Normative Femoral and Tibial Lengths in a Modern Population of Twenty-First-Century U.S. Children.

BACKGROUND: The Green-Anderson (GA) leg-length data remain the gold standard for the age-based assessment of leg lengths in children despite their methodologic weaknesses. We aimed to summarize current growth trends among a cross-sectional cohort of modern U.S. children using quantile regression methods and to compare the median femoral and tibial lengths of the modern U.S. children with those of the GA cohort. METHODS: A retrospective review of scanograms and upright slot-scanning radiographs obtained in otherwise healthy children between 2008 and 2020 was completed. A search of a radiology registry revealed 3,508 unique patients between the ages of 2 and 18 years for whom a standard-of-care scanogram or slot-scanning radiograph had been made. All patients with systemic illness, genetic conditions, or generalized diseases that may affect height were excluded. Measurements from a single leg at a single time point per subject were included, and the latest available time point was used for children who had multiple scanograms made. Quantile regression analysis was used to fit the lengths of the tibia and femur and overall leg length separately for male patients and female patients. RESULTS: Seven hundred patients (328 female and 372 male) met the inclusion criteria. On average, the reported 50th percentile tibial lengths from the GA study at each time point were shorter than the lengths in this study by 2.2 cm (range, 1.4 to 3.3 cm) for boys and 2 cm (range, 1.1 to 3.1 cm) for girls. The reported 50th percentile femoral lengths from the GA study at each time point were shorter than the lengths in this study by 1.8 cm (range, 1.1 to 2.5 cm) for boys and 1.7 cm (range, 0.8 to 2.3 cm) shorter for girls. CONCLUSIONS: This study developed new growth charts for femoral and tibial lengths in a modern U.S. population of children. The new femoral and tibial lengths at nearly all time points are 1 to 3 cm longer than traditional GA data. The use of GA data for epiphysiodesis could result in underestimation of expected childhood growth. LEVEL OF EVIDENCE: Prognostic Level IV . See Instructions for Authors for a complete description of levels of evidence.

Excision of Physeal Bars of the Distal Femur, Proximal and Distal Tibia Followed to Maturity.

OBJECTIVE: In the 50 years since a premature partial physeal arrest (a physeal bar) was first excised from an epiphysis there have been no large in-depth studies reporting the results in patients followed to skeletal maturity. This paper reports the results of physeal bar resection surgery in a group of patients followed to skeletal maturity, documenting the restored growth of the affected physis, the affected bone, and the final limb-length discrepancy. METHODS: Forty-eight patients underwent physeal bar resection of the distal femur (21), proximal tibia (9), and distal tibia (18) by 1 surgeon (H.A.P.) from 1968 through 1996, and were followed prospectively to skeletal maturity with clinical and radiologic examinations. Factors such as sex, age at time of injury, etiology of the bar, physeal bar location and size, age at time of bar excision, interposition material, and additional surgical procedures were analyzed with respect to physis, bone, and limb growth following bar resection. RESULTS: The mean growth for the entire bone following physeal bar excision was 7.6 cm for the distal femur, 4.7 cm for the proximal tibia, and 7.5 cm for the distal tibia, compared with growth in the contralateral control bone of 6.8 cm in the femur, 5.0 cm in the proximal tibia, and 7.8 cm in the distal tibia. The maximum bone growth following bar excision in a single patient was 21.3 cm for the distal femur, 10.3 cm for the proximal tibia, and 18.6 cm for the distal tibia. The mean limb-length discrepancy at maturity was -1.7 cm for the distal femur, -1.3 cm for the proximal tibia, and -1.1 cm for the distal tibia (all sites combined -1.4 cm). Fourteen patients (29%) had only the 1 bar excision with no other accompanying or subsequent surgery. Thirty-four patients (71%) had 1 to 4 accompanying or subsequent leg length or angular correcting procedures. CONCLUSIONS: Physeal bar excision to restore growth when applied to the appropriate patient is a useful, rewarding procedure, reducing the number of surgical limb length equalizing procedures. It is a demanding surgical procedure and requires diligent and careful follow-up until maturity. Additional limb length equalizing surgery is frequently needed. LEVEL OF EVIDENCE: Case series, level IV.

