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Outcomes of total hip arthroplasty are similar for patients with displaced femoral neck fractures and osteoarthritis.
This study attempted to evaluate whether total hip arthroplasty for displaced femoral neck fractures had significantly different outcomes when compared with total hip arthroplasty for osteoarthritis. This is a retrospective study of 60 patients who had total hip arthroplasties between 1997 and 2001. Thirty patients (mean age, 79.7 years) had total hip arthroplasties for displaced femoral neck fractures; 30 patients (mean age, 76.9 years) were treated with total hip arthroplasties for osteoarthritis. The same surgeon used the modified lateral approach for all surgeries. All patients had radiographic assessment, physical examination, and evaluation with the Harris hip score. The mean followup was 38 months. The mean Harris hip score for the 25 patients treated with a total hip arthroplasty for a femoral neck fracture was 81 points; the mean hip score for the 27 patients treated with a total hip arthroplasty for osteoarthritis was 87 points. No statistically significant differences between these groups were observed. Patients who were treated with a total hip arthroplasty for a femoral neck fracture did not have increased perioperative morbidity compared with patients who had a total hip arthroplasty for osteoarthritis. This study suggests that the outcomes for total hip arthroplasties in this consecutive series of patients treated for displaced femoral neck fractures and osteoarthritis are comparable.
Right bundle-branch block ventricular tachycardias: septal versus lateral ventricular origin based on activation time to the right ventricular apex.
BACKGROUND: Identifying the septal versus lateral site of origin of ventricular tachycardia (VT) with a right bundle-branch block (RBBB)-type pattern and an R-S ratio >1 in lead V1 is difficult with the 12-lead ECG, especially in patients with prior apical infarction. METHODS AND RESULTS: We prospectively evaluated 58 patients with VT. Sixteen patients had apical infarcts (group 1), 29 had nonapical infarcts (group 2), and 13 had no heart disease (group 3). QRS complex onset to activation at the right ventricular apex (stim-RVA) was measured during left ventricular (LV) apical septal and lateral pacing, and 47 RBBB-type VTs (QRS-RVA) were localized to the septal or lateral apex by using entrainment techniques. Pacing and VT site of origin were confirmed by electroanatomic mapping. The stim-RVA time was 59+/-16 ms for septal versus 187+/-24 ms for lateral sites in group 1, P<0.001; 70+/-14 ms for septal versus 169+/-19 ms for lateral sites in group 2, P<0.001; and 42+/-15 ms for septal versus 86+/-16 ms for lateral sites in group 3, P<0.005. The QRS-RVA time was 50+/-13 ms for apical septal VTs versus 178+/-21 ms for lateral VTs in group 1, P<0.001; 71+/-17 ms for apical septal versus 157+/-20 ms for lateral VTs in group 2, P<0.001; and 32+/-12 ms for septal versus 71+/-16 ms for lateral VTs in group 3, P<0.01. CONCLUSIONS: The QRS-RVA differs for the VT site of origin from the LV septal versus lateral apex. These data prove useful in rapidly regionalizing the VT site of origin with a V1 R-S ratio >1, particularly in instances of an apical infarct, where surface ECG distinctions are less identifiable.
Strength and knot security of braided polyester and caprolactone/glycolide suture.
BACKGROUND: Appropriate suture selection is necessary in providing mechanical stability to soft tissue reconstructions. Caprolactone/glycolide (Panacryltrade mark) became a popular suture, possessing excellent handling properties; however, clinical observations questioned the knot security of caprolactone/glycolide. Caprolactone/glycolide is still available on many commercial suture anchor systems. This study compared the security of the knots and ultimate tensile strength of braided caprolactone/glycolide suture to that of a commonly used suture material, braided polyester (Ethibondtrade mark). MATERIALS: Suture knots of No. 2 braided polyester suture and No. 2 braided caprolactone/glycolide suture were submersed in a physiologic saline solution and stressed using a continuous (non-cyclic) load, simulating a single maximal loading event in a clinical setting. Continuous loading was done to achieve clinical suture knot failure (3-mm knot slippage), then continued until catastrophic suture failure (suture breakage) occurred. Ten trials of each suture were tested. RESULTS: Force required to cause knot slippage of 3 mm was greater for braided polyester than for braided caprolactone/glycolide (p <. 0001, unpaired Students' t-test). Forces resulting in catastrophic failure were greater for braided polyester than braided caprolactone/glycolide (p = .0284, unpaired Students' t-test). CONCLUSIONS: These data have important implications in the selection of suture materials for repair of soft tissue injuries. In the clinical setting, a single maximal loading event may result in suture failure. These data indicate that braided polyester possesses superior in-vitro mechanical properties and suggest that braided polyester may provide greater security in-vivo than braided caprolactone/glycolide suture.
