Corticosteroid injection for trigger finger: blinded or ultrasound-guided injection?

INTRODUCTION: Trigger digit is one of the most common causes of pain and disability in the hand. The mainstay of conservative treatment of this disease has been local steroid injection into the tendon sheath. The aim of this study was to investigate the clinical benefit of an ultrasound-guided corticosteroid injection compared to a blinded application. MATERIALS AND METHODS: 74 patients, who suffered from persistent or increasing symptoms of a single trigger digit, were enroled in this prospective, randomised case-control study. All patients were treated with an injection of 40 mg/1 ml methylprednisolone acetate into the flexor tendon sheath at the level of the A1 pulley. Half of the patients had their injections under ultrasound control (USG) and half without (blinded injection group, BIG). Associated metabolic diseases were recorded. At the 6-week and 6-month follow-up examinations, the complication rate and the need for a second injection were assessed. The outcome was rated using the Quinnell grading. The pain level was assessed using the visual analogue scale. RESULTS: Four patients were excluded due to lack of follow-up. Both study groups were comparable in respect of age, hand dominance and associated diseases. There were significantly more female patients in the USG group (32 versus 23 %). After the corticosteroid injections, all patients improved significantly in terms of pain level and the Quinnell grading at 6 weeks and 6 months after the intervention in comparison to the pre-injection status. There were no significant differences between the groups. 9 patients (13 %) needed a second injection (6 of BIG, 3 of USG), all of whom had diabetes mellitus. No local complications were seen after the injections. CONCLUSION: The use of ultrasound-guided injection of corticosteroid may be associated with extra time and effort, with no superior clinical benefits compared to the blinded technique. LEVEL OF EVIDENCE: Level 1(prospective randomised study).

Sheehan's syndrome co-existing with Graves' disease.

Sheehan's syndrome (SS), which is an important cause of hypopituitarism, is common in developing countries. The most common presentation is the absence of lactation and amenorrhea. Hypothyroidism rather than hyperthyroidism is the usual expected phenomenon in SS. Postpartum hyperthyroidism is also common and Graves' disease (GD) is an important cause of postpartum hyperthyroidism. Here we report a case of a 22-year-old female patient in our clinic presented symptoms of amenorrhea, lack of lactation, palpitations and sweating. Her physical examination revealed goiter, moist skin and proptosis. Her laboratory evaluation showed suppressed thyroid stimulating hormone, elevated levels of free thyroxine and free triiodothyronine. Thyroid antibodies were positive. Tec 99m thyroid scintigraphy results were gland hyperplasia and increased uptake consistent with GD. She gave birth 7 months ago; after delivery she had a history of prolonged bleeding, amenorrhea and inability to lactate. She had hypogonadotropic hypogonadism, hyperprolactinemia and growth hormone deficiency. Serum cortisol and adrenocorticotropic hormone levels were normal. Her magnetic resonance imaging was empty sella. Our diagnosis was GD co-existing with SS. GD with concomitant hypopituitarism is rare but has been described previously, but there are no reports of GD occurring with SS. In this case study, we report a patient with GD associated with SS.

A study of 60 patients with percutaneous trigger finger releases: clinical and ultrasonographic findings.

We present the clinical results and ultrasonographic findings of 61 trigger digits treated with percutaneous A1 pulley release. An endoscopic carpal tunnel knife was used for the release in the outpatient department. The mean follow-up period was 3.5 months. A total of 55 digits (90%) had complete relief of their triggering postoperatively. Six digits (10%) had Grade 2 triggering clinically in the early postoperative period.The complications included six cases of insufficient release (10%), scar sensitivity in one patient, short-term hypoaesthesia in three digits (5%), and flexor tendon laceration noted on postoperative ultrasonography in eight digits (13%). No neurovascular damage was noted on the postoperative ultrasonography. Ultrasonograpy provides information about tendon laceration and changes in thickness of the pulleys and confirm A1 pulley release after surgery, but it does not alter clinical decision-making. We believe that pre- and postoperative ultrasonograpy does not need to be included as a routine examination.

Prevalence of primary Sjogren's syndrome in Turkey: a population-based epidemiological study.

