent of bone mineral density [20]. Other
determinants of peak bone mass in men include age at puberty, dietary calcium intake and exercise during childhood and
adolescence [21].
Bone loss starts between the ages of 35 and 50 years in men and women and continues into old age in both sexes [22], with
men losing 15-45% of trabecular bone and 5-15% of cortical bone with advancing age, whereas women lose 35-50% and 25-30%
respectively. Trabecular bone loss is less in men than women when expressed as a percentage of their higher peak bone mass,
but is accompanied by trabecular thinning, rather than the reduction in trabecular number seen in women [23]. Cortical bone
loss is also lower in men, because endocortical resorption is less and periosteal bone formation is greater than in women
[24]. Biochemical and histological studies suggest that bone formation decreases with advancing age in men, but there is
some evidence of increased bone resorption in elderly men [1].
Although heredity is an important determinant of peak bone mass in men, it has much less effect on age related bone loss
[17]. The age related decrease in circulating free testosterone, adrenal androgens, growth hormone and insulin-like growth
factor 1 (IGF1) may contribute to the observed reduction in bone formation and continuing bone loss with age in men [24]. It
is now apparent that the actions of testosterone on the male skeleton may be mediated in part by aromatization to
oestradiol, such that oestrogen deficiency may contribute to age related bone loss in men [25,26]. Case reports have
described osteoporosis in men with mutations in the oestrogen receptor or aromatase genes [27,28]. There is also a positive
correlation between bone density and serum oestradiol in healthy older men, with only a weak inverse relationship with
circulating testosterone [29]. A number of other factors have been implicated in bone loss in men including physical
inactivity, tobacco and alcohol consumption, poor dietary calcium intake, low vitamin D levels, decreased calcium absorption
and secondary hyperparathyroidism [21].
The development of osteoporosis may be accelerated by underlying secondary causes of bone loss, which are found in 33-78%
of men presenting with symptomatic vertebral crush fractures [10,23,30-33]. The major secondary causes of osteoporosis in
men with vertebral fractures are hypogonadism, oral steroid therapy and alcohol abuse.
Case-control studies from the US and UK show a significantly increased risk of symptomatic vertebral fractures in men with
smoking, alcohol consumption and underlying secondary causes of osteoporosis [10,30]. Case-control studies of hip fractures
in men have shown an increased risk of fracture with disorders associated with secondary osteoporosis, such as
thyroidectomy, gastric surgery and hypogonadism [34,35]. There is also a greater risk of hip fracture with conditions
related to an increased risk of falling, such as hemiparesis, Parkinson-s disease, dementia, vertigo, alcoholism and
blindness [34]. A prospective study from Australia showed a higher risk of hip fracture in men with low hip bone density,
quadriceps weakness, increased body sway, falls in past year, previous fractures, low body weight and short stature [36].
It has also been suggested that bone size is an important determinant of fracture risk in men [24]. A study in 38 men with
idiopathic osteoporosis and vertebral fractures showed reduced BMD and vertebral dimensions compared with aged-matched
control subjects [37]. This suggests that the achievement of a reduced bone size at the end of the growth period or failure
of periosteal increase during adulthood may contribute to the pathogenesis of vertebral fractures in older men [37].
Diagnosis of Osteoporosis in Men
Until recently the diagnosis of osteoporosis in men was based on the development of fractures after minimal trauma. The
introduction of Dual Energy X-ray Absorptiometry (DXA) bone density measurement has stimulated interest in the diagnosis of
osteoporosis before fractures occur. The World Health Organization (WHO) has defined osteoporosis as a BMD 2.5 standard
deviations or more below the mean value for young adults (T score < -2.5), but this has only been established for women
[38]. Nevertheless, there is a similar relationship between BMD and fracture risk in both sexes [39,40], suggesting that the
WHO criteria may be applicable in men and women. Furthermore, work from the US shows the prevalence of osteoporosis at the
hip, spine or forearm using the WHO criteria is 35% in women over the age of 50 years, compared with 19% in men [41]. These
figures are broadly comparable to those reported for the lifetime risk of fractures at these sites in 50 year old women
(39.7%) and men (13.1%) in the US [42].
Investigation and Management of Osteoporosis in Men
To exclude underlying causes of secondary osteoporosis, the following investigations should be considered in men with
osteoporotic fractures: full blood count, ESR, serum biochemical profile, thyroid function tests, serum testosterone, sex
hormone binding globulin, gonadotrophins, prostate specific antigen and serum and urine immunoelectrophoresis [31]. The
identification of secondary osteoporosis is important, as treatment of conditions such as hypogonadism may increase bone
density [43,44].
All men with osteoporosis should be given advice on lifestyle measures to decrease bone loss. These include eating a
balanced diet rich in calcium, stopping smoking, moderating alcohol consumption and maintaining regular physical activity
and exposure to sunlight throughout life. Where there is a history of falls, attempts should be made to identify and modify
underlying causes. There is also growing interest in the use of hip protectors, which may potentially decrease the risk of
hip fractures in frail elderly people with recurrent falls.
There is no well established treatment for idiopathic osteoporosis in men, as few clinical trials have specifically
examined the effects of treatment on bone density and fracture incidence in men. Observational studies in men with
idiopathic and secondary osteoporosis suggest that intermittent cyclical etidronate therapy increases bone density at the
lumbar by 5-10%, with smaller increases at the hip [45]. In an uncontrolled study in 42 men with vertebral fractures
followed for a median of 31 months, intermittent cyclical etidronate increased spine bone density by 3% annually, whilst hip
bone density showed a non-significant rise of 0.7% per year [46]. It would therefore appear that cyclical etidronate has
comparable effects on bone density in men and women, although the effect on fracture incidence in men remains unclear.