Effects of ethanol in an open field apparatus: modification by U50488H and WIN 44441-3.
The effects of U50488H, a kappa agonist, and WIN 44441-3, a kappa antagonist, and their modification of the effects of ethanol, on the behavior of rats in a modified open field apparatus, was examined. Crossover activity was increased by U50488H. Headpoke activity was decreased by WIN 44441-3 and increased by U50488H. Rearing activity was increased by WIN 44441-3 but was not affected by U50488H. The effect of both drugs was dose related, with the largest doses having no effect. Ethanol (0.5 g/kg) stimulated crossover activity while it depressed rearing, headpoke and corner activities; except for crossover activity the 2.0 g/kg dose of ethanol depressed these activities. Pretreatment with WIN 44441-3 (0.5 mg/kg) potentiated the stimulant effect of ethanol on crossover activity and partially reversed the depressant effect of ethanol on rearing and headpoke activities. U50488H potentiated the ethanol-induced depression of headpoke and reversed the depression of corner activity. Pretreatment with U50488H had no effect on ethanol's action on crossover and rearing behaviors. Our results indicate that kappa opiate receptors may mediate some behaviors exhibited by rats in a modified open field apparatus. Activation of these receptors increases locomotor and headpoke activity but had no effect on rearing activity. Furthermore, the 0.5 g/kg dose of ethanol has differential effects on different measures of open field behavior, while the 2.0 g/kg dose was largely depressant. Our data suggest that some of these effects of ethanol may be mediated via kappa opioid receptors.
Effects of ethanol on plasma corticosterone and rectal temperature modification by U50488H and WIN 44441-3.
Endogenous opiates are believed to subserve various behaviors and physiological functions. We have examined the effect of U50488H (0-12 mg/kg), a kappa agonist, and WIN 44441-3 (0-4.0 mg/kg), a kappa antagonist, on ethanol (ET)-induced changes in rectal temperature and in plasma corticosterone (CS) levels in rats. The 12 mg/kg dose of U50488H produced marked hypothermia, the other doses either produced hyperthermia comparable to that seen in control animals, or had no effect. The 0.5 mg/kg of WIN44441-3 had a small hypothermic effect while the 4.0 mg/kg produced hyperthermia. U50488H potentiated and the low dose of WIN 44441-3 reversed the hypothermic effect of ethanol. By contrast, neither WIN 44441-3 nor U50488H pretreatments affected the ethanol-induced elevation in plasma CS. These results indicate that kappa agonists increase plasma CS concentration and affect thermoregulatory mechanisms. Furthermore, our data indicate a possible role of endogenous kappa opioids in the hypothermic effect of ethanol, but not in the elevation of plasma CS.
Subtrochanteric shortening and derotational osteotomy in primary total hip arthroplasty for patients with severe hip dysplasia: 5-year follow-up.
Twenty-one primary hip arthroplasties were performed in Crowe grade 3 or 4 hip dysplasia using a subtrochanteric shortening osteotomy. Average patient age was 48.2 years. Average follow-up was 5.8 years (minimum, 2 years). Femoral fixation was cemented in 10 hips and uncemented in 11 hips. All acetabular components were uncemented, with 33% requiring structural autograft. Ninety-one percent of femoral osteotomies healed without complication. Two osteotomy nonunions required revision. Two acetabular revisions were performed for malposition and polyethylene failure. Three patients experienced postoperative dislocation. One cemented femoral component was revised for loosening. However, no neurologic deficiencies were identified. Harris hip score improved from 32.5 to 73.6. Limp improved in 60% of patients and dependence on assistive walking device improved in 40% of patients. Subtrochanteric shortening osteotomy is a safe and predictable method of restoring the anatomic hip center in high developmental hip dislocation. However, the complication rate in these patients is higher than primary hip arthroplasty for osteoarthritis.
Fluorescent image correlation for nanoscale deformation measurements.
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Plasma matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-2, and CD40 ligand levels in patients with stable coronary artery disease.