OBJECTIVES: The aim of this study was to determine the prevalence of primary Sjogren's syndrome (pSS) in a general Turkish population according to the latest proposed American-European Consensus Group (AECG) criteria and European-1 (EU-1) criteria. METHODS: The study was conducted in two districts of Izmir and involved 2835 subjects 20 years of age and older. In the first stage, face-to-face interviews were performed at the registered households. In the second stage, subjects reporting symptoms of both dry eye and dry mouth were invited to the hospital for a full examination, which included Schirmer-1, sialometry and serologic tests. In the third stage, a minor salivary gland biopsy was performed as required. RESULTS: A total of 2887 subjects were contacted and a complete interview was obtained for 2835 (1551 female, 1284 male) subjects. A total of 159 subjects (126 female, 33 male) confirmed oral and ocular dryness, and 86 of these patients (54.1%) underwent a detailed clinical examination in the hospital. pSS was diagnosed in 10 patients (nine females) according to the EU-1 criteria, and in six patients (six females) according to the AECG criteria. We found a minimum crude prevalence of 0.21% [95% confidence interval (CI): 0.03-0.29] in the sample population and an age-sex adjusted prevalence of 0.16% (95% CI: 0.06-0.35), according to AECG criteria. According to EU-1 criteria, these prevalence rates were found to be 0.35% (95% CI: 0.10-0.45) and 0.28% (95% CI: 0.13-0.51) respectively. CONCLUSION: The pSS prevalence rates found in the Turkish population in this study were lower than the estimated prevalence rate in a general population.

Blood coagulation, fibrinolysis and lipid profile in patients with primary hyperparathyroidism: increased plasma factor VII and X activities and D-Dimer levels.

BACKGROUND AND OBJECTIVES: Primary hyperparathyroidism (PHPT) is associated with an increased cardiovascular mortality and morbidity rate. However, the exact role of PTH and/or calcium in the development of cardiovascular disease (CVD) is still controversial. The influence of PHPT on hemostasis is yet unknown. Therefore, the main purpose of this study was to investigate the markers of endogenous coagulation/fibrinolysis and to evaluate the relationships between these hemostatic parameters, serum lipid profile and serum calcium and PTH in patients with PHPT. DESIGN AND METHODS: Twenty-three patients with PHPT and 20 age-matched healthy controls were included in the study. Fibrinogen, factors V, VII, VIII, IX and X activities, von Willebrand factor (vWF), antithrombin III (AT III), protein C, protein S, tissue plasminogen activator (t-PA) and tissue plasminogen activator inhibitor-1 (PAI-1), as well as common lipoprotein variables, were measured. The relationships between biochemical parameters and these hemostatic parameters were examinated. RESULTS: Compared with the control subjects, platelet count, FVII, FX activities, and D-Dimer levels were significantly increased in patients with PHPT (p<0.001, p<0.05, p<0.001, and p<0.05, respectively). Among the lipids, the levels of TC, TG and LDL-C were significantly increased in patients with PHPT (p<0.01, p<0.001, p<0.001, respectively) than those in controls. In patients with PHPT, we showed a positive correlation between urinary phosphorus excretion and factors VIII, IX, and X (r: 0.572, p<0.01; r: 0.543, p<0.01; r: 0.532, p<0.01, respectively). F IX activity was positively correlated with TC (r: 0.463, p<0.05) and LDL-C (r: 0.549, p<0.01) There was a positive correlation between serum ALP and PAI-1 levels (r: 0.451, p<0.05). ApoB was positively correlated with D-Dimer (r: 0.421, p<0.05). We did not find any significant correlation between iPTH and serum calcium and the hemostatic parameters that we measured. INTERPRETATION AND CONCLUSIONS: In conclusion, we found some important differences in the hemostatic parameters between the patients with PHPT and healthy controls. Increased platelet count, F VII and FX activities and D-Dimer levels in patients with PHPT represent a potential hypercoagulable state, which might augment the risk for atherosclerotic and atherothrombotic complications. This condition may contribute to the excess mortality rate due to CVD in patients with PHPT.

Hyperuricemia influences chronic cyclosporine nephropathy.

