Tc-99m HMPAO SPECT imaging of the central nervous system in tuberous sclerosis

Tc-99m HMPAO was used to evaluate cerebral perfusion in a patient with tuberous sclerosis. The SPECT images demonstrated reduced HMPAO uptake in regions corresponding with MRI-confirmed locations of cortical tubers. These results indicate that the lesions are characterized by vascular perfusion deficits and support the hypothesis that cortical tubers result from developmental abnormalities of the embryonic central nervous system.     

Drug mixture which improves survival of ischemic rabbit epigastric skin flaps

The chief aim of this study was to maximize flap survival by counteracting the pathophysiological changes occurring during ischemia-reperfusion. Rabbit epigastric skin flaps given 21 hours of ischemia were infused intra-arterially with selected drugs at the start of reperfusion. Compared with control infused ischemic flaps, which had a 33% survival rate on day 7 post-ischemia, significant improvement was found with vasodilators nitrendipine (61%) and prostacyclin (65%) and the thrombolytic agent urokinase (65%); marginal improvement with the free radical scavenger desferrioxamine (53%); but no change with streptokinase (44%), heparin (21%), and ATP-MgCl₂ (35%). A drug mixture comprising all of these agents except streptokinase and urokinase produced 87% survival, suggesting an additive effect. Biochemical assays on skin homogenates and blood implicated oxygen free radicals, neutrophil infiltration, and thromboxane in flap failure. These results imply that multiple factors are responsible for ischemic flap failure and that a mixture of drugs needs to be infused to counteract all of the detrimental changes. © 1994 Wiley-Liss, Inc.     

Capillary anastomosis in vena caval thrombosis

A 29-year-old woman presented with recurrent diffuse histiocytic lymphoma. Bilateral brachial venous catheters were placed for chemotherapy, which resulted in thrombotic occlusion of the superior vena cava. A lung scan with Tc-99m MAA (flow study and static images) demonstrated extensive collateral vessels in the upper thorax and trapping of particles in the right upper abdomen, anteriorly. A simultaneous liver scan with Tc-99m sulfur colloid (flow and delayed images) illustrated a normal liver with no other abnormal sites of tracer deposition. The accumulation of a lung imaging agent in the anterior abdominal wall was secondary to capillary anastomosis between the superior and inferior epigastric veins.     

Infection and immunoregulation of T lymphocytes by parainfluenza virus type 3.

Human parainfluenza virus type 3 (HPIV3) is a major cause of disease in newborns and infants. It also has a striking potential to reinfect individuals throughout their lives, suggesting that HPIV3 does not induce lifelong immunity; however, the operative mechanism for the failure to prevent reinfection is not known. We have assessed the potential of the virus to infect nontransformed human T lymphocytes and have found that T cells are readily infected by the virus. Productive infection requires activation of the T cells and results in a marked inhibition of proliferation. Furthermore, our results indicate that exposure to the virus, even without overt expression of viral proteins as detected by immunohistology, profoundly alters the functional capacity of the T cells. The capacity of the virus to regulate T-lymphocyte function may play an important role in the failure of the virus to induce lifelong immunity.     

T-cell influence on the B-cell differentiation process induced by Klebsiella

Klebsiella pneumoniae K43 cell membrane preparations (Klebs M) have been characterized previously as a human polyclonal B cell activator (PBA) that stimulates purified B cells to differentiate into immunoglobulin (Ig) secreting cells with negligible prior or parallel proliferation and in the absence of T cells. The aim of the present study was to define the cellular interactions in the regulation of Klebs M induced B-cell differentiation. For this purpose OKT4+ and OKT8+ cell populations were negatively selected with reasonable purity by means of a panning technique or by complement-mediated cytolysis using monoclonal OKT4 and OKT8 antibodies. The resulting cell populations were added to purified autologous B cells exposed to Klebs M or, as a control, pokeweed mitogen (PWM). In the Klebs M system both the OKT4+ and the OKT8+ cell subsets markedly enhanced IgM production; however, the helper effect of the OKT4+ cell subset was much more intense than that of the OKT8+ subset. In the PWM system only the OKT4+ cells provided help for B-cell differentiation. The OKT8+ subset demonstrated suppressor activity in the presence of an adequate helper cell (OKT4+ subset) function. These results indicate that Klebs M behaves like a "relatively T cell-independent PBA".     