Endogenous matrix metalloproteinases (MMPs) and their inhibitors, tissue inhibitor of metalloproteinases (TIMPs), are important mediators of extracellular matrix remodeling, which is integral to plaque progression in coronary artery disease. In addition, high levels of the soluble fragment of CD40 ligand (sCD40L) have previously been associated with adverse cardiovascular outcomes. We hypothesized that circulating levels of MMP-9, TIMP-1, TIMP-2, and sCD40L were abnormal in patients who had stable coronary artery disease, and these levels were compared with those in matched controls. We also hypothesized correlations of MMPs, TIMPs, and sCD40L to each other and to high-sensitivity C-reactive protein (a proinflammatory marker), white blood cell count, severity of coronary artery disease (based on angiographic measurements of atherosclerotic burden), and coronary collateralization. We studied 204 adult patients who attended our unit for outpatient diagnostic cardiac catheterization for the investigation of suspected coronary artery disease. Coronary angiograms were scored for atheroma burden and stenosis by 2 independent observers. Circulating levels of MMP-9, TIMP-1, TIMP-2, and sCD40L were measured by enzyme-linked immunosorbent assay. Plasma levels of MMP-9 (p = 0.0099), TIMP-2 (p = 0.0019), and sCD40L (p <0.001), but not TIMP-1 (p = 0.463) were high in patients compared with healthy controls. In patients who had coronary artery disease, MMP-9 and high-sensitivity C-reactive protein levels were significantly higher in women than in men. Only MMP-9 correlated modestly with total white blood cell count (Spearman's correlation, r = 0.274, p = 0.002). Logistic regression of cardiovascular risk factors showed that only white blood cell count was independently associated with MMP-9 (p = 0.02). After standardizing for atheroma and stenosis scores, there were no statistically significant differences in our research indexes in patients who had angiographic collaterals compared with those who did not. In conclusion, stable coronary artery disease is associated with abnormal circulating levels of MMP-9, TIMP-2, and sCD40L, which do not appear to related to each other or to severity of coronary artery disease or collateralization. The gender difference in high-sensitivity C-reactive protein and MMP-9 levels may provide insight into the pathophysiology of coronary artery disease in men and women, and further studies are warranted to explore this potential link.
Elevations in ventricular pacing threshold with the use of the Y adaptor: implications for biventricular pacing.
Cardiac resynchronization therapy (CRT) is a new and promising therapeutic option for patients with severe heart failure and intraventricular conduction delay. Patients who are candidates for CRT and have a previously implanted device may utilize a "Y" IS 1 connector to accommodate the coronary sinus lead. This modification has the potential to alter biventricular pacing thresholds. During an 18 month period, successful biventricular pacemaker implantation was performed in 72 patients (age: 67 +/- 11 years, left ventricular ejection fraction: 20.5 +/- 5.6%). All of these patients had severe symptomatic congestive heart failure (NYHA Class III and IV). In 20 patients a special "Y" adaptor that bifurcates the ventricular IS 1 bipolar output to two bipolar outputs or one unipolar and one bipolar output was utilized. During initial implantation, LV thresholds obtained in a unipolar configuration prior to connecting to the "Y" adaptor were significantly lower than thresholds obtained after connecting to the "Y" adaptor (1.7 +/- 1.11 V at 0.5 ms pulse width versus 2.8 +/- 1.5 V at 0.5 ms pulse width [P = 0.01]). Two patients (10%) required left ventricular lead revisions due to unacceptably high left ventricular thresholds during device follow-up. The difference in measured left ventricular thresholds between the two configurations is best explained by a resistive element that is added to the circuit when performing threshold measurement of the LV lead through the "Y" adaptor (combined tip to RV ring configuration) versus measurement of the LV lead in a unipolar configuration. This resistive element represents multiple factors including anode surface area, resistive polarization at the tissue-electrode interface, and transmyocardial resistance. LV thresholds should be measured in an LV tip to RV ring configuration or ideally in a combined tip (LV and RV) to shared ring configuration in order to accurately assess LV thresholds. This observation has significant clinical implications as loss of capture may occur as a result of improper measurement of left ventricular thresholds at the time of implantation.
A whole-genome scan for obstructive sleep apnea and obesity.