BACKGROUND: The observation that long-standing hyperuricemia is associated with chronic tubulointerstitial disease, afferent arteriolopathy, intrarenal vasoconstriction, and increased vascular resistance raises the hypothesis that hyperuricemia might contribute to chronic cyclosporine (CsA) nephropathy. The aim of the present study was to investigate the effect of hyperuricemia on chronic CsA nephropathy. METHODS: Patients who were treated with CsA-based immunsuppressive regimens and underwent a renal biopsy were enrolled in this case-control study. We retrospectively obtained posttransplant baseline serum creatinine, uric acid (UA), mean serum UA, and creatinine values 3 months prior to biopsy. CsA trough levels, mean blood pressure, diuretic and antihypertensive treatment were recorded. Biopsy specimens showing CsA nephropathy (n = 34) were revaluated by a pathologist to score CsA nephropathy according to recent quantitative criteria for calcineurin inhibitor arteriolopathy as proposed by M.J. Mihatsch. RESULTS: As compared with the non-CsA nephropathy group, recipient and donor ages, donor origin and cold ischemia times were similar for the CsA nephropathy group (P > .05). Mean CsA doses, CsA trough (C(0)), and C(2) levels were not different between the groups (P > .05). Systolic and diastolic blood pressure, glomerular filtration rate, diuretic usage, and antihypertensive treatment were also similar in CsA nephropathy and non-CsA nephropathy groups (P > .05). Mean serum UA level within 3 months prior to biopsy in the CsA nephropathy and non-CsA nephropathy groups were 7.5 +/- 1.4 mg/dL versus 5.7 +/- 1.4 mg/dL, respectively (P < .001). CONCLUSION: Hyperuricemia seems to exacerbate CsA-induced nephropathy.

Evaluation of telomerase activity in gingival fibroblasts of cyclosporine-treated patients.

Gingival overgrowth (GO) is a common side effect following administration of cyclosporin A (CsA). Various case reports have shown that squamous cell carcinomas could arise in GO induced by CsA and phenytoin. It is also known that human telomerase activated in about 90% of cancers is mainly composed of hTR, hTERT, and TPI. The aim of this study was to investigate the potential role of telomerase activity in the pathogenesis of CsA-induced GO. Included in the study were 9 patients on CsA: 4 with and 5 without GO. Gingival tissues were obtained during gingivectomy or flap procedures; gingival fibroblasts were cultured in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10,000 U/mL penicillin, 10 mg/mL streptomycin, 2 mmol/L l-glutamine, and 10% heat-inactivated fetal bovine serum at 37 degrees C under a humidified 95% air virgule 5% CO(2) atmosphere. Quantitative detection of hTERT mRNA was performed with the commercially available LightCycler Telo TAGGG hTERT Quantification Kit using real-time online PCR. The hTERT mRNA expression was positive in one patient, while hTERT mRNA expression was negative in the others. Because results indicated that there may be a relationship between CsA-induced GO and positive telomerase activity, detailed studies should be performed to confirm the present findings.

Vascular endothelial growth factor expression and vascularity in renal allograft biopsies.

BACKGROUND: Vascular endothelial growth factor (VEGF) expression influences tubular repair and promotes angiogenesis. The aim of the present study was to determine the relation of VEGF expression and cortical vascularity with renal pathological changes and clinical parameters in allograft biopsies. MATERIALS AND METHODS: Sections from 50 renal allograft biopsies were evaluated by streptavidine-biotin immunohistochemistry by primary antibodies against VEGF and CD34. Cortical tubulointersititial (TI) VEGF expression was scored by light microscopic examination considering intensity and density. Glomerular expression was scored as 0: no staining; 1: faint staining in less than 50% of glomeruli; 2: moderate to strong staining in more than 50% of glomeruli. We determined the number of vessels per cortical high power field (Nves) highlighted by CD34 staining. The clinical and pathological features were retrieved from patient files. RESULTS: Nves was decreased with interstitial fibrosis (IF): 56.3 +/- 3.7; 53.3 +/- 9.8, 46.6 +/- 10.5, 36.75 +/- 1.89 for cases with no IF to mild, moderate, and severe forms, respectively (P << .000). There was increased TI VEGF expression: 1.86 +/- 2.12, 5.8 +/- 3.1, 5.85 +/- 4.4, 10.25 +/- 2.06, respectively (P = .004). The NVes values were not different for cases with high and low to negative VEGF expression scores. There was a negative correlation between Nves values and creatinine at the time of biopsy and time from transplantation to biopsy (r = -.325, P = .024 and r = -.294, P = .038, respectively). Nves and VEGF scores were not different when acute rejection scores or cyclosporine toxicity were considered (P > .05), while Nves were significantly different for chronic allograft nephropathy scores (P = .05). CONCLUSIONS: Chronic renal changes seemed to be associated with decreased cortical vascularity in renal allografts, while the TI VEGF expression was increased. In contrast Nves was not increased with VEGF expression in this series. It seems that along with VEGF, other factors are required for protection against vascular reduction. The aging of the allograft is also a negative influence on cortical vascularity.

Successful therapy with rituximab of refractory acute humoral renal transplant rejection: a case report.