Physeal bar equivalent.

Premature partial physeal arrest without the formation of an osseous bar - physeal bar equivalent (PBE) - is uncommon. Four children with a PBE had an infection near the distal femoral physis before the age of 11 months. Some growth was achieved after resection of the PBE in each case. Of two cases diagnosed and treated early, one required only contralateral physeal arrests to achieve limb-length equality at maturity. The other, currently 8 years and 4 months old, has a 1.1-cm limb-length discrepancy 6 years after PBE resection and will require observation until maturity. Of two cases diagnosed and treated late, one required ipsilateral femoral lengthening and contralateral femoral shortening and physeal arrests to treat the limb-length discrepancy and angular deformity. The other, currently 7 years and 1 month old, has a 4.8-cm discrepancy and will need future surgical limb-length equalization. Early recognition and treatment of PBE is required to avoid severe limb-length inequality and angular deformity.

The fate of hips that are not prophylactically pinned after unilateral slipped capital femoral epiphysis.

BACKGROUND: The indications for prophylactic pinning of the contralateral hip after unilateral slipped capital femoral epiphysis (SCFE) remain controversial in part because the natural history of the contralateral hip is unclear. QUESTIONS/PURPOSES: We therefore determined (1) the incidence of contralateral slips in patients with unilateral SCFE, (2) the rate of subsequent corrective surgery, and (3) the Harris hip score (HHS) and VAS pain score for hips that sustained a contralateral slip after unilateral pinning. METHODS: We retrospectively reviewed 226 patients with unilateral SCFE at initial presentation between 1965 and 2005; of these, 133 met our inclusion criteria and were followed at least 2 years. Latest followup included examination and radiographs for 52 patients and HHS (without radiographs) and VAS pain score for 81 hips. Minimum followup was 2 years (median, 13 years; range, 2-43 years). RESULTS: Of the 133 patients at risk for a subsequent slip, 20 patients developed a contralateral slip (15%). One patient developed avascular necrosis requiring arthroplasty, and another patient had a mild contralateral slip with disabling pain. For the 15 patients with contralateral slips and scores available, the mean HHS was 90 (range, 49-100) and the mean VAS pain score was 20 of 100. Six found the contralateral hip painful. CONCLUSIONS: The contralateral slip sustained by the majority of patients was for the most part mild. However, nearly 1/3 of the contralateral slipped hips were painful. One patient has severe pain, and a second required THA for avascular necrosis after an unstable slip. These may have been preventable by prophylactic pinning. LEVEL OF EVIDENCE: Level III, therapeutic study. See Instructions for Authors for a complete description of levels of evidence.

Incidence of slipped capital femoral epiphysis: a population-based study.

The incidence of slipped capital femoral epiphysis (SCFE) remains controversial. A population-based database was used to identify all residents of a Midwestern American county treated for a new diagnosis of SCFE. Between 1965 and 2005, 49 patients (aged 9-16 years) underwent treatment of SCFE. This represents an annual incidence of 8.3 unilateral cases and 0.5 bilateral cases per 100,000 children. In patients with unilateral disease, mild slips developed in nine contralateral hips (19%) at a mean of 166 days (range: 6-432 days). As all contralateral slips were mild, we recommend careful follow-up rather than prophylactic pinning of the contralateral hip.

The treatment of congenital pseudarthrosis of the tibia with ipsilateral fibular transfer to make a one-bone lower leg: a review of the literature and case report with a 23-year follow-up.