Assessment of the viability of microvascularized bone grafts after mandibular reconstruction by means of bone SPET and semiquantitative analysis

The purpose of this study was to investigate the value of bone scintigraphy including single-photon emission tomography (SPET) and semiquantitative analysis for the assessment of graft viability following microvascularized bone transplantation. We evaluated 60 scintigraphic studies of 36 patients with 39 bone grafts. Thirty-four investigations were performed 6-11 days (early bone scans) and 26 up to 11 months (late bone scans) after mandibular reconstruction. After administration of 550 MBq technetium-99m methylene diphosphonate, planar scintigrams and a SPET study were performed. The data were reconstructed iteratively. Scans were evaluated visually and semiquantitatively by a region of interest technique using the ratio between transplant and cranium (T/C). Patients with uncomplicated healing showed a T/C ratio >1.0 in early and late bone scans. In cases with necrosis, the T/C ratio was below 1.0 when performing early bone scans. However, in late bone scans, some patients with necrosis showed a slightly increased uptake and a T/C ratio >1.0. The data demonstrate that as early as 6-11 days after mandibular reconstruction, increased tracer uptake proves that the surgery has been successful and indicates a normal healing process. Especially in the early bone scans no false-positive or false-negative results were observed and the T/C ratio clearly differentiated between vital and non-vital bone grafts. At later times false-positive findings could be observed; these were, however, rare because of the significantly higher tracer uptake of the healthy grafts when compared with completely or partially necrotic transplants.     

Relevance of underlying disease and bacterial vacA and cagA status on the efficacy of Helicobacter pylori eradication

AIM: To study the effects of Helicobacter pylori associated diseases and the bacterial vacA and cagA statuses on the efficacy of H. pylori eradication. METHODS: A prospective study in a consecutive series of outpatients of a gastroenterological institution and of a primary practice. A series of 146 H. pylori positive patients with peptic ulcer disease (PUD; n = 40) or nonulcer dyspepsia (NUD; n = 106) were evaluated. H. pylori vacA genotpyes and cagA status were determined directly in gastric biopsy specimens by polymerase chain reaction. The patients were treated with triple-therapy regimens consisting of a proton pump inhibitor and two antibiotics twice daily for 7 days. Reevaluation of H. pylori was determined 4-5 weeks later by endoscopy or 13C urea breath test. RESULTS: 123 patients completed the study. In 8 patients, colonization with two or more H. pylori strains was found. The overall cure rate was 84.6% (104/123). The eradication rates were significantly higher in patients with PUD (94.4%, 34/36) than in those with NUD (81.6%, 71/87; p < 0.05). In patients with cagA-positive H. pylori strains, the eradication rate was 89.0% (73/82) as compared with 78.8% (26/33) in those with cagA-negative strains (p = 0.15). The vacA genotype had no effect on the efficacy of H. pylori eradication. CONCLUSION: Using 1-week triple-therapy regimens, treatment of H. pylori infection is more effective in patients with PUD than in those with NUD.     

Thyroxine-binding globulin--not a tumor marker of hepatocellular cancer]

Thyroxin-binding globulin (TBG) is secreted by human hepatoma cell lines and was suggested as a tumor marker of primary hepatocellular carcinoma (HCC). However, the results of several clinical studies are contradictory. Therefore, we decided to investigate whether TBG is a valuable marker for early detection and/or followup of HCC. In 30 patients with HCC we determined TBG, thyroxine (T4), trijodothyronine (T3), alpha-feto-protein, ferritin and the sonographically determined tumor size. Twenty one of these patients had liver cirrhosis. In 19 patients hepatitis B-markers could be detected, 9 of whom with positive HBs antigen. Twenty two patients with liver cirrhosis served as controls. Serum TBG in HCC and liver cirrhosis was not significantly different (21.1 +/- 6.9 vs. 18.7 +/- 5.1 micrograms/ml). T4 (p less than 0.04) and the T4/TBG ratio (p less than 0.0002) were significantly lower in HCC. T3 and ferritin were comparable in both groups. TBG correlated with T4 (r = 0.6), but not with the sonographic tumor size, alpha-fetoprotein or ferritin. In 3 patients alpha-fetoprotein and TBG could be determined 3 to 36 months prior to the primary diagnosis of HCC. In none of these patients an increase of TBG was detected before diagnosis of HCC. In the 4 patients under chemotherapy, TBG decreased after the first course. Three of these patients showed further decreasing TBG values in spite of an increasing tumor size. We conclude that in our patients TBG is no valuable tumor marker for the early diagnosis or follow up of HCC.