Acute humoral rejection (AHR) is generally less responsive to conventional anti-rejection treatment with consequent allograft losses. Therapeutic options include antilymphocyte antibody (ATG), intravenous immunglobulin (IVIG), plasmapheresis, or immunoadsorption with protein A together with intensification of immunsuppression with a tacrolimus/mycophenolate mofetil combination. This report describes a transplant recipient who responded to rituximab therapy as treatment for steroid-, ATG-, IVIG-, and plasmapheresis-resistant AHR.

A renal transplant recipient with delayed gastric emptying in amyloidosis due to familial Mediterranean fever improved with erythromycin: a case report.

Patients with systemic amyloidosis often have symptoms related to impared gastrointestinal motility due to delayed gastric emptying, which results from autonomic nerve or smooth muscle infiltration with amyloid. There is no current report about gastric delaying secondary to amyloidosis due to familial Mediterranean fever. In this report, we have described a renal transplant recipient with delayed gastric emptying secondary to amyloidosis due to familial Mediterranean fever, which improved with erithromycin treatment.

Outcome of kidney transplantation for renal amyloidosis:a single-center experience.

The aim of this retrospective study was to investigate the results of kidney transplantation in patients with renal amyloidosis. We analyzed the results of renal transplantation in 13 amyloidotic transplant recipients compared with those in a control group of 13 nonamyloidotic patients. While the etiology of amyloidosis was rheumatoid arthritis in one patient, in all of the others it was secondary to familial Mediterranean fever. Acute rejection episodes developed once in six and twice in one patient. The renal function in these patients was improved by antirejection treatment. Chronic rejection did not develop in any patient. However six patients (46%) died due to various complications despite functional grafts. The others are still being followed with well-functioning grafts. Among the control group, acute and chronic rejection were diagnosed in three and two patients, respectively: one patient returned to hemodialysis after 26 months of transplantation, while the others are still alive with functional grafts. There was no death in the control group. The 5- and 10-year actuarial patient survival rates of the amyloidosis and control groups were 52.2%, 26.6%, and 100%, 100%, respectively (P = .002). However, the graft survivals of the amyloidosis versus control groups were 100%, 100%, versus 87.5%, 87.5, respectively (P = .47). In conclusion, we observed a high rate of early mortality among recipients with amyloidosis associated with infectious complications. Moreover, patient survivals were lower among amyloidotic renal recipients.

Association of corticosteroids and factor V, prothrombin, and MTHFR gene mutations with avascular osteonecrosis in renal allograft recipients.

The mechanism of posttransplantation avascular osteonecrosis (AVN) is controversial. Besides an increased bone marrow pressure due to reduced blood supply, enhanced coagulation has been considered. We investigated the associations of factor V Leiden, prothrombin G20210A, and MTHFR C677T mutations as well as cumulative corticosteroid doses with AVN in renal allograft recipients. The records of 39 volunteer patients and 11 patients in whom osteonecrosis was previously identified were reviewed for cumulative corticosteroid dosages during the first year. All patients were screened for factor V Leiden, prothrombin G20210A, and MTHFR C677T mutations by direct sequencing of genomic DNA. The cumulative corticosteroid dosages at 3, 6, and 12 months in the osteonecrotic group (5033.5 +/- 1565.3, 7164.9 +/- 2063.1, 8835.1 +/- 2216.8 mg) were significantly higher than in the control group (3629 +/- 1504.1, 4784.5 +/- 1568.7, 6322.4 +/- 1686.6 mg; P = .013, P = .001, P = .001, respectively). No significant difference in factor V Leiden, prothrombin G20210A, and MTHFR C677T mutations was observed between the osteonecrotic and control groups (P > .05). In conclusion, an association between the first year (3, 6, and 12 month) cumulative corticosteroid dosages and AVN was demonstrated in renal transplant recipients. However, no correlation was determined between factor V Leiden, prothrombin G20210A, and MTHFR C677T mutations and osteonecrosis.

Does hepatic vein outflow obstruction contribute to the pathogenesis of hepatocellular carcinoma?