BACKGROUND: The surgical making of a one-bone lower leg is, in a way, an operation of necessity or last resort. It has been attempted for many conditions and by many techniques. METHODS: This is a review of the literature and a case report of transferring a congenitally pseudarthritic fibula to replace an ipsilateral pseudarthritic tibial diaphysis without exposing the fibular vascular pedicle, or using microvascular techniques, and with the specific aim of purposely creating a true one-bone lower leg, the tibula. RESULTS AND CONCLUSION: The concept and surgical technique used here leave the contralateral leg undisturbed and are less demanding, time consuming, and costly than a vascularized pedicle graft or bone transport. This procedure is new and can also be applied when the fibula is normal and to repair tibial diaphyseal deficiency from any cause in both children and adults.

The ulnius: a one-bone forearm in children.

Surgical creation of a one-bone forearm is appropriately utilized for a variety of underlying conditions. It functions best when the proximal ulna and distal radius are available for use. A variety of surgical techniques have been utilized. This report reviews the pediatric literature and presents four personal cases, each with a different underlying abnormality. The rotational position of forearm fusion is discussed.

Management of distal tibial medial malleolus type-6 physeal fractures.

PURPOSE: Type 6 is an open fracture in which part of the physis is missing. It is the least common physeal fracture, but has the highest rate of complications, particularly the formation of a physeal bar. Without preemptive treatment, a physeal bar always forms, producing growth retardation and angular deformity, and excision of these physeal bars has been uniformly unsuccessful. The distal medial malleolus is a common site for the fracture. METHODS: Strategies for the treatment of two varieties of acute medial malleolar type-6 fractures and two types of late deformities following type-6 fracture are given. The acute fractures were treated with either fat or cartilage applied to the exposed physis. The late deformities were treated with corrective iliac bone grafting. RESULTS: The acute fractures were prevented from forming physeal bars and the two late deformities were fully corrected with good outcomes. CONCLUSION: Fat applied to an acute type-6 physeal fracture has a good chance of preventing bar formation. Ankle deformities due to bars can be corrected by means of iliac bone grafting.

Metallic implant removal in children.

The indications for removing metal that was implanted in children and the practice of removing it have changed dramatically during the past century, but this subject is rarely discussed in publications, oral presentations, or resident training curricula. Thus, during their training, residents learn about the topic only sporadically from evaluating patients. This article presents the cases for and against metallic implant removal and identifies situations in which removal is appropriate and situations in which it is not.

Differences in surface-exposed antigen expression between Helicobacter pylori strains isolated from duodenal ulcer patients and from asymptomatic subjects.

We have analyzed possible qualitative and quantitative differences in antigen expression between Helicobacter pylori strains isolated from the antrum and different locations in the duodenum of 21 duodenal ulcer (DU) patients and 20 asymptomatic subjects (AS) by enzyme-linked immunosorbent assay (ELISA) and inhibition ELISA. Almost all antral and duodenal strains grown in vitro expressed the N-acetyl-neuroaminyllactose-binding hemagglutinin, flagellins (subunits FlaA and FlaB), urease, a 26-kDa protein, and a neutrophil-activating protein. In 75% of both the DU patients and the AS, antral H. pylori strains expressed either the blood group antigen Lewis y (Le(y)) alone or together with the Le(x) antigen. However, duodenal H. pylori strains of DU patients expressed Le(y) antigen more frequently than corresponding strains of AS (P < 0.05). Presence of Le(y) on H. pylori was related to the degree of active duodenitis (P < 0.05). Duodenal H. pylori strains isolated from AS were significantly more often Lewis nontypeable than duodenal strains of DU patients (P < 0.01). Presence of H. pylori blood group antigen-binding adhesin (BabA) was significantly higher on both antral and duodenal strains isolated from DU patients than on corresponding strains isolated from AS (P < 0.05). BabA-positive duodenal H. pylori strains isolated from DU patients were associated with active duodenitis more frequently than corresponding strains isolated from AS (P < 0.01). Infection with H. pylori strains positive for Le(y) and BabA in the duodenum is associated with development of duodenal ulcer formation.

Conceivable mechanisms by which Helicobacter pylori provokes duodenal ulcer disease.

