Rickets disease. Presentation on the topic "Rachitis" Changes in the chest

Ministry of Health of the Russian Federation. Federal State Budgetary Educational Institution of Higher Education "Northern State Medical University" Department of the Ministry of Health of the Russian Federation.
FSBEI HE "Northern State Medical University"
Department of Pediatrics
Head department: professor, doctor of medical sciences Malyavskaya S. I.
Teacher: Candidate of Medical Sciences, Associate Professor Kopalin A.K.
Rickets-like diseases in children
Performed:
VI year student, 2nd group
Faculty of Pediatrics
Musinskaya L.Yu.
Arkhangelsk
2017

Pathogenesis

Classification

Main signs of RPD

Differential diagnosis of radiological signs of RPD

Vitamin D-resistant rickets

Renal tubular acidosis

De Toni-Debreu–Fanconi disease

Vitamin D-dependent rickets

Differential diagnosis of rickets-like diseases in children (according to A.V. Shilov and P.V. Novikov)

Bibliography

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-1.jpg" alt=">Presentation on the subject of pediatrics. Topic: Rickets in children Completed by student 31 Maksimenko group"> Презентация по предмету педиатрия. Тема: Рахит у детей Выполнила студентка 31 группы Максименко Екатерина!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-2.jpg" alt=">Contents Rickets is Prevalence Etiology Vitamin D Role"> Содержание Рахит – это Распространенность Этиология Витамин Д Роль питания Физиологические потребности в витамине Д Патогенез Начальный период Период разгара Период реконвалесценции Период остаточных явлений!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-3.jpg" alt="> Rickets is Rickets (Greek rhahis - spinal ridge) - children's disease"> Рахит - это Рахит (греч. rhahis – спинной хребет) – заболевание детей раннего возраста, при котором в связи с дефицитом витамина Д нарушены кальциево-фосфорный обмен, процессы костеобразования и минерализации костей, а также функция нервной системы и внутренних органов.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-4.jpg" alt=">Prevalence “Classic” rickets remains a very common disease. It affects infants during the period of rapid"> Распространенность “Классический” рахит остается весьма распространенным заболеванием. Он поражает младенцев в период быстрого роста в возрасте 2 мес – 2 года с частотой 10 -35% .!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-5.jpg" alt=">Etiology The occurrence of rickets in young children is associated with insufficient intake of"> Этиология Возникновение рахита у детей раннего возраста связано с недостаточным поступлением в организм ребенка витаминов группы Д.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-6.jpg" alt=">Vitamin D The name “vitamin D” is assigned to a group of substances represented by more than 10 structural analogues,"> Витамин Д Название “витамин Д” присвоено группе веществ, представленной более чем 10 структурными аналогами, обладающими антирахитическими свойствами различной активности. Основные из них витамины Д 2, или эргокальциферол, и витамин Д 3, или холекальциферол.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-7.jpg" alt=">Source of Vitamin D Vitamin D 2, or ergocalciferol, was obtained from purple ergot,"> Источник витамина Д Витамин Д 2, или эргокальциферол, был получен из спорыньи пурпурной, в небольших количествах содержится в растительном масле, маргарине и в ростках пшеницы. Витамин Д 3, или холекальциферол, обнаружен в жире трески, тунца, в яичном желтке. Тем не менее витамин Д поступает в организм с пищей в основном в виде предшественников. Главный из них 7 - дегидрохолестерин.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-8.jpg" alt=">The role of nutrition The importance of nutrition in obtaining vitamin D is important in case of disruption of endogenous"> Роль питания Значение питания в получении витамина Д важно в случае нарушения эндогенного синтеза активных форм витамина Д. Поэтому принципиальное значение принадлежит поступлению с едой прежде всего холекальциферола, что осуществляется через продукты животного происхождения.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-9.jpg" alt=">Physiological needs for vitamin D Everyday diet is not rich in vitamin D, which is To"> Физиологические потребности в витамине Д Повседневное питание небогато витамином Д, который относится к витаминам, мало распространенным в природе, физиологические суточные потребности в витамине Д определяются, по данным ВОЗ, следующим образом: для взрослых – 100 МЕ, для детей – 400 МЕ, для беременной или кормящей женщины – 1000 МЕ.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-10.jpg" alt=">Table 1. Clinical classification of rickets Period of the disease Severity of the process Nature of the course Initial I degree"> Таблица 1. Клиническая классификация рахита Период болезни Тяжесть процесса Характер течения Начальный I степень – легкая Острое Разгар болезни II степень – средней Подострое тяжести Реконвалесценции III степень – тяжёлая Рецидивирущее!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-11.jpg" alt=">Regulation of calcium metabolism The main physiological function of vitamin D and its metabolites is to maintain"> Регуляция обмена кальция Основной физиологической функцией витамина Д и его метаболитов является поддержание гомеостаза кальция и фосфора в организме, что необходимо для нормального созревания костной ткани, хода обменных и физиологических процессов. Дефицит поступления в организм солей кальция, фосфора, магния, меди, цинка, железа, кобальта и некоторых других микроэлементов, белка и отдельных аминокислот также сопровождается нарушениями фосфорно-кальциевого обмена и возникновением клинической картины рахита.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-12.jpg" alt="> The body's calcium supply is largely associated with the activity of the parathyroid glands, which produce two"> Обеспеченность организма кальцием во многом связана с деятельностью паращитовидных желез, вырабатывающих два гормона – паратгормон и кальцитонин, которые вместе с витамином Д обеспечивают регуляцию кальциевого обмена. Секреция паратгормона зависит от концентрации ионизированного кальция в сыворотке крови: повышение концентрации ионизированного кальция снижает секрецию, снижение – повышает. Мишени для паратгормона: почки, костная ткань, желудочно-кишечный тракт. Рецепторно- клеточная связь гормона реализуется через мембранно-связанную аденилатциклазу и характеризуется преимущественно изменением обмена кальция.