Geriatri Pratiğinde Koruyucu Hekimlik

Osteoporoz, bozulmuş kemik mikromimarisi ve kemik kütlesindeki azalma sonucu ortaya çıkanve kemik kırılganlığına neden olan ilerleyici bir metabolik kemik hastalığıdır. Osteoporozun en önemliklinik sonucu morbidite ve mortalitede önemli artışa neden olan frajilite kırıklarıdır. Kırıklar sağlık sistemleri için önemli bir yüktür. İlerleyen yaş, osteoporoz için önemli ve değiştirilemez bir risk faktörüdür. Bu nedenle yaşlılarla ilgilenen klinisyenler osteoporozu değerlendirebilecek niteliklere sahipolmalıdır. Osteoporoz gelişimini önlemek için değiştirilebilir risk faktörleri düzeltilmeli, 65 yaş üstü kadınlar ve 70 yaş üstü erkekler dual enerji x-ray absorpsiyometri (DEXA) ile taranmalıdır. Osteoporozdafarmakolojik olmayan tedavi yöntemlerine (egzersiz, diyet , yaşam tarzı değişikliği) ek olarak hasta özellikleri, ilaç etkileri ve yan etkiler göz önünde bulundurularak bifosfonatlar, denosumab gibi anti-rezorptif tedavi ajanları veya teriparatid, abaloparatid, romosuzumab gibi anabolik tedavi ajanları arasındanuygun olan ajan seçilerek uygulanmalıdır. Tedavi yanıtı takip edilmeli ve hiçbir tedavi ajanının kullanımısüresiz olarak kabul edilmemelidir.&nbsp;Osteoporosis is a progressive metabolic bone disease that results from deteriorated bonemicroarchitecture and a decrease in bone mass, which causes bone fragility. The most important clinical result of osteoporosis is fragility fractures that result in significant increase in morbidity and mortality. The age is an important risk factor for osteoporosis. Therefore, clinicians interested in older peopleshould have the qualifications to evaluate osteoporosis. To prevent osteoporosis development, the interchangeable risk factors must be corrected, and men over 65 and over 70 must be scanned with dual energy x-ray absorphaly (DEXA). In addition to non-pharmacological treatment methods (exercise, diet,lifestyle change) in the osteoporosis, patient characteristics, drug effects and side effects should be considered, and the appropriate agent must be applied between treatment agents such as biphosphanates,denosumab, teriparatid, abaloparatid, romosuzumab. The treatment response should be monitored, andno treatment agent should be considered indefinitely.&nbsp;&nbsp;</p

Natural history of ROHHAD syndrome: development of severe insulin resistance and fatty liver disease over time

Background:&nbsp;Rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation (ROHHAD) is a rare syndrome with unknown etiology. Metabolic abnormalities are not known to be part of the syndrome. We present one of the oldest cases reported in the literature, who developed severe metabolic abnormalities and hepatic disease suggesting that these features may be part of the syndrome.Case presentation:&nbsp;A 27-year-old woman, diagnosed with ROHHAD syndrome at age 15, who previously developed diabetes insipidus, growth hormone deficiency, hyperprolactinemia, and hypothyroidism in her first decade of life. This was followed by insulin resistance, NAFLD, liver fibrosis, and splenomegaly before age 14 years. Her regimen included a short course of growth hormone, and cyclic estrogen and progesterone. Her metabolic deterioration continued despite treatment with metformin. Interestingly, she had a favorable response to liraglutide therapy despite having a centrally mediated cause for her obesity. At age 26, a 1.6 cm lesion was found incidentally in her liver. Liver biopsy showed hepatocellular carcinoma which was successfully treated with radiofrequency ablation.Conclusion:&nbsp;Metabolic abnormalities, Insulin resistance and fatty liver disease are potentially part of the ROHHAD syndrome that may develop over time. GLP1 agonists were reasonably effective to treat insulin resistance and hyperphagia. Patients with ROHHAD may benefit from close follow up in regards to liver disease.Keywords:&nbsp;Atypical diabetes; GLP-1 agonists; Insulin resistance; Obesity; ROHHAD.</p