Obstructive sleep apnea (OSA) is a common, chronic, complex disease associated with serious cardiovascular and neuropsychological sequelae and with substantial social and economic costs. Along with male gender, obesity is the most characteristic feature of OSA in adults. To identify susceptibility loci for OSA, we undertook a 9-cM genome scan in 66 white pedigrees (n=349 subjects) ascertained on the basis of either an affected individual with laboratory-confirmed OSA or a proband who was a neighborhood control individual. Multipoint variance-component linkage analysis was performed for the OSA-associated quantitative phenotypes apnea-hypopnea index (AHI) and body mass index (BMI). Candidate regions on chromosomes 1p (LOD score 1.39), 2p (LOD score 1.64), 12p (LOD score 1.43), and 19p (LOD score 1.40) gave the most evidence for linkage to AHI. BMI was also linked to multiple regions, most significantly to markers on chromosomes 2p (LOD score 3.08), 7p (LOD score 2.53), and 12p (LOD score 3.41). Extended modeling indicated that the evidence for linkage to AHI was effectively removed after adjustment for BMI, with the exception of the candidate regions on chromosomes 2p (adjusted LOD score 1.33) and 19p (adjusted LOD score 1.45). After adjustment for AHI, the primary linkages to BMI remained suggestive but were roughly halved. Our results suggest that there are both shared and unshared genetic factors underlying susceptibility to OSA and obesity and that the interrelationship of OSA and obesity in white individuals may be partially explained by a common causal pathway involving one or more genes regulating both AHI and BMI levels.
Whole genome scan for obstructive sleep apnea and obesity in African-American families.
Obstructive sleep apnea (OSA) is a common, chronic disease associated with obesity. OSA and obesity are both prevalent in African Americans, who are also at increased risk for secondary complications. To identify susceptibility loci for OSA, we undertook a 9-centimorgans genome scan in 59 African-American pedigrees ascertained on the basis of either an affected individual with laboratory-confirmed disease or a proband who was a neighborhood control subject. Variance component linkage analysis was performed for the quantitative phenotypes apnea-hypopnea index (AHI) and body mass index. A candidate region on chromosome 8q (logarithm of odds [LOD] = 1.29, p = 0.006) gave the only evidence for linkage to the AHI. Body mass index was linked to multiple regions, most significantly to markers on chromosome 4q (LOD = 2.63, p = 0.0006) and 8q (LOD = 2.56, p = 0.0007). Evidence of linkage to the AHI was only slightly reduced after adjustment for body mass index. After adjustment for the AHI, some of the primary linkages to body mass index were greatly reduced whereas others remained suggestive. Our results suggest that there are both shared and unshared genetic factors underlying susceptibility to OSA and obesity, and that the genetic determinants of obesity in this population may be modulated by apnea severity.
Ghrelin exerts a proliferative effect on a rat pituitary somatotroph cell line via the mitogen-activated protein kinase pathway.
OBJECTIVES: Ghrelin is a brain-gut peptide with GH-releasing and appetite-inducing activities and a widespread tissue distribution. Ghrelin is the endogenous ligand of the GH secretagogue receptor type 1a (GHS-R1a), and both ghrelin and the GHS-R1a are expressed in the pituitary. There are conflicting data regarding the effects of ghrelin on cell proliferation. A positive effect on proliferation and activation of the mitogen-activated protein kinase (MAPK) pathway has been found in hepatoma, adipose, cardiomyocyte and prostate cell lines. However, ghrelin has also been shown to have anti-proliferative effects on breast, lung and thyroid cell lines. We therefore examined the effect of ghrelin on the rat pituitary cell line GH3. METHODS: RT-PCR was used for the detection of GHS-R1a and pre-proghrelin mRNA expression in GH3 cells. The effect of ghrelin on cell proliferation was studied using [(3)H]thymidine incorporation; cell counting and the activation of the MAPK pathway were studied using immunoblotting and inhibitors of the extracellular signal-regulated kinase 1 and 2 (ERK 1/2), protein kinase C (PKC) and tyrosine phosphatase pathways. RESULTS: GHS-R1a and ghrelin mRNA expression were detected in GH3 cells. Ghrelin, at 10(-10) to 10(-6) M concentrations, significantly increased [(3)H]thymidine incorporation (at 10(-9) M, 183+/-13% (means+/-s.e.m.) compared with untreated controls), while 12-phorbol 13-myristate acetate (PMA) at 10(-7) M (used as a positive control) caused a 212+/-14% increase. A reproducible stimulatory effect of desoctanoyl ghrelin was also observed on [(3)H]thymidine incorporation (135+/-5%; P<0.01 at 10(-9) M compared with control), as well as on the cell count (control 6.8 x 10(4)+/-8.7 x 10(3) cells/ml vs desoctanoyl