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-13.jpg" alt=">The effect on bone tissue is characterized by three main effects: Ø inhibition of collagen synthesis in active"> Действие на костную ткань характеризуется тремя основными эффектами: Ø торможением синтеза коллагена в активных остеобластах; Ø активацией остеолизиса остеокластами; Ø ускорением созревания клеток- предшественников остеобластов и остеокластов.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-14.jpg" alt=">Pathogenesis The development of the disease is largely determined by the anatomical and physiological characteristics of the child’s body. In particular, intensive"> Патогенез Развитие заболевания во многом обусловлено анатомо-физиолгическими особенностями детского организма. В частности, интенсивный рост ребенка грудного возраста, требующий поступления большого количества пластического материала, лабильный и напряженный обмен веществ и особое строение костной ткани, представленное не кристаллами оксиапатита, а легкорастворимым кальций- фосфатом, в значительной мере способствуют возникновению рахита.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-15.jpg" alt=">Table 2. Hereditary and acquired nephropathies and RD Hereditary Acquired nephropathies Congenital familial Glomerulonephritis"> Таблица 2. Наследственные и приобретенные нефропатии и РЗ Наследственные Приобретённые нефропатии Врожденный семейный Гломерулонефрит с Гипофосфатемический рахит нефротическим синдромом или фосфат-диабет Хроническая почечная Аутосомно-доминантный недостаточность Аутосомно-рецессивный Дисметаболическая Сцепленный с Х-хромосомой нефропатия с кристаллурией Тубулопатии Тип 1 – дистальный, синдром Баттлера – Олбрайта Тип 2 – проксимальный Болезнь де Тони – Дебре – Фанкони Наследственный нефрит!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-16.jpg" alt=">Table 3. Malabsorption syndrome, liver disease and RD Malabsorption syndrome Diseases liver celiac disease atresia"> Таблица 3. Синдром мальабсорбции, болезни печени и РЗ Синдром мальабсорбции Болезни печени Целиакия Атрезия и аномалии развития Муковисцидоз желчных путей Экссудативная энтеропатия Гепатиты и циррозы печени Энтерит, энтероколит Болезни накопления Резекция участка желудка (гликогенозы, болезнь или тонкой кишки Вильсона – Коновалова) Лекарственные поражения!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-17.jpg" alt=">Predisposing factors Numerous perinatal factors (diseases of the mother during time"> Предрасполагающие факторы Предрасполагают к возникновению рахита многочисленные перинатальные факторы (заболевания матери во время беременности, гестоз, неблагоприятное течение родов и др.). Благодаря тому что интенсивное поступление кальция и фосфора от матери к плоду происходит в последние месяцы беременности, ребенок менее 30 нед гестации уже при рождении имеет часто остеопению – более низкое содержание минеральных веществ в кости. Этому же способствуют нерациональные питание и режим жизни беременной.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-18.jpg" alt="> Immaturity of enzyme systems of the liver, kidneys, skin, as well as their diseases , provoke development"> Незрелость ферментных систем печени, почек, кожи, как и их заболевания, провоцируют развитие рахита у детей. Особенно часто рахит возникает у недоношенных детей. Для нормального процесса окостенения важно достаточное содержание в пище белка, кальция и фосфора при правильном их соотношении, микроэлементов магния и цинка, витаминов группы В и А. К рахиту приводит недостаточная двигательная активность ребенка, так как кровоснабжение кости и электростатическая напряженность существенно повышаются при мышечной деятельности.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-19.jpg" alt=">Initial period In the initial period in children of the first year of life, changes are noted with"> Начальный период В начальном периоде у детей первого года жизни изменения отмечаются со стороны нервной и мышечной систем. Ребенок становится раздражительным, часто беспокойным, вздрагивает при громких звуках, появлении яркого света, тревожно спит. У него появляются потливость, особенно головы, облысение затылка. Через 2 -3 нед от начала заболевания обнаруживается мягкость костных краев в области большого родничка, по ходу стреловидного и ламбдовидного швов. Тонус мышц снижается. Содержание кальция в крови остается нормальным, уровень фосфора несколько снижается. При исследовании мочи обнаруживается фосфатурия.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-20.jpg" alt=">The height of the disease During the height of the disease, symptoms from the nervous and muscular"> Период разгара В период разгара болезни прогрессируют симптомы со стороны нервной и мышечной систем. Усиливаются потливость, слабость, гипотония мышц и связочного аппарата, заметным становится отставание в психомоторном развитии. Этому периоду особенно свойственно быстрое прогрессирование костных изменений: размягчение плоских костей черепа, появление краниотабеса, уплощение затылка, асимметричная форма головы. Разрастание остеоидной ткани в точках окостенения плоских костей черепа ведет к образованию лобных и затылочных бугров. Из-за этого голова приобретает квадратную или ягодицеподобную форму. Могут возникнуть деформации лицевой части черепа – седловидный нос, “олимпийский” лоб, нарушения прикуса и пр.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-21.jpg" alt=">Period of convalescence During this period, the child has no signs of active rickets, gradually"> Период реконвалесценции В этот период у ребенка не определяются признаки активного рахита, постепенно исчезают вегетативные и неврологические симптомы, улучшается общее самочувствие, нормализуется концентрация кальция и фосфора в крови, хотя уровень кальция может быть и сниженным из-за интенсивного его отложения в костях. Средние сроки – от 6 мес до 2 лет жизни.