A conceivable concept for the development of duodenal ulcers in Helicobacter pylori (H. pylori) infected subjects is presented in this chapter. The concept includes an explanation of the fact that only a minority of all H. pylori-infected subjects will develop a duodenal ulcer. Helicobacter pylori infection of the antrum induces a hypersecretion of gastric acid secretion, giving rise to gastric metaplasia in the duodenal bulb. This gastric metaplasia is a prerequisite for H. pylori colonization of the bulb. These events are common to all H. pylori-infected subjects. However, a much higher density of H. pylori bacteria and colonization with virulent organisms has been found in the bulb of duodenal ulcer patients, resulting in a much stronger inflammatory reaction with active duodenitis and an impaired bicarbonate secretion. These characteristics, together with acid hypersecretion, seem to be the important factors in evoking a duodenal ulcer.

[When is H pylori a cause of duoenal ulcer? Hypersecretion of gastric acid, active duodenitis and reduced bicarbonate secretion are links in the chain]. / När ger H pylori ulcus duodeni? Hypersekretion av syra, aktiv duodenit och nedsatt bikarbonatsekretion är länkar i kedjan.

Helicobacter pylori infection engaging mainly the gastric antrum causes hypersecretion of gastric acid. The increased duodenal acid load gives rise to islands of gastric mucosa in the proximal duodenum. As these bacteria thrive only on gastric mucosa it presents an opportunity for Helicobacter pylori to colonize the duodenum. A much higher density of virulent Helicobacter pylori has been found in the duodenum of duodenal ulcer patients in comparison to infected subjects without duodenal ulcer. The high density of virulent Helicobacter pylori in the proximal duodenum results in a strong inflammatory reaction with active duodenitis and impaired bicarbonate secretion. These characteristics of duodenal ulcer patients, together with the acid hypersecretion, seem to be the key factors in evoking a duodenal ulcer.

Role of local cytokines in increased gastric expression of the secretory component in Helicobacter pylori infection.

Using immunohistochemical staining, we examined the presence of secretory component (SC) on epithelial cells in gastric and duodenal biopsy specimens collected from Helicobacter pylori-infected individuals and healthy controls. Gastric epithelial cells from healthy volunteers expressed low, but detectable, levels of SC. In contrast, significantly higher level of expression of SC (P < 0.001) was observed on epithelial cells in the antra of H. pylori-infected individuals. The antral SC expression correlated with staining for gamma interferon of intraepithelial and lamina propria lymphocytes (r(s) = 0.76 and 0.69, respectively, P < 0.001) and correlated weakly with production of tumor necrosis factor alpha (r(s) = 0.43, P < 0.05), but it did not correlate at all with interleukin-4 production.

A novel tablet-based 13C urea breath test for Helicobacter pylori with enhanced performance during acid suppression therapy.

BACKGROUND: The urea breath test (UBT) can still be improved in terms of user-friendliness and accuracy during acid-suppression therapy. This study was designed to evaluate a novel, rapidly disintegrating 13C UBT tablet, which was supplemented with citric acid to facilitate diagnosis of Helicobacter pylori in the hypochlorhydric stomach. METHODS: The efficacy of a fasting 13C tablet-based UBT (TUBT) was compared with that of a standard 13C UBT (SUBT) during 40 min after dosing, and optimal sampling points were determined. The single-point TUBT was validated against a 'gold standard' (GS) including a TUBT, culture, histology, and a CLO test in 134 dyspeptic patients, and its optimal cut-off point was determined by means of a biometric method. In addition, 20 SUBT-positive patients were randomized to perform either the TUBT or the SUBT after 7 days of omeprazole therapy (20 mg twice daily). RESULTS: Compared with a SUBT, the TUBT gave a quicker and wider separation between positive and negative results and an earlier optimal sampling point (10 versus 40 min). At 10 min the TUBT correctly classified 40 of 42 GS-positive subjects (sensitivity, 95%) and all of 92 GS-negative patients (specificity, 100%), and the optimal cut-off point was 1.8 delta per mil. Furthermore, when optimal sampling points were used, the TUBT (t = 10 min) proved to be more accurate than the SUBT (t = 40 min) during omeprazole treatment, correctly identifying all of 10 and 3 of 9 H. pylori-infected patients, respectively. CONCLUSIONS: By supplying 13C urea and citric acid as a rapid-release tablet, it is possible to shorten the duration of the 13C UBT to 10 min, omit the test meal, and still maintain excellent accuracy, even during acid suppression therapy.