ghrelin (10(-9) M) 1.04 x 10(5)+/-7.5 x 10(3) cells/ml; P<0.01). Ghrelin caused a significant increase in phosphorylated ERK 1/2 in immunoblotting, while desoctanoyl ghrelin showed a smaller but also significant stimulatory effect. The positive effect of ghrelin and desoctanoyl ghrelin on [(3)H]thymidine incorporation was abolished by the MAPK kinase inhibitor U0126, the PKC inhibitor GF109203X and the tyrosine kinase inhibitor tyrphostin 23, suggesting that the ghrelin-induced cell proliferation of GH3 cells is mediated both via a PKC-MAPK-dependent pathway and via a tyrosine kinase-dependent pathway. This could also be clearly demonstrated by Western blot analysis, where a transient increase in ERK 1/2 phosphorylation by ghrelin was attenuated by all three inhibitors. CONCLUSION: We have shown a novel role for ghrelin in stimulating the proliferation of a somatotroph pituitary tumour cell line, suggesting that ERK activation is involved in mediating the effects of ghrelin on cell proliferation. Desoctanoyl ghrelin showed a similar effect. As ghrelin has been shown to be expressed in both normal and adenomatous pituitary tissue, locally produced ghrelin may play a role in pituitary tumorigenesis via an autocrine/paracrine pathway.
The relationship of in vivo 31P MR spectroscopy to histology in chronic hepatitis C.
Liver biopsy remains the gold standard for characterizing diffuse liver disease and is associated with significant morbidity and, rarely, mortality. Our aim was to investigate whether a noninvasive technique, in vivo phosphorus 31 ((31)P)-magnetic resonance spectroscopy (MRS), could be used to assess the severity of hepatitis C virus (HCV)-related liver disease. Fifteen healthy controls and 48 patients with biopsy-proven HCV-related liver disease were studied prospectively. Based on their histologic fibrosis (F) and necroinflammatory (NI) scores, patients were divided into mild hepatitis (F or= 4/18), and cirrhosis (F = 6/6). Hepatic (31)P MR spectra were obtained using a 1.5-T spectroscopy system. Quantitation of the (31)P signals was performed in the time domain using the Advanced MAgnetic RESonance algorithm. There was a monotonic increase in the mean +/- 1 standard error phosphomonoester (PME) to phosphodiester (PDE) ratios for the control, mild disease, moderate disease, and cirrhosis groups: 0.15 +/- 0.01, 0.18 +/- 0.02, 0.25 +/- 0.02, 0.38 +/- 0.04, respectively (ANOVA, P <.001). An 80% sensitivity and specificity was achieved when using a PME/PDE ratio less than or equal to 0.2 to denote mild hepatitis and a corresponding ratio greater than or equal to 0.3 to denote cirrhosis. No other significant spectral changes were observed. In conclusion, (31)P MRS can separate mild from moderate disease and these 2 groups from cirrhosis. The ability to differentiate these populations of patients has therapeutic implications and (31)P MRS, in some situations, would not only complement a liver biopsy but could replace it and be of particular value in assessing disease progression.
Spontaneous long-term remission in a patient with premature ovarian failure.
OBJECTIVE: To describe a patient with premature ovarian failure who after a pregnancy achieved a prolonged remission, which has lasted for more than 10 years. METHODS: Clinical and laboratory data of a patient who had premature ovarian failure with a spontaneous pregnancy and a prolonged remission are described. The pertinent literature is reviewed and summarized. RESULTS: A 26-year-old woman presented with secondary amenorrhea of 6 months' duration in 1984. Her serum total estrogen level was low, and gonadotropins were in the postmenopausal range. She also had a history of primary hypothyroidism, diagnosed in 1979. The physical examination showed normal findings, except for an enlarged thyroid gland and a few areas of vitiligo on her back, arms, and legs. Antithyroid antibodies were present. Adrenal insufficiency was excluded on the basis of results of the cosyntropin stimulation test. She had a normal 46,XX karyotype. A diagnosis of premature ovarian failure was made, and therapy with cyclic estrogen and progesterone was initiated. In 1991, she spontaneously conceived and gave birth to a healthy baby. After delivery, the patient began to have normal menstrual cycles and continues to do so without hormone replacement therapy. Subsequently, serum estrogen and gonadotropins were in the normal range. Her thyroid antibodies also became negative. When last contacted by her primary-care physician in November 2002, she was still having normal menstrual periods, and the patches of vitiligo were no longer present. CONCLUSION: It is well known that many autoimmune diseases subside during pregnancy; however, most of them relapse in the postpartum period. The mechanism of the prolonged remission in our patient is unknown, but hormonal as well as autoimmune changes related to pregnancy and the post partum period might have had a role.