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-22.jpg" alt=">Period of residual effects Signs of the clinical picture of rickets weaken as slows down"> Период остаточных явлений Признаки клинической картины рахита ослабевают по мере того, как замедляется рост ребенка. При выздоровлении в возрасте 2 -3 лет остаточные явления, приводящие к выраженным деформациям, продолжают оставаться в позвоночнике и костях конечностей. При рентгенологическом обследовании заметно появление и увеличение объема костных точек роста, утолщение с классическим признаком “черного контура” и очертаний кости, утолщение коркового слоя кости (надкостница, формирующая контурную линию кости) и видимость двойного контура, представляющего собой старую кость, окруженную чехлом новой кости.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-23.jpg" alt=">Severity The diagnosis of mild rickets (I) is made based on the presence changes characteristic"> Тяжесть течения Диагноз рахита легкой степени (I) ставят на основании наличия изменений, характерных для начального периода рахита. Средней тяжести рахит (II степень) характеризуется умеренно выраженными изменениями костной системы и внутренних органов. Тяжелый рахит (III степень) диагностируется при обнаружении у ребенка выраженных деформаций костей, тяжелых поражений нервной системы и внутренних органов, анемии, приведших к отставанию в физическом и нервно-моторном развитии. Могут появиться такие осложнения, как вторичные инфекции или тетания, судороги, сердечная недостаточность, ларингоспазм (спазм голосовых связок), гипокальциемия (недостаток кальция) и даже внезапная смерть.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-24.jpg" alt="> Acute rickets The acute course of rickets is marked by signs of osteomalacia of the skeletal system, expressed by neurological"> Острый рахит Острое течение рахита знаменуется признаками остеомаляции костной системы, выраженными неврологическими симптомами.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-25.jpg" alt=">Subacute rickets The subacute course is characterized by severe symptoms of osteoid hyperplasia, the simultaneous presence of child lesions"> Подострый рахит Подострое течение характеризуется выраженными симптомами остеоидной гиперплазии, одновременным наличием у ребенка поражений костей в разные периоды первого года жизни, так как при рахите череп поражается в первые 3 мес жизни, деформации грудной клетки возникают, как правило, в 3 -6 мес, а деформации нижних конечностей – во втором полугодии жизни.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-26.jpg" alt=">Recurrent rickets Recurrent, or wave-like, course of rickets is established, if any clinical, laboratory and"> Рецидивирующий рахит Рецидивирующее, или волнообразное, течение рахита устанавливают, если имеются клинические, лабораторные и рентгенологические признаки активного рахита, выявленные у ребенка с клиническими и рентгенологическими указаниями на закончившийся в прошлом активный рахит (наличие полосок обызвествления).!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-27.jpg" alt=">Bone signs The leading clinical signs of rickets are bone changes. Head: craniotabes"> Костные признаки Ведущими клиническими признаками рахита являются костные изменения. Голова: краниотабес определяется в затылочной или теменной области, где череп размягчается настолько, что поддается сдавливанию. Ряд авторов рассматривают данный симптом как физиологическое явление до 4 мес; продолжительность времени, в течение которого роднички и швы между костями черепа зарастают, также должна инерпретироваться как состояние с большими индивидуальными отклонениями; запаздание появления зубов.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-28.jpg" alt="> Chest: rachitic “rosary” as a result of hypertrophy of the cartilage between the ribs And"> Грудная клетка: рахитические “четки” как результат гипертрофии хряща между ребрами и грудиной в форме утолщений по обе стороны грудины; деформация грудной клетки. Позвоночник: изменения в костях позвоночника реализуются в отсутствие физиологических изгибов и появлении патологических искривлений по типу кифозов, лордозов и сколиозов.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-29.jpg" alt="> Extremities: classic epiphyseal swelling, epiphyseal thickening due to proliferation, poor calcified bone"> Конечности: классическая эпифизарная припухлость, утолщение эпифиза из-за пролиферации плохо кальцифицированного костного матрикса, что особенно заметно на лодыжках и запястьях; деформация развития тазобедренных суставов и костей нижних конечностей, появляющаяся в конце первого и в начале второго года жизни (0 -, К- и Х-образные ноги, плоский рахитический таз)!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-30.jpg" alt=">Nonspecific treatment methods Nonspecific therapy includes organizing proper sanitary and hygienic mode"> Неспецифические методы лечения Неспецифическая терапия включает в себя организацию правильного санитарно- гигиенического режима с достаточным пребыванием ребенка на свежем воздухе, прогулками в любой сезон года, полноценным сном при условии охраны ребенка от излишних внешних раздражителей (шума, света). В период бодрствования следует стимулировать психическую и двигательную активность ребенка.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-31.jpg" alt=">Prevention Vitamin D deficiency is eliminated by systematically taking it in the form of a drug, beginning"> Профилактика Недостаточность витамина Д ликвидируется систематическим приемом его в виде лекарственного препарата, начиная с первых недель жизни до 1, 5 -4 лет. Детям с 3 -месячного возраста надо давать ударные дозы величиной 200 000 ME, т. е. 5 мг витамина Д 3 каждые 5 -6 мес. Риск гипервитаминоза при этом, за исключением случаев повышенной чувствительности к витамину Д, исключительно мал. С другой стороны, профилактику рахита начинают еще до рождения ребенка. При патронаже беременных женщин обращают внимание будущей матери на необходимость соблюдения правильного режима дня с чередованием труда и отдыха, исключения физических перегрузок, достаточного пребывания на свежем воздухе, рационального питания.!}