Nevertheless, a postmarketing surveillance study using the UK General Practice Research Database shows a significant
reduction in the risk of vertebral fractures (relative risk 0.44; 95% confidence intervals 0.20-0.97) in osteoporotic men
treated with cyclical etidronate compared with untreated osteoporotic men [47]. Controlled studies of other bisphosphonates
such as clodronate, alendronate and risedronate in men with osteoporosis are either under way or planned.
In addition to improving bone density in men with hypogonadal osteoporosis, testosterone also appears to increase spine
bone density in eugonadal men with vertebral fractures. An uncontrolled study of testosterone treatment in 21 eugonadal men
with vertebral osteoporosis showed a significant increase in spine bone density of 5% in six months, although no change in
hip bone density was seen [48]. Subsequent analysis of the biochemical markers of bone turnover showed a reduction in bone
resorption with testosterone, which may be mediated by conversion to oestradiol [48]. An earlier uncontrolled study of
testosterone treatment in 14 eugonadal men with vertebral fractures showed an increase in spine bone density of 6.1% after
three years treatment [49]. A randomised controlled crossover study in 15 men on long-term corticosteroid treatment showed
an increase in spine bone density of 5% after 12 months treatment with testosterone, whilst no change was observed during
the control period of 12 months observation [50]. A multi-centre randomised controlled trial is due to start shortly in the
UK, to assess the safety and efficacy of testosterone supplementation in eugonadal men with osteoporosis.
A randomised controlled trial in 21 men with idiopathic osteoporosis showed an increase in bone density after three months
treatment with weekly intramuscular injections of 50 mg nandrolone decanoate, but this decreased to basal levels after one
year of treatment [51]. The apparent lack of benefit with nandrolone may be related to suppression of endogenous
testosterone production and the inability to aromatize anabolic steroids such as nandrolone to oestradiol.
A controlled study from Germany shows that low dose intermittent monofluorophosphate and calcium increases bone density and
decreases the risk of vertebral fractures in men with osteoporosis [52]. Nevertheless, this treatment is not widely
available and the therapeutic window is likely to be narrow.
The role of calcium and vitamin D supplementation in the management of osteoporosis in men remains unclear. An early
controlled trial in normal men with a wide age range showed no effect of calcium and vitamin D on bone loss from the forearm
or spine [53]. In contrast, a recent study in older men and women (mean age 70 years) demonstrated that 700 IU vitamin D3
and 500 mg elemental calcium daily had a modest beneficial effect on bone density and decreased the incidence of
non-vertebral fractures [54]. Other potential treatments for osteoporosis in men include calcitonin, anabolic steroids,
parathyroid hormone and growth hormone, but there is relatively little published information on their use in men [1].
Conclusions
It is now realised that osteoporotic fractures pose an important public health problem in men and women. Further work is
required to clarify the pathogenesis of osteoporosis and fractures in men and to develop appropriate criteria for the
diagnosis of male osteoporosis. Randomised controlled trials are also needed to establish the most effective treatment for
osteoporosis in men. In the meanwhile, testosterone replacement should be considered in men with hypogonadism, whereas
bisphosphonates are probably the treatment of choice in men with idiopathic osteoporosis. Calcium and vitamin D supplements
may be useful in frail, elderly men with osteoporosis, who are likely to have vitamin D deficiency and secondary
hyperparathyroidism.
References
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Russell RG, Stevenson JC (1998) Management of male osteoporosis: Report of the UK Consensus Group. QJM 91: 71-92.
2. Cooper C (1996) Epidemiology and definition of osteoporosis. In: Compston JE (ed) Osteoporosis. New perspectives on
causes, prevention and treatment. Royal College of Physicians of London, London, p1-10.
3. O'Neill TW, Felsenberg D, Varlow J, Cooper C, Kanis JA, Silman AJ (1996) The prevalence of vertebral deformity in
european men and women: The European Vertebral Osteoporosis Study. J Bone Miner Res 11: 1010-1018.
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5. Royal College of Physicians of London (1989) Fractured neck of femur: prevention and management. Royal College of
Physicians of London, London.
6. Boyce WJ, Vessey MP (1985) Rising incidence of fracture of the proximal femur. Lancet 1: 150-151.
7. Obrant KJ, Bengner U, Johnell O, Nilsson BE, Sernbo I (1989) Increasing age-adjusted risk of fragility fractures: a sign
of increasing osteoporosis in successive generations? Calcif Tissue Int 44: 157-167.
8. Francis RM, Sutcliffe A (1990) Implications of osteoporotic fractures in the elderly. In: Drife JO and Studd JWW (eds)
HRT and osteoporosis. Springer-Verlag, Berlin, p87-93.
9. Spector TD, Cooper C, Lewis AF (1990) Trends in admissions for hip fracture in England and Wales, 1968-85. BMJ 300:
1173-1174.
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L European Calcified Tissue Society 1999
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Re: Системный прогрессирующий остеопороз
Peter Romchuk 15 Июнь 2003, 23:58
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if all causes for secondary osteoporosis, mentioned by doctor aid, are excluded,
you may also think about Osteogenesis imperfecta tarda (OI congenita with multiple fractures of extremities).
It affects both sexes and varies greatly in clinical presentation. Possible concurrent
symptoms are thin, transparent sclerae, which appear blue, and hearing loss from
otosclerosis. I have had one female patient with OI. Surprisingly, she had her bones united in normal terms, just to have shortly new fracture in some other place.
We treated her conservatively + some supplements (vit D3, Ca).
"Merck Manual" recommends pamindronate given IV.
Regards,
Peter Romchuk
orthopedic surgeon,
Central City Hospital,
Rivne, Ukraine
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Системный прогрессирующий остеопороз