Duodenal Helicobacter pylori infection differs in cagA genotype between asymptomatic subjects and patients with duodenal ulcers.

BACKGROUND & AIMS: It is unclear why only a minority of subjects infected by Helicobacter pylori develop duodenal ulcers (DU). The aim of this study was to investigate whether the number and type of H. pylori strains in the duodenum of patients with DU may play a critical role. METHODS: Twenty-one patients with DU and 20 asymptomatic subjects with antral H. pylori infection were studied. Paired biopsy specimens were taken from the antrum and from each quadrant of the duodenal bulb. Analyses included extent of duodenal gastric metaplasia, severity of duodenitis, bacterial density, presence of the cagA gene, and vacuolating cytotoxin activity. RESULTS: H. pylori was cultured from duodenal biopsy specimens in 95% of patients with DU and 80% of asymptomatic subjects. Both groups had a similar bacterial density and proportion of cagA-positive strains in the antrum (86% vs. 75%), but patients with DU had a 20-fold higher density of H. pylori and a higher proportion of cagA-positive strains in the duodenal bulb (81% vs. 30%). Active duodenitis was present only in patients with DU infected by cagA positive strains in the duodenum. CONCLUSIONS: The results suggest that a high density of cagA-positive strains in the duodenum with severe duodenitis are important determinants of DU disease.

Local cytokine response in Helicobacter pylori-infected subjects.

The host immune response to Helicobacter pylori infection might be of importance with regard to the outcome of infection by this organism, e.g., to explain why only a proportion of infected subjects develop peptic ulcers. In this study we have analyzed the local response of different cytokines-i.e., the proinflammatory interleukin-1beta, (IL-1beta), IL-6, tumor necrosis factor alpha, and IL-8; the immunoregulatory gamma interferon (IFN-gamma); and IL-4; and the anti-inflammatory transforming growth factor beta (TGF-beta)-in antral biopsy specimens from H. pylori-infected duodenal ulcer (DU) patients and asymptomatic (AS) carriers (i.e., with chronic gastritis only). For comparison, biopsy specimens from uninfected healthy individuals were also analyzed. An immunohistochemical technique was used to allow quantification of the cytokine responses as well as identification of the cell types associated with the cytokine expression. We found that the levels of all of the studied cytokines except IL-4 were increased in the H. pylori-infected subjects compared to the levels in the healthy individuals. Our results indicate that the antral cytokine response is of the Th1 type since IFN-gamma, but not IL-4, was up-regulated both in H. pylori-infected DU patients and in AS carriers. However, there were no significant differences in either proinflammatory or immunoregulatory cytokine levels when H. pylori-infected subjects with and without peptic ulcers were compared. Some of the cytokines, particularly IL-1beta and TGF-beta, were also found in the gastric mucosae of healthy, uninfected subjects. We also showed that the gastric epithelium contributes substantially to the antral cytokine response of the proinflammatory cytokines IL-1beta and IL-6 in addition to IL-8.

Specific antibodies in sera and gastric aspirates of symptomatic and asymptomatic Helicobacter pylori-infected subjects.