Src="https://present5.com/presentation/3/73752168_33949279.pdf-img/73752168_33949279.pdf-32.jpg" alt="> Pregnant women should eat enough vitamins, micro- and macroelements,"> Беременные женщины должны употреблять в пищу достаточное количество витаминов, микро- и макроэлементы, продукты, содержащие полноценные белки, ненасыщенные жирные кислоты. Обязательным является соблюдение правил личной гигиены, полезны занятия лечебной физкультурой. Во время беременности происходит адаптация фосфорно-кальциевого метаболизма матери к потребностям плода. Общий уровень кальция у беременной женщины уменьшается примерно на 8% по сравнению с содержанием кальция до момента беременности.!}

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Disorders of calcium metabolism are called calcinosis. Two forms of calcinosis: systemic and limited. Three forms of calcification: metastatic, dystrophic and metabolic. Rickets. Alcoholic hepatitis. Tuberculosis. Generalized hematogenous tuberculosis.

At 1 year of life, the following occurs: intensive remodeling of the bone structure intensive remodeling of the bone structure tension of mineral metabolism tension of mineral metabolism bone tissue is very sensitive to adverse effects. bone tissue is very sensitive to adverse effects. The first three years of life are the most critical for bone mass formation.

Reasons contributing to the development of rickets: malnutrition malnutrition hypokinesia hypokinesia prematurity prematurity insufficiency of natural insolation insufficiency of natural insolation climatic conditions climatic conditions environmental features of the region environmental features of the region

Not only the lack of nutrients plays a role in the development of the disease, but also their excess. For example, an excess of P in food (feeding with cow's milk, flour, and cereal products) inhibits the absorption of Ca in the small intestine and the synthesis of the active form of vitamin D in the kidneys. Not only the lack of nutrients plays a role in the development of the disease, but also their excess. For example, an excess of P in food (feeding with cow's milk, flour, and cereal products) inhibits the absorption of Ca in the small intestine and the synthesis of the active form of vitamin D in the kidneys.

Excess Fe in food, stearic and palmitic acids reduce the absorption of calcium in the intestine. The deposition of Ca and P in the fetus occurs most intensively from the 32nd week of pregnancy. The shorter the child's gestational age at birth, the more susceptible he is to rickets. Acute and chronic diseases influence the development of rickets.

Vitamin D absorption occurs in the small intestine with a sufficient amount of bile. Intestinal diseases (malabsorption, etc.) and impaired bile secretion impair absorption, contributing to the development of the disease. Vitamin D enters the bloodstream into the liver, where, under the action of the liver enzyme 25 hydroxylase, the first active metabolite is formed - 25 hydroxy cholecalciferol (calcidiol).

Calcidiol has no effect on bone metabolism. Liver diseases lead to disruption of its formation. Calcidiol is then transported to the kidneys using vitamin D binding protein, where active metabolites are formed in the renal tubules with the participation of renal enzymes.

The 1st metabolite - 24.25 dihydroxy cholecalciferol - ensures the fixation of Ca and P in bone tissue (skeletal mineralization) and suppresses the secretion of PTH. 2nd metabolite - calcitriol - hormonally active substance - affects phosphorus-calcium metabolism - acts on target organs (intestines, kidneys, bones)

Violations of vitamin D metabolism can occur at any level. Insufficient intake of vitamin D from food and insufficient formation of it in the skin contribute to the development of “classic” vitamin D deficiency rickets. Violations of vitamin D metabolism (pathology of the kidneys, intestines, liver, genetic defects) lead to secondary, endogenous rickets and its hereditary variants.

The pathogenesis of rickets is considered from the characteristics of those processes in which vitamin D is involved. Vitamin D regulates phosphorus-calcium metabolism. How? 1. Stimulates the absorption of Ca and P in the intestine 2. Being an antagonist of parathyroid hormones that regulate the reabsorption of P in the renal tubules, regulates the level of P in the body

3. Has a direct effect on the mineral metabolism of bone tissue (deposition and resorption) 4. In conjunction with parathyroid hormone and thyrocalcitonin, plays a role in the homeostasis of Ca and P in body fluids and tissues 5. Participates in the Krebs cycle, i.e. into the transformation of pyruvic acid into oxaloacetic acid, and then into citric acid 6. Promotes the elimination of inorganic P from inorganic compounds.

Parathyroid hormone, by reducing the reabsorption of Ca in the renal tubules, promotes its excretion from the body, causing hypophosphatemia and hyperphosphaturia. Alkaline phosphatase increases, which leads to an increase in the activity of osteoblasts and the circle closes (the norm according to Kay is 0.17 - 0.35 units. Alkaline phosphatase can remain within the normal range if there is a deficiency of protein or zinc in the diet. Decreased absorption of Ca: excess filates excess filates high level of stearic acid and palmitic acids high levels of stearic and palmitic acids Phosphorus absorption decreases with excess iron in the diet.

Changes in the skeletal system during rickets. Head: craniotabes (softening of areas of the parietal bones, less often areas of the occipital bone), deformation of the skull bones, increase in the frontal and parietal tubercles, deformation of the skull bones, increase in the frontal and parietal tubercles, violation of the relationship between the upper and lower jaws, violation of the relationship between the upper and lower jaws, later closure of the large fontanel, late closure of the large fontanel, impaired teething (untimely, incorrect), defects in tooth enamel, tendency to caries. violation of teething (untimely, incorrect), defects in tooth enamel, tendency to caries.

Chest: deformation of the clavicle (increased curvature), deformation of the clavicle (increased curvature), “costal beads” (hemispherical thickening at the junction of the cartilaginous part of the rib with the bone), “rib beads” (hemispherical thickening at the junction of the cartilaginous part of the rib with the bone) , expansion of the lower and narrowing of the upper operations, expansion of the lower and narrowing of the upper operations, compression of the chest from the sides, compression of the chest from the sides, scaphoid depressions on the lateral surfaces of the chest, scaphoid depressions on the lateral surfaces of the chest, deformation of the sternum (chicken "chest, cobbler's chest), sternum deformation (chicken breast, cobbler's chest), Harrison's groove Harrison's groove

Upper limbs: curvature of the humerus, curvature of the humerus, curvature of the bones of the forearms, curvature of the bones of the forearms, deformation in the joint area: “bracelets” (thickening in the area of ​​the wrist joints), “strings of pearls” (thickening in the area of ​​the diaphysis of the phalanges of the fingers) deformation in the joint area: “bracelets” (thickening in the area of ​​the wrist joints), “strings of pearls” (thickening in the area of ​​the diaphysis of the phalanges of the fingers)

Spine: kyphosis in the lower thoracic vertebrae, kyphosis in the lower thoracic vertebrae, kyphosis or lordosis in the lumbar region, kyphosis or lordosis in the lumbar region, scoliosis in the thoracic region. scoliosis in the thoracic region. Pelvic bones: flat pelvis, narrowing of the entrance to the small pelvis.

Lower extremities: curvature of the hips forward and outward, curvature of the hips forward and outward, various curvatures of the lower extremities (O- or X-shaped deformities), various curvatures of the lower extremities (O- or X-shaped deformities), deformities in the joint area, deformations in the area joints

"Exogenous" rickets is rarely severe. This clinical symptomatology is more typical for rickets-like diseases (secondary rickets, hereditary rickets).