Hepatocellular carcinoma (HCC) is one of the more common malignant diseases in the world. Here we have investigated role of hepatic venous outflow obstruction in the development of HCC. During a 10-year period from November 1986 to December 1996, 1,748 patients with clinical evidence of either portal hypertension, hepatic venous outflow obstruction, or inferior vena cava obstruction without Behçet's disease (BD) and 512 patients with Behçet's disease were examined at Hacettepe University Hospital. The presence of and the effect of hepatic venous obstruction on the subsequent development of HCC was assessed. In each case, hepatic vein thrombosis was assessed by hepatic venography and by digital subtraction angiography (DSA), computed tomography (CT), ultrasonography (US), and liver biopsy. Coagulation factors, including protein C, protein S, anti-thrombin III, and routine laboratory studies assessing the coagulability of blood were also investigated. The role of hepatic venous outflow obstruction on the subsequent development of HCC was determined by periodic laboratory investigations that included alpha-fetoprotein (AFP), ultrasonography, and when indicated liver biopsy. During the same time period all patients diagnosed as having HCC were investigated to identify all potential etiologic factors responsible for the HCC. Fifty-five (10.7%) of the 512 patients with BD were found to have one or more large vein thromboses. Sixteen of these 55 (29%) patients had hepatic vein thrombosis. During the follow-up period HCC developed in 2 of these 16 patients (12.5%), 34 and 21 months after a diagnosis of hepatic vein thrombosis was established. Forty patients from a total of 1,748 patients with clinical evidence of portal hypertension and cirrhosis, but without BD, were found to have evidence of hepatic vein thrombosis. Twenty-one of these 40 patients had an identifiable underlying disorder responsible for their hepatic vein thrombosis. Despite a full clinical and laboratory investigation in the other 19 patients, the etiologic factor responsible for the hepatic vein thrombosis remained obscure. Only one of these 19 patients, who also had portal vein thrombosis, developed HCC during a 9-year follow-up. Thus, a total of three of the 56 (5.36%) of cases of hepatic vein thrombosis developed an HCC. All of the hepatic tumors were of the multicentric, nodular, rapidly growing type. Despite the presence of hepatic vein thrombosis, there was no clear-cut histologic evidence for cirrhosis. Our experience suggests that hepatic vein thrombosis may be a contributing factor responsible for HCC development. Moreover, we advise that individuals with hepatic vein thrombosis should be assessed periodically for the development of HCC.

What is the association of primary sclerosing cholangitis with sex and inflammatory bowel disease in Turkish patients?

BACKGROUND/AIMS: In the Western world, primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease that is associated with inflammatory bowel disease (IBD), particularly chronic ulcerative colitis and, to a lesser degree, Crohn's disease. The goal of this study was to determine the prevalence of PSC in Turkish patients with IBD and chronic amebic colitis, a disease that is endemic in Turkey. METHODOLOGY: During a 10-year period, between 1986 and 1996, a total of 81 IBD (64 ulcerative colitis and 17 Crohn's disease) patients and 127 patients with chronic amebic colitis were seen and evaluated with radiologic, serologic, immunologic and pathologic tests. Whenever a clinical or biochemical finding suggested the presence of co-existent hepatic and/or biliary disease, the patient was further evaluated by liver biopsy, auto-antibodies and endoscopic retrograde cholangiopancreatography (ERCP) to determine whether they also had PSC or some other form of liver disease. As a disease control group, a total of 752 patients with clinical and/or laboratory evidence of pancreaticobiliary disease were also studied. In 86 of these 752 patients (10%), a primary disorder of the biliary tree was diagnosed by ultrasonography, computed tomography, peritoneoscopy, liver biopsy, ERCP and abdominal laparotomy. In addition, all 86 patients of the control group were evaluated endoscopically in order to determine whether they had any associated gastrointestinal condition of the upper or lower gastrointestinal tracts. After establishing final diagnoses of IBD, amebic colitis and PSC, these patients were evaluated with respect to their socio-economic status. A high protein diet (1.8 gram/kg/day) was administered to those patients with chronic amebic colitis and IBD during the active period of the disease. RESULTS: Of the 208 patients (81 with IBD and 127 with chronic amebic colitis), no cases of PSC were identified. Of the 86 patients in the control group with primary biliary tract disease, 45 had a biliary system malignancy, 14 had primary biliary cirrhosis (PBC), 16 had PSC, 3 had Caroli's disease, 6 had a common bile duct cyst, and 2 had gallbladder adenomatosis. All but 1 of the 16 patients with PSC were female. CONCLUSIONS: These data suggest that, in contrast to findings in Western Europe and the USA, in Turkey: 1) PSC is not regularly associated with idiopathic IBD; 2) most patients with PSC are female; 3) PSC accounts for only 18% of patients with a primary disorder of the biliary tree; 4) the incidence of small-duct primary sclerosing cholangitis is greater than that reported in the literature; and, 5) the incidence of IBD and PSC in Turkey is relatively lower than in other countries.