In this study we have determined systemic and local antibody responses against different Helicobacter pylori antigens in H. pylori-infected and noninfected subjects. In addition, we studied whether differences in antibody responses between patients with duodenal ulcers and asymptomatic H. pylori carriers might explain the different outcomes of infection. Sera and in most instances gastric aspirates were collected from 19 duodenal ulcer patients, 15 asymptomatic H. pylori carriers, and 20 noninfected subjects and assayed for specific antibodies against different H. pylori antigens, i.e., whole membrane proteins (MP), lipopolysaccharides, flagellin, urease, the neuraminyllactose binding hemagglutinin HpaA, and a 26-kDa protein, by enzyme-linked immunosorbent assay. The H. pylori-infected subjects had significantly higher antibody titers against MP, flagellin, and urease in both sera and gastric aspirates compared with the noninfected subjects. Furthermore, the antibody titers against HpaA were significantly elevated in sera but not in gastric aspirates from the infected subjects. However, no differences in antibody titers against any of the tested antigens could be detected between the duodenal ulcer patients and the asymptomatic H. pylori carriers, either in sera or in gastric aspirates.

Aspirin-induced gastritis, like Helicobacter pylori-induced gastritis disinhibits acid secretion in humans: relation to cytokine expression.

BACKGROUND: Helicobacter pylori infection contributes to hypergastrinemia and hypersecretion of acid by blocking inhibitory reflex pathways to gastrin and parietal cells normally activated by antral distention. Our aim was to investigate whether a similar blockade of inhibitory responses could be provoked by inducing gastritis with aspirin, thus implicating a common inflammatory component, possibly a proinflammatory cytokine(s). METHODS: We studied the effects of antral distention on stimulated acid secretion and gastrin release in H. pylori-negative volunteers, before and after 3 days of aspirin therapy (2 g daily). Immediately before the examinations, the severity of gastric mucosal injury was evaluated macroscopically and histologically, and the production of interleukin (IL)-1beta, IL-6, IL-8, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma was determined by immunohistochemistry. RESULTS: Most subjects had severe gastric injury after aspirin therapy, resulting in a substantially increased production of IL-1beta, IL-6, and IL-8 but not of TNF-alpha and IFN-gamma in the antral mucosa. In these subjects the acid-inhibitory response was abolished or markedly reduced. Conversely, aspirin therapy failed to affect the gastrin release in all subjects studied. CONCLUSIONS: The disinhibition of acid secretion in response to antral distention is a joint feature of the gastritis induced by aspirin and H. pylori infection, possibly related to the increased production of IL-1beta, IL-6, and IL-8. The H. pylori-related hypergastrinemia apparently has a different background.

Antibody-secreting cells in the stomachs of symptomatic and asymptomatic Helicobacter pylori-infected subjects.

In this study we analyzed whether infection with Helicobacter pylori gives rise to specific B-cell responses against a number of putative virulence factors of H. pylori, e.g., urease, flagellin, and different bacterial surface antigens, locally in the gastric mucosa. This was studied in antrum and corpus biopsies collected from 11 H. pylori-infected patients with duodenal ulcers, 11 asymptomatic H. pylori carriers, and 13 noninfected, healthy controls. Mononuclear cells were isolated from the biopsies and assayed for frequencies of total and H. pylori-specific antibody-secreting cells (ASCs) by means of the enzyme-linked immunospot technique. The H. pylori-infected subjects had remarkably higher frequencies of total immunoglobulin A (IgA)- and IgM-secreting cells than the noninfected subjects, while the frequencies of IgG-secreting cells were virtually the same in the different groups. In addition, most of the infected subjects had IgA ASCs reacting with H. pylori membrane proteins, flagellin, and urease, while none of the noninfected subjects had any detectable H. pylori-reactive ASCs. Furthermore, half of the infected subjects also had ASCs reacting with a Helicobacter-specific 26-kDa protein, while only a few of them had ASCs reacting with neutrophil-activating protein, the neuraminyllactose-binding hemagglutinin HpaA, or lipopolysaccharides purified from different H. pylori strains. The frequencies of H. pylori-specific ASCs in the antrum and corpus were almost identical, and no differences in either antigen specificity or magnitude of the B-cell response in the stomach could be detected between the ulcer patients and the asymptomatic H. pylori carriers. This study demonstrates that H. pylori infection induces strong antibody responses in the human gastric mucosa, both in asymptomatic carriers and in duodenal ulcer patients. However, the outcome of infection could not be explained by differences in the local B-cell response to any of the antigens used in this study.