The initial period is not recognized by all pediatricians, and at present the St. Petersburg school considers it inappropriate to include this period of the disease in the classification of rickets. The initial period is not recognized by all pediatricians, and at present the St. Petersburg school considers it inappropriate to include this period of the disease in the classification of rickets.

The period at the height of rickets is characterized, in addition to bone deformations corresponding to varying degrees of rickets, severe muscle hypotonia (frog stomach, loose ligaments and joints, the “penknife” symptom, the “muffler” symptom). The period at the height of rickets is characterized, in addition to bone deformations corresponding to varying degrees of rickets, severe muscle hypotonia (frog stomach, loose ligaments and joints, the “penknife” symptom, the “muffler” symptom).

Due to muscle hypotonia, late development of static and motor functions is noted. Children begin to sit, stand, and walk later. Muscular hypotonia in combination with chest deformities contributes to impaired pulmonary ventilation and increased respiratory morbidity. Due to muscle hypotonia, late development of static and motor functions is noted. Children begin to sit, stand, and walk later. Muscular hypotonia in combination with chest deformities contributes to impaired pulmonary ventilation and increased respiratory morbidity.

During the height of the disease, the child may experience pain in the bones, which intensifies with movement and palpation. Passive movements in the limbs cause negative emotions in the child. During the height of the disease, the child may experience pain in the bones, which intensifies with movement and palpation. Passive movements in the limbs cause negative emotions in the child.

During the period of convalescence, muscle hypotension decreases, which is accompanied by the acquisition of new motor skills, and autonomic disorders disappear. Bone changes have clinically clear positive dynamics only in the acute course of rickets (craniotabes, bone compliance along the cranial sutures disappears). During the period of convalescence, muscle hypotension decreases, which is accompanied by the acquisition of new motor skills, and autonomic disorders disappear. Bone changes have clinically clear positive dynamics only in the acute course of rickets (craniotabes, bone compliance along the cranial sutures disappears).

The period of residual effects of rickets is diagnosed in children who have persistent significant deformations of the skeletal system, which requires further observation and treatment not only from a pediatrician, but also from an orthopedist. The period of residual effects of rickets is diagnosed in children who have persistent significant deformations of the skeletal system, which requires further observation and treatment not only from a pediatrician, but also from an orthopedist.

In some children, there may be a change in the axis of the lower extremities and “rachitic flatfoot.” Deformations of flat bones decrease, but remain. In children who have suffered from rickets, an enlargement of the parietal and frontal tubercles, flattening of the occiput, malocclusion, deformation of the chest and pelvic bones remain. In some children, there may be a change in the axis of the lower extremities and “rachitic flatfoot.” Deformations of flat bones decrease, but remain. In children who have suffered from rickets, an enlargement of the parietal and frontal tubercles, flattening of the occiput, malocclusion, deformation of the chest and pelvic bones remain.

Acute rickets occurs in children in the first half of life, more often in premature babies, in children from multiple pregnancies who do not receive prophylactic doses of vitamin D. Acute rickets occurs in children in the first half of life, more often in premature babies, in children from multiple pregnancies, not receiving preventive doses of vitamin D.

The subacute course of rickets is characterized by a predominance of osteoid tissue hyperplasia in bone growth zones (excessive formation of fibrous tissue instead of normal calcified tissue). The subacute course of rickets is characterized by a predominance of osteoid tissue hyperplasia in bone growth zones (excessive formation of fibrous tissue , instead of normal calcified),

The recurrent course of rickets is a repeated exacerbation of an already subsided rickets process. An X-ray examination of this type of progression reveals stripes of calcification in the metaphyseal zones of the tubular bones. This course of the disease is more typical for secondary or hereditary forms of rickets. The recurrent course of rickets is a repeated exacerbation of an already subsided rickets process. An X-ray examination of this type of progression reveals stripes of calcification in the metaphyseal zones of the tubular bones. This course of the disease is more typical for secondary or hereditary forms of rickets.

In recent years, calcium-deficiency rickets has begun to be identified, which occurs as a result of insufficient calcium intake into the child’s body. This applies primarily to breastfed children whose mothers do not consume or consume little dairy products. In recent years, calcium-deficiency rickets has begun to be identified, which occurs as a result of insufficient calcium intake into the child’s body. This applies primarily to breastfed children whose mothers do not consume or consume little dairy products.

Calcium-deficiency rickets can occur at any age, but more often in children in the first months of life who are breastfed Calcium-deficiency rickets can occur at any age, but more often in children in the first months of life who are breastfed

In the diagnosis of this variant of rickets, medical history (maternal nutrition) and laboratory tests are helpful, in which there is a decrease in Ca content in the urine, normal concentrations of P and Ca in the blood serum, and an increase in the activity of the enzyme alkaline phosphatase (ALP). In the diagnosis of this variant of rickets, medical history (maternal nutrition) and laboratory tests are helpful, in which there is a decrease in Ca content in the urine, normal concentrations of P and Ca in the blood serum, and an increase in the activity of the enzyme alkaline phosphatase (ALP).

The biochemical variants of rickets include: hypocalcemic (calcipenic), hypophosphatemic (phosphopenic) and a variant with the absence of pronounced deviations from the norm in calcium and phosphorus levels in the blood. The biochemical variants of rickets include: hypocalcemic (calcipenic), hypophosphatemic (phosphopenic) and a variant with the absence of pronounced deviations from the norm in calcium and phosphorus levels in the blood.

Differential diagnostic signs of vitamin D-deficient rickets rickets-like diseases Signs of vitamin D-deficient rickets Phosphate diabetes Renal tubular acidosis De-Toni-Debreu-Fanconi disease Type of inheritance Not traced Dominant, linked to the X chromosome Sporadic cases, possible autosomal recessive or autosomal - dominant autosomal recessive, dominant is possible Time of manifestation 1.5-3 months 1 year 3 months; 1 year 6 months 5-6 months; 2-3 years 2 years 6 months 3 years First clinical manifestations Changes in the nervous system, irritability, tearfulness, sleep disturbance, sweating, decreased appetite, muscle hypotonia Severe deformation of the lower extremities, rachitic “bracelets”, muscular hypotonia of the lower extremities Polyuria , polydipsia, irritability, tearfulness, sharp muscle pain, muscle hypotension Unreasonable increases in temperature, Polyuria, polydipsia.