The effect of interferon and desferrioxamine on serum ferritin and hepatic iron concentrations in chronic hepatitis B.

BACKGROUND/AIMS: Recent reports indicate that an individual's iron status might affect the response rate achieved with Interferon therapy for the treatment of chronic viral hepatitis. METHODOLOGY: Forty individuals, 29 men and 11 women, with chronic viral hepatitis B, who had elevated serum ferritin levels, were randomized to receive either Interferon (IFN) 5 MU TIW SQ for 6 months alone (n=21) or Interferon in combination with repetitive cycles of desferrioxamine infused at a dose of 80 mg/kg per cycle (n=19) over 3 consecutive days in an effort to reduce their metabolically active iron pool during the course of IFN treatment. These cycles were continued until a serum ferritin level of less than 250 ng/ml (normal values <220 ng/ml) was achieved. Additionally, all desferrioxamine treated subjects were placed on a low iron containing diet. An interferon response was defined as normalization of the serum ALT and seroconversion from eAg positive to eAb positive. All other responses were defined as failures. RESULTS: The mean ages of the subjects in the 2 groups were 39+/-6 and 38+/-5 years. The initial serum ALT levels were 150+/-27 and 151+/-13 IU/l. The hepatic iron concentrations were 916+/-29 and 896+/-15 microg/g/dry liver weight. The serum ferritin levels were 386+/-12 and 393+/-18 ng/ml. None of these values differed significantly between the 2 treatment groups. The desferrioxamine treated group consisted of 14 men and 5 women. This group experienced a reduction in their serum ferritin to a level of 237+/-13 ng/ml as a result of the desferrioxamine treatment (p<0.05). Additionally, a reduction in their hepatic iron concentration, to a level 766+/-29 microg/g/dry liver weight, occurred with treatment (p<0.05). Twelve of the 19 (63%) desferrioxamine-treated subjects and 8 of the 21 (38%) control subjects experienced a normalization of their serum ALT levels with treatment (p<0.05). Thirteen of 19 (68%) of the desferrioxamine-treated subjects but only 8 of 21 (38%) of the IFN alone treated group seroconverted to anti-e positive (p<0.05). Moreover, a greater improvement in the hepatic histologic score and rate of HBV-DNA loss occurred in the desferrioxamine-treated group. CONCLUSIONS: Based upon these data, it can be concluded that desferrioxamine infusion to achieve a normal serum ferritin level enhances the likelihood of an individual with chronic hepatitis B responding to IFN therapy. The precise mechanism responsible for this phenomenon is not clear, but would appear to be due to a reduction in the hepatic free iron pool as reflected by sequential changes in the serum ferritin and hepatic iron concentrations.

Comparative SEM study on the effect of different demineralization methods with tetracycline HCl on healthy root surfaces.

Periodontal regeneration through the use of root demineralization received a lot of interest in periodontology. Topical application of acid to dentin surfaces produced a zone of demineralization, exposing dentin collagen fibrils and opening dentin tubules. In this study, the in vitro effects of different tetracycline HCl application techniques were investigated. According to the results of this SEM study, it may be desirable to apply tetracycline HCl using burnishing technique to expose maximum intertubular fibrils and for the tubular openings. However, this technique should be studied when placed in an in vivo system.

Human papillomavirus in a patient with severe gingival overgrowth associated with cyclosporine therapy. A case report.

Cyclosporin a is an endecapeptide that has been used clinically since 1978 as an immunosuppressant agent. Although cyclosporine appears to be uniformly beneficial in the treatment of a wide variety of disorders, its use may result in a number of side effects. One of the most important adverse effects is gingival overgrowth. This report relates a case of severe gingival overgrowth in a 31-year-old female who had received cyclosporine therapy in conjunction with a kidney transplant. Because of the severe gingival overgrowth, we analyzed a biopsy, which was positive for human papillomavirus. The case was treated and followed for 18 months.

Infantile genetic agranulocytosis (Kostmann type). A case report.

Severe periodontitis in a patient with infantile genetic agranulocytosis (Kostmann syndrome) is presented. This rare syndrome is inherited as an autosomal recessive pattern and characterized by severe neutropenia. The periodontal status and treatment of the patient is described. It is concluded that periodontal therapy including scaling, root planning, soft tissue curettage, and the use of selected antimicrobial agents can be successful in this particular syndrome.