Effect of age at menarche on microvascular complications among women with Type 1 diabetes.

AIM: To test the hypothesis that delayed menarche is associated with an increased microvascular complication risk among women with Type 1 diabetes. METHODS: We studied the female participants of an ongoing prospective study of childhood-onset Type 1 diabetes diagnosed during the period 1950-1980. Of 325 women, we included data from 315 who had reached menarche by the study baseline (1986-1988) and who self-reported their age at menarche. Both cross-sectional and prospective analyses over the 25-year follow-up were used to assess the relationship of age at menarche with the prevalence, incidence and cumulative incidence of microvascular complications, comprising overt nephropathy, proliferative retinopathy and confirmed distal symmetric polyneuropathy. RESULTS: In cross-sectional analyses at baseline, the odds of overt nephropathy increased 1.24 times (P=0.02) with each annual increase in age at menarche, and 3.2 times (P=0.009) in those with delayed menarche compared with women with normal menarche onset, after adjustment. Similarly, the cumulative incidence of overt nephropathy increased 1.16 times (P=0.01) with each older year of menarche and women with delayed menarche were at twofold increased risk of overt nephropathy (hazard ratio 2.30, P=0.001) compared with women with normal menarche onset. However, age at menarche was not significantly associated with either proliferative retinopathy or confirmed distal symmetric polyneuropathy after adjusting for covariates. CONCLUSIONS: Age at menarche was significantly associated with the prevalence and cumulative incidence of overt nephropathy, but not with proliferative retinopathy or confirmed distal symmetric polyneuropathy in Type 1 diabetes. Women with delayed menarche may therefore be targeted for early screening and timely interventions to prevent the development of nephropathy.

Glucose and glycogen metabolism in erythrocytes from normal and glycogen storage disease type III subjects.

Active glycogen metabolism has been demonstrated in both normal and glycogen-rich erythrocytes taken from patients with type III glycogen storage disease. Activity of all enzymes catalyzing the reactions required for the synthesis and degradation of glycogen have been demonstrated in the mature erythrocytes. Uniformly labeled glucose-(14)C is incorporated into glycogen in intact cells of both types during incubation. Replacement of the glucose-(14)C by unlabeled glucose in the medium resulted in a significant loss of radioactivity from cellular glycogen. In the absence of the substrate a progressive shortening of outer branches occurred during incubation of intact glucogen-rich cells. Using cells from patients with type III glycogen storage disease, which have sufficient glycogen content to be analyzed by beta-amylolysis, we demonstrated that the glucosyl units are first incorporated in the outer tiers, then transferred to the core where they tend to accumulate due to the absence of amylo-1,6-glucosidase. The glycogen-rich cells have a more rapid rate of glucose utilization upon incubation which is not reflected by a higher lactate production. The increased rate of glucose utilization did not result from an increased rate of glucose incorporation into glycogen in affected cells. The rate of (14)CO(2) production from glucose-1-(14)C during incubation was not significantly different in the two types of cells unless methylene blue was added as an electron acceptor, in which case the glycogen-rich cells oxidized glucose to CO(2) more rapidly.

Transcription of genes encoding granulocyte-macrophage colony-stimulating factor, interleukin 3, and interleukin 6 receptors and lack of proliferative response to exogenous cytokines in nonhematopoietic human malignant cell lines.