Specific signs Bone changes: craniotabes, frontal tuberosities, rachitic rosaries, “bracelets”, 0- and X-shaped deformities of the legs Progressive varus deformity of the legs Polyuria, polydipsia, muscle hypotonia to atony, adynamia. Enlarged liver. Constipation. Valgus deformity of the legs. Periodic fever, progressive multiple bone deformities. Increased liver size. Blood pressure is reduced. Tendency to constipation Signs Vitamin D-deficient rickets Phosphate-diabetes Renal tubular acidosis De-Toni-Debreu-Fanconi disease Physical development No features Growth deficiency with unchanged weight Combination of short stature and sharply reduced nutrition

Biochemical blood parameters Calcium Reduced Normal More often normal Phosphorus Reduced Significantly reduced Reduced Significantly reduced Potassium Normal Reduced Sodium Normal Reduced Acid-base status Normal or compensated metabolic acidosis Metabolic acidosis Severe compensated metabolic acidosis Severe metabolic acidosis Signs Vitamin D-deficient rickets Phosphate- diabetes Renal tubular acidosis De-Toni-Debreu-Fanconi disease

Changes in urine Aminoaciduria PresentNormal Severe Phosphaturia PresentSignificant ModerateSignificant Calciuria ReducedNormal Significant Reduced X-ray of the skeletal bones Absence of a line of preparatory calcification, torch symptom, goblet-shaped dilatation of the metaphyses. Osteoporosis Severe goblet deformations of the metaphyses. Thickening of the cortical layer of the periosteum Acute systemic osteoporosis, blurring, unclear contours of the metaphyses. Often concentric bone atrophy. Severe osteoporosis. Trabecular exhaustion in the distal and proximal parts of the diaphysis Effect of treatment vit. D High, moderate doses, duration 4-6 weeks Satisfactory, high doses, taken constantly Minor Satisfactory, high doses, taken constantly Signs Vitamin D - deficiency rickets Phosphate - diabetes Renal tubular acidosis De-Toni-Debreu-Fanconi disease

Prevention of rickets in children in the first two years of life is mandatory. 1. Antenatal prevention - daily stay of the pregnant woman in the fresh air, a healthy lifestyle, proper nutrition with an optimal content of vitamin D and Ca, other macro and microelements, vitamins, proteins.

2. Specific antenatal prophylaxis All pregnant women are prescribed vitamin D at a dose of 400 IU per day for 8 weeks (28–32 weeks of pregnancy) during the winter-spring period. For women at risk: preeclampsia, diabetes mellitus, hypertension, rheumatism, etc., vitamin D is prescribed in a dose of 400 IU for 8 weeks from 28 to 32 pregnancies, regardless of the time of year.

4. Specific prevention - for full-term babies, breastfed from 3-4 weeks. age in the autumn – winter – spring periods, with the exception of the summer period. If the child was born at the end of spring, then prevention begins in the fall. The preventive dose is 500 IU daily.

Full-term children at risk (chronic extragenital pathology of the mother, twins, convulsive syndrome, congenital pathology of the hepatobiliary system, malabsorption syndrome, prolonged immobilization) are prescribed 1000 IU daily, excluding the summer months.

Premature babies with the 1st stage of prematurity are prescribed a prophylactic dose of vitamin D from the day of life in a dose of IU, premature babies of the 2-3rd stage - from the day of life in a dose of IU

Contraindications to the administration of a prophylactic dose of vitamin D are: Hypophosphatasia Hypophosphatasia Idiopathic calciuria (Williams-Bournet disease) Idiopathic calciuria (Williams-Bournet disease) Microcephaly Microcephaly Craniostenosis Craniostenosis

In the treatment of rickets, specific and nonspecific methods of therapy are used: adherence to the regimen; adherence to the regimen; sufficient physical activity; sufficient physical activity; staying in the fresh air; staying in the fresh air; correct nutrition, appropriate for the age of the child; correct nutrition, appropriate for the age of the child;

Drug Active ingredient Release form and dosage Aqueous solution of vitamin D3 Cholecalciferol Aqueous solution, 1 drop 500 IU Oil solution of vitamin D3 Cholecalciferol Oil solution, 1 drop 500 IU Oil solution 0.0625% (1 drop 625 IU) 0.125% (1 drop 1250 IU ) Ergocalciferol Vitamin D2 oil solution

Vitamin D is prescribed depending on the period of the disease: 1 st, 2 st of severity - 2000 - 2500, 3 st - 3000 - 5000 per day, for 30 days, treatment is monitored with the Sulkovich test, every day during therapy. After achieving a therapeutic effect, they switch to a prophylactic dose of vitamin D; the child receives this dose daily during the first 2 years of life and in the winter in the third year of life.

Rickets is a polyetiological disease of early age, which is a consequence of metabolic disorders, mainly phosphorus-calcium, and is accompanied by damage to many organs and systems and the development of skeletal deformation. The disease has been known since ancient times. The first medical description of this pathology was given by the English anatomist and orthopedist F. Glisson in 1656. The name of the disease comes from the Greek word “rachis”, which means “spine” (spine), the curvature of which is one of the symptoms of the disease. Rickets is one of the most common diseases in young children. According to various researchers, rickets occurs in 20-60% of children. Reliable data are unknown, since mild forms of the disease and initial manifestations are often missed.

Etiology The causes of rickets are divided into endogenous and exogenous. Endogenous: 1. Insufficient supply of vitamin D, phosphates, calcium, magnesium, zinc and other microelements, vitamins, amino acids. 2. Insufficient exposure of the child to fresh air and insufficient insolation, which leads to disruption of the formation of vitamin D from 7-dehydrocholesterol in the epidermis under the influence of ultraviolet rays. Exogenous factors: 1. Disruption of the absorption of vitamin D in the intestines. 2. Disruption of the processes of hydroxylation of inactive forms of vitamin D into active forms (D) in the liver and kidneys. 3. Impaired absorption of phosphorus and calcium in the intestine, their increased excretion in the urine, impaired utilization of bone tissue. 4. Impaired functional activity of vitamin D receptors.