Steroidogenic factor-1 and the gonadotrope-specific element enhance basal and pituitary adenylate cyclase-activating polypeptide-stimulated transcription of the human glycoprotein hormone alpha-subunit gene in gonadotropes.
In the anterior pituitary, expression of the common glycoprotein hormone alpha-subunit (alphaGSU) is mediated in part by multiple response elements residing in the distal promoter (-435 bp). One such site is the gonadotrope-specific element (GSE), which is bound by the orphan nuclear receptor steroidogenic factor-1 (SF-1) and confers pituitary adenylate cyclase-activating polypeptide (PACAP)-stimulated alphaGSU expression. Here we investigated the functional importance of the GSE and SF-1 phosphorylation in both basal and stimulated alphaGSU transcription. Mutation of the GSE reduced basal and PACAP-stimulated alphaGSU promoter activity in the alphaT3-1 gonadotrope cell line. Overexpression of wild-type SF-1, but not an S203A mutant form of SF-1, enhanced basal and PACAP-stimulated alphaGSU promoter activity. The effect of PACAP on alphaGSU promoter activity was inhibited after overexpression of MAPK phosphatase. Helix assembly of the SF-1 ligand-binding domain was stimulated by PACAP in vitro via a MAPK-dependent pathway, as determined using a mammalian two-hybrid assay. PACAP quickly activated MAPK (within 5 min) and also resulted in elevated levels of phospho-cAMP response element-binding protein and phospho-SF-1, as judged by a specific antiphospho-S203 antibody; this effect was blocked by the MAPK kinase inhibitor, UO126. Collectively, these data demonstrate that SF-1 binds to the GSE and activates both basal and PACAP-stimulated alphaGSU transcription, which is further increased by phosphorylation at Ser203 via MAPK. These data suggest strongly that the induction of alphaGSU gene expression by peptide hormone signaling is coupled directly to the posttranslational status of SF-1.
Caloric restriction attenuates Abeta-deposition in Alzheimer transgenic models.
Dietary influences on Alzheimer disease (AD) are gaining recognition. Because many aging processes are attenuated in laboratory mammals by caloric restriction (CR), we examined the effects of short-term CR in two AD-transgenic mice, APP(swe/ind) (J20) and APP(swe) + PS1(M146L) (APP + PS1). CR substantially decreased the accumulation of Abeta-plaques in both lines: by 40% in APP(swe/ind) (CR, 6 weeks), and by 55% in APP + PS1 (CR, 14 weeks). CR also decreased astrocytic activation (GFAP immunoreactivity). These influences of CR on AD-transgenic mice are consistent with epidemiological reports that show that high caloric diets associate with the risk of AD, and suggest that dietary interventions in adult life might slow disease progression.
Infections due to nontuberculous mycobacteria in kidney, heart, and liver transplant recipients.
Infections due to nontuberculous mycobacteria (NTM) in solid-organ transplant recipients are infrequent but may be a major cause of morbidity. We describe four cases of NTM infection in solid-organ transplant recipients. The manifestations included a nodule secondary to Mycobacterium kansasii infection in a heart transplant recipient, a cutaneous lesion and a pulmonary nodule secondary to M. kansasii infection in a renal transplant recipient, tenosynovitis secondary to Mycobacterium chelonae infection in a renal transplant recipient, and cutaneous lesions secondary to M. chelonae infection in a liver transplant recipient. We also summarize previously reported cases of NTM infections in solid-organ transplant recipients; common manifestations of NTM infections in solid-organ transplant recipients include cutaneous lesions of the extremities, tenosynovitis, and joint infection. Histopathologic examination of aspirates or biopsy specimens from involved areas and staining and culture for mycobacteria are essential for diagnosis. Treatment of NTM infection most commonly involves surgery, reduction in doses of immunosuppressive medications, and/or therapy with antimycobacterial medications; these treatments are often associated with a good outcome.