Generalized Increase In Bone Density Research Articles

Renal Osteodystrophy in Mullerian, Renal, Cervicothoracic Somite Abnormalities (MURCS Association): A Logical, However Hitherto Unknown Entity

The MURCS association which stands for Mullerian, Renal, Cervicothoracic Somite Abnormalities is a rare developmental anomaly seen in females. The clinical course of this disorder is not clearly defined as of yet-which may range from asymptomatic to severe disability. Here we present the case of a young 22-year-old female who was incidentally detected to have a generalized increase in bone density with an absent uterus. Further workup revealed a case of MURCS association with renal osteodystrophy. This is an as of yet unreported complication/association and must be kept in mind in the treatment of these patients.

Back pain in chronic renal failure

Patient SK, a 40-yr-old female, resident of Bhagalpurvillage in Bihar, India, was operated for gallstones3 years previously. On pre-operative checkup, mildrenal dysfunction was detected. She was asymptomaticfor renal disease with serum creatinine of 159mmol/l(1.8mg/dl), bland urinary sediment and small echo-genic kidneys on ultrasound. She was puton conservative management for chronic renal failure(CRF) and was doing well till 1 year ago. Since thenshe developed back pain, which increased on walking.Pain was dull in character without any radiation. Therewere no systemic complaints. In the past month whenher pain increased substantially, causing discomfort inday-to-day activities. On investigation she was foundto have moderate renal failure with blood ureanitrogen (BUN) of 11.8mmol/l and serum creatinineof 309mmol/l (3.5mg/dl). Other labs showed serumcalcium of 2.4mmol/l, phosphorus 1.1mmol/l, alkalinephosphatase 243U/l, uric acid 381mmol/l and intactparathyroid hormone (iPTH) of 182.0pg/ml. X-raysof bilateral forearms, pelvis and spine were taken(Figures 1–3, respectively), which revealed generalizedincrease in bone density, degenerative changeswith osteophytes in lumber vertebra, calcification ofbilateral iliolumbar and sacrospinous ligaments andinterosseous membrane calcification in forearms.Definitive diagnosis was reached with estimation offluoride levels in blood and urine, which were0.291mg/l and 0.962mg/l (15.3 and 50.6mmol/l),respectively. Her drinking water source, ground waterfrom a tubewell, was found to contain 3.910mg/l(205.9mmol/l) of fluoride. She was diagnosed to havefluorosis with moderate CRF and was advised to usedomestic reverse-osmosis-treated water for cookingand drinking.Main sources of fluoride include food and water.About 50–70% of fluoride is excreted by the kidneys[1]. Individuals with kidney disease have decreasedability to excrete fluoride in urine and are at risk ofdeveloping fluorosis even at normal recommendedlimit of 0.7 to 1.2mg/l (37–63mmol/l) of fluoride indrinking water [2]. In fluorosis with normal renalfunction, urine fluoride rises above 0.5–4.48mg/l(26–236mmol/l) and may reach 1.5–13.0mg/l(79–685mmol/l) [3]. Serum fluoride rises to0.04–0.28mg/l (2.1–14.7mmol/l) in such patients [1].Fluoride is bone-seeking due to its high affinity forcalcium phosphate and therefore accumulates in bone.Radiological changes can be quite similar to changesof renal osteodystrophy, and therefore the diagnosismay be missed unless specifically investigated.

Osteopetrosis: Further heterogeneity

A form of osteopetrosis is described in two sibs which differs from the well-established autosomal dominant and recessive forms. The clinical course is mild with no evidence of clinically important encroachment upon the bone marrow or cranial nerve foramina; the skeletal radiographs show a mild generalized increase in bone density and metaphyseal modeling defects affecting primarily the distal femurs. The inheritance pattern is compatible with either an autosomal or X-linked recessive mode. The histologic features are distinct as well, and suggest that the pathogenesis of the condition differs from that of the usual forms of osteopetrosis.

Clinical and Experimental Lead Poisoning: Some Roentgenologic and Anatomic Changes in Growing Bones

THE purpose of this report is to present and correlate some roentgenologic and anatomic changes occurring in the growing skeleton during both clinical and experimental lead poisoning, and to consider the roentgenologic sequelæ in the bones of two children who recovered from chronic lead poisoning. The selective deposition of lead in the skeleton has been clearly shown in the extensive studies of Minot and Aub (1). Their demonstration chemically of lead storage in bone first suggested to me that retention of lead in bones might also be shown roentgenologically. Aub and his co-workers (2) concluded that a high concentration of lead occurs in the solid portion of the bone, whereas the marrow contains only traces of lead. They did not mention the ends of the diaphyses as special sites of lead deposit. We had anticipated that the roentgenologic findings in lead poisoning might be a generalized increase in bone density. Therefore, the pronounced changes limited to the ends of the shafts first seen in Case 1, October, 1929, were unexpected. Case 1. M. K., 18 months of age, was admitted to the Babies' Hospital on Oct. 21, 1929, from the Out-patient Department, with the diagnosis of chronic poisoning by lead. The familial, natal, and developmental histories were normal. Three months previously the child had begun to vomit. The vomiting had increased in both frequency and severity until, during the few weeks just past, emesis had occurred after all attempts to take food or even water. About four months previous to admission there had been a decided change in the child's disposition and activity. This previously normal child had become hyperirritable, crying most of the day and “shaking continually and waving her arms frantically in the air.” The infant had begun to walk about the fourteenth month, and the mother thought that she had walked as well as most children of this age, until the last two months before admission to the hospital, when she “fell down frequently” and finally stopped walking (one month before). Attempts to encourage her to begin walking again were unsuccessful. The child “staggered badly.” No convulsive seizures had been observed. She was supposed to have gained normally during this time. Two and one-half months before admission, pallor was first noted, which had gradually increased up to the day of admission. The mother offered the information that at the fourteenth month, the approximate date when she started to walk, the infant was first seen to chew on the painted surfaces of woodwork about the household—window-cases, doors, crib, beds, and chairs. This perversion of appetite had continued throughout the last four months, and during this time several “large areas of paint had been chewed off” these surfaces. Physical Examination Measurements: head 18½ inches, length 30¼ inches.