Factors contributing to the development of rickets in children. 1. Artificial feeding 2. Prematurity of children (multivitaminosis, including hypovitaminosis D, increased need for vitamin D, immaturity of morphological and functional systems). 3. High rates of skeletal growth, rapid remodulation of bone tissue. 4. Poor child care.

Consumption of large quantities of grain products with food Insufficient UV irradiation Insufficient intake of vitamin D from food Lack of vitamin D Reduced reabsorption of P in the kidneys Hypophosphatemia Detachment of P from the myelin of nerve trunks Muscle hypotension Decreased synthesis of CaSB Decreased intestinal absorption of Ca Hypocalcemia Hyperproduction of PTH Inhibition of citrate activity tetasi Inhibition of citrate synthesis Acidosis Impaired protein and other types of metabolism Aminoaciduria Impaired collagen synthesis Impaired formation and deposition of CaHPO in bones Stimulation of osteoclasts Inhibition of osteoblasts Demineralization of bones Impaired bone formation

Working classification of Lukyanova E.M. (1988) distinguish: 1) Classic vitamin D-deficient rickets. 2) Vitamin D-dependent rickets is associated with a genetic defect in the synthesis of 1,25(OH) D in the kidneys or with resistance of target organs to it. 3) Vitamin D-resistant rickets (tubulopathies, hypophosphatasia). 4) Secondary rickets in liver diseases, malabsorption syndrome, etc.

Diagnosis of rickets 1. Clinical data. 2. Biochemical blood test: decreased phosphorus concentration; decrease in phosphorus concentration; increased alkaline phosphatase activity; increased alkaline phosphatase activity; calcium content – ​​N or hypocalcemia; calcium content – ​​N or hypocalcemia; decreased citric acid content (hypocitremia). decreased citric acid content (hypocitremia). 3. X-ray of skeletal bones – osteoporosis.

Clinical manifestations of rickets (S.O. Dulitsky, 1947) I degree 1. The first symptoms of rickets are autonomic disorders: sleep disturbances; sleep disorders; irritability; irritability; tearfulness; tearfulness; increased sweating: most of the face, scalp; increased sweating: most of the face, scalp; “sour” sweat, rubbing the head against the pillow, baldness of the back of the head; “sour” sweat, rubbing the head against the pillow, baldness of the back of the head; Red dermographism. Red dermographism. 2. Bone compliance – edges of the greater fontanelle, lesser fontanelle, sagittal suture, (minor osteoporosis).

II degree More pronounced bone changes appear: 1. Head: craniotabes (softening of areas of the parietal bones, less often areas of the occipital bone); craniotabes (softening of areas of the parietal bones, less often areas of the occipital bone); deformations of the skull bones; deformations of the skull bones; frontal and parietal tubercles; frontal and parietal tubercles; violation of the relationship between the upper and lower jaws; violation of the relationship between the upper and lower jaws; late closure of the large fontanelle, impaired teething (untimely, incorrect), defects in tooth enamel. late closure of the large fontanelle, impaired teething (untimely, incorrect), defects in tooth enamel.

2. Chest: deformation of the collarbones (increased curvature); deformation of the clavicle (increased curvature); “rib beads” (hemispherical thickening at the junction of the cartilaginous part of the rib into the bone); “rib beads” (hemispherical thickening at the junction of the cartilaginous part of the rib into the bone); expansion of the lower aperture and narrowing of the upper one, compression of the chest from the sides; expansion of the lower aperture and narrowing of the upper one, compression of the chest from the sides; Scaphoid depressions on the lateral surfaces of the chest; Scaphoid depressions on the lateral surfaces of the chest; Deformation of the sternum (“keeled”, “lake-shaped” chest). Deformation of the sternum (“keeled”, “lake-shaped” chest). 3. Spine: Kyphosis in the lower thoracic vertebrae, kyphosis or lordosis in the lumbar region, scoliosis in the thoracic region, flat pelvis. Kyphosis in the lower thoracic vertebrae, kyphosis or lordosis in the lumbar region, scoliosis in the thoracic region, flat pelvis.

III degree 1. Deformation of the bones of the skull, chest, spine + various changes in the tubular bones: a) upper limbs: curvature of the humerus and bones of the forearm; curvature of the humerus and forearm bones; Deformation in the joint area: “bracelets” (thickening in the area of ​​the wrist joints), “strings of pearls” (thickening in the area of ​​the diaphysis of the phalanges of the fingers). Deformation in the joint area: “bracelets” (thickening in the area of ​​the wrist joints), “strings of pearls” (thickening in the area of ​​the diaphysis of the phalanges of the fingers). b) lower limbs: curvature of the hips forward and outward; curvature of the hips forward and outward; various curvatures of the lower extremities (O- or X-shaped deformities); various curvatures of the lower extremities (O- or X-shaped deformities); deformities in the joint area. deformities in the joint area.

Initial period 1. Occurs at 2, 3 months. life, in premature babies - at the end of the first month. In the first place are changes in the nervous system: anxiety, slight excitability, flinching at a sharp sound, anxious sleep, increased sweating, mild muscle hypotension. restlessness, slight excitability, flinching at a sharp sound, anxious sleep, increased sweating, mild muscle hypotension.

Heightened period 1. Bone deformations of varying degrees. 2. Severe muscle hypotonia: “frog” belly; "frog" belly; loose ligaments and joints; loose ligaments and joints; "pocket knife" symptom; "pocket knife" symptom; muffler symptom; muffler symptom; "Harrison's furrow" "Harrison's furrow" 3. Late development of static and motor functions (children later begin to sit, stand, and walk). 4. Muscular hypotonia, deformation of the chest, impaired pulmonary ventilation, increased respiratory morbidity.

Period of residual effects 1. Deformations of flat bones decrease, but enlarged parietal and frontal tubercles, flattening of the back of the head, deformation of the chest, pelvic bones, and malocclusion remain. 2. Deformations of tubular bones disappear over time. 3. “Rachitic flatfoot” – changes in the axis of the lower extremities – in some children.

Acute course The predominance of osteomalacia processes over osteoid tissue hyperplasia (“craniotabes”, softening of the edges of the fontanelles and sutures) is more common in children in the first six months of life, in premature infants, in children from multiple pregnancies who do not receive prophylactic doses of vitamin D. The predominance of osteomalacia processes over osteoid tissue hyperplasia (“craniotabes”, softening of the edges of the fontanelles and sutures) more often in children in the first six months of life, in premature infants, in children from multiple pregnancies who do not receive prophylactic doses of vitamin D.

Subacute course Predominance of hyperplasia of osteoid tissue in areas of bone growth (“rib rosary”, “bracelets”, “tubercles”, etc.). The predominance of hyperplasia of osteoid tissue in areas of bone growth (“rib rosary”, “bracelets”, “tubercles”, etc.). More common in the second half of the year, in children receiving an insufficient prophylactic dose of vitamin D. More common in the second half of the year, in children receiving an insufficient prophylactic dose of vitamin D.

Recurrent course Repeated exacerbation of a subsided rachitic process. Repeated exacerbation of a subsided rachitic process. An X-ray examination of the bones reveals stripes of calcification in the metaphyseal zones of the tubular bones. An X-ray examination of the bones reveals stripes of calcification in the metaphyseal zones of the tubular bones. This course is more typical for secondary or hereditary forms of rickets. This course is more typical for secondary or hereditary forms of rickets.

Treatment of rickets It is necessary to eliminate the causes that led to the development of the disease; pathological changes that have occurred in the body. Treatment is divided into nonspecific and specific. Nonspecific treatment: rational nutrition; balanced diet; correct child routine; correct child routine; sufficient exposure to fresh air; sufficient exposure to fresh air; daily hygienic, periodically medicinal coniferous and with sea salt. daily hygienic, periodically medicinal coniferous and with sea salt.

Specific treatment Specific treatment depends on the period of the disease and its course. In the initial period of the disease during the subacute course in full-term infants, general ultraviolet radiation is prescribed every day or every other day, sessions. Start UV treatment with 1/8 biodose and increase to 1.5 biodose. In the initial period of the disease during the subacute course in full-term infants, general ultraviolet radiation is prescribed every day or every other day, sessions. Start UV treatment with 1/8 biodose and increase to 1.5 biodose. At the height of the disease, vitamin D is prescribed IU per day for 3-4 weeks. An aqueous solution of vitamin D (cholecalciferol) is mainly used; 1 drop contains 500 IU. During treatment with vitamin D, it is advisable to perform a Sulkovich test (determining the level of calcium in urine) once a week. At the height of the disease, vitamin D is prescribed IU per day for 3-4 weeks. An aqueous solution of vitamin D (cholecalciferol) is mainly used; 1 drop contains 500 IU. During treatment with vitamin D, it is advisable to perform a Sulkovich test (determining the level of calcium in the urine) once a week. After achieving a therapeutic effect, they switch to a prophylactic dose (IU per day), which is prescribed to the child for 2 years.

Prevention Antenatal and postnatal prevention is carried out. Antenatal prevention 1. Nonspecific measures: Rational nutrition of the pregnant woman, adequate lifestyle, sufficient exposure to fresh air. A balanced diet for a pregnant woman, an adequate lifestyle, and sufficient exposure to fresh air. Prevention of bacterial and other diseases in a pregnant woman. Prevention of bacterial and other diseases in a pregnant woman. Timely treatment of gestosis in pregnant women. Timely treatment of gestosis in pregnant women. Prevention of miscarriage. Prevention of miscarriage. 2. Specific prevention: Carried out in the last 2-3 months of pregnancy during the autumn-winter period of the year. Prescribe vitamin D by IU every day or ultraviolet radiation, sessions every day or every other day (start with ¼ biodose and increase to 2.5-3 biodoses). It is carried out in the last 2-3 months of pregnancy in the autumn-winter period of the year. Prescribe vitamin D by IU every day or ultraviolet radiation, sessions every day or every other day (start with ¼ biodose and increase to 2.5-3 biodoses).

Postnatal prevention 1. Nonspecific: Breastfeeding, timely introduction of supplements and complementary foods. Breastfeeding, timely introduction of supplements and complementary foods. Carrying out massage and gymnastics (30-40 minutes a day). Carrying out massage and gymnastics (30-40 minutes a day). Sufficient exposure to fresh air, air baths. Sufficient exposure to fresh air, air baths.

2. Specific prevention: Starts from 3-4 weeks (in premature infants from the day of life). Every day the child is given IU vitamin D until he is one year old. In the summer months (2-3 months), vitamin D is not given due to intense sun exposure. For premature babies and children with increased skin pigmentation, the daily dose of vitamin D is increased to IU and given for 1.5-2 years, excluding the summer months. For premature babies and children with increased skin pigmentation, the daily dose of vitamin D is increased to IU and given for 1.5-2 years, excluding the summer months. If children are fed with adapted formulas, vitamin D is not prescribed. If children are fed with adapted formulas, vitamin D is not prescribed. To prevent hypervitaminosis D, it is necessary to perform a Sulkovich test once every 2-7 weeks. To prevent hypervitaminosis D, it is necessary to perform a Sulkovich test once every 2-7 weeks.

Literature 1. Handbook for students of higher medical degrees of the IV level of accreditation / Ed. prof. O.V. Tyazhkoy / Seeing a friend. – Vinnytsia: New book, – from Pediatrics: Textbook for higher medical students. Textbook Institutions of III-IV levels of accreditation. – 2nd ed., rev. and additional /V.G.Maidannik. – Kharkov: Folio, – Rickets (Manual for doctors)/Romanyuk F.P., Alferov V.P., Kolmo A.E., Chugunova O.V. – St. Petersburg, – 62 p.

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