Studies in recent years have suggested that human tumor cell lines are capable of responding in vitro to hematopoietic growth factors. In the present study, we investigate the transcription of the alpha and beta subunits of granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor, the alpha and beta subunits of interleukin 3 (IL-3) receptor, and the single subunit of interleukin 6 (IL-6) receptor and its associated gp130 transduction protein by PCR amplification of reverse-transcribed cellular mRNA in 34 malignant cell lines derived from a variety of histological cell types. mRNA for only a single subunit polypeptide was found in a significant minority of cell lines (23%), while in 20% both the alpha and beta subunits of either the GM-CSF receptor or the IL-3 receptor were detected among a number of different histological cell types. Transcription of the gene encoding the IL-6 receptor was found in 38% of cell lines, and all lines transcribed the gp130 transduction protein, consistent with previous observations on the ubiquity of that polypeptide. In order to test the in vitro effect of exogenously added growth factors on those malignant cell lines transcribing complete cytokine receptor, either GM-CSF, IL-3, or IL-6 was added in therapeutic concentrations (20-500 ng/ml) and cellular proliferation was measured by incorporation of [3H]thymidine. No stimulation was seen at either 3 and 6 days of culture. Production of cytokine by these cell lines was investigated at the level of transcription and by assay of peptide product. None transcribed mRNA for either GM-CSF or IL-3, while 5 of 6 (STD, DOZ, ADE, Hep-2, and Detroit) expressed IL-6 mRNA. Of these latter, 2 cell lines (ADE and Hep-2) produced IL-6 as determined by bioassay, while none produced GM-CSF or IL-3 by enzyme-linked immunosorbent assay. This suggests that in the case of GM-CSF and IL-3, failure to proliferate on addition of cytokine is not due to the prior presence of endogenous production. In contrast, at least a subset of malignant cell lines may involve a closed IL-6 autocrine loop saturating cell surface sites. These findings suggest that the ability to transcribe the genes encoding cytokine receptor is by itself insufficient to render cells cytokine responsive and that malignant cells may lack the cellular machinery for cytokine-induced proliferation. This in turn suggests that therapeutic administration of either GM-CSF, IL-3, or IL-6 may involve no additional risk of tumor regrowth in vivo.

Defective cytokine production following autologous stem cell transplantation for solid tumors and hematologic malignancies regardless of bone marrow or peripheral origin and lack of evidence for a role for interleukin-10 in delayed immune reconstitution.

A substantial body of evidence accumulated in recent years indicates a protracted delay in immune reconstitution following autologous stem cell transplantation. In order to investigate the cellular basis of this phenomenon, peripheral blood mononuclear cells were studied from recipients of autologous stem cell transplantation for solid tumors and hematological malignancies. On stimulation with phytohemagglutinin and phorbol 12-myristate 13-acetate, transplant-derived peripheral blood mononuclear cells demonstrate statistically significant depressed production of interleukin 3 (IL-3), IL-4, granulocyte-macrophage-colony-stimulating factor, and gamma-interferon as compared to normal controls, during the first 6 months following engraftment, which recover to normal levels 6 months or more posttransplant. When the overall group of transplant recipients is compared to the control group, there is a statistically significant lower production of IL-2. In addition, no differences were observed regardless of the source of the engrafted stem cells, whether from bone marrow alone (autologous bone marrow transplantation), from peripheral blood stem cells alone, or from a combination of autologous bone marrow transplantation and peripheral blood stem cells. The defect persisted past 6 months postengraftment. Transplant-derived peripheral blood mononuclear cells were stimulated with combinations of either phytohemagglutinin plus the calcium ionophore A23187, thereby circumventing the requirement for accessory cell function, or with phorbol 12-myristate 13-acetate plus anti-CD28 monoclonal antibody, mimicking the CD28-B7 cell surface-ligand interaction capable of triggering and stabilizing IL-2 gene transcription. In both situations, decreased production of IL-2 as compared to controls was observed in individuals within 6 months of transplantation. Quantitative polymerase chain reaction indicates that decreased transcription of IL-2 mRNA following transplantation is not due solely to a decrease in the absolute numbers of CD4+ T-cells but is secondary to reduced numbers of transcript copies per cell. Production of IL-10 was found to be decreased regardless of whether the autologous graft was of bone marrow or peripheral blood origin. These findings are consistent with the conclusion that: (a) multiple dysregulations exist in the production of cytokines important in immune homeostasis; (b) a defect occurs at or prior to the level of transcription of IL-2 mRNA; (c) IL-10 does not play a direct role in the pathogenesis of posttransplantation immunosuppression; and (d) there is no evidence that peripheral blood stem cells may be superior to bone marrow-derived stem cells in accelerating immune reconstitution.

The catabolism of human and rat very low density lipoproteins by perfused rat hearts.

The catabolism of human and rat 125I-labelled very low density lipoproteins (VLDL) was compared by perfusing the lipoproteins through beating rat hearts. Triacylglycerol was removed from the VLDL to a greater extent than the protein moiety, leaving remnants containing relatively more apo-B and less apo-C. The change in apo-C content of the remnants correlated with the loss of triacylglycerol. The extent of removal of triacylglycerol from the rat and human VLDL was similar and in most cases appeared to saturate the heart lipoprotein lipase. The remnants were slightly smaller in size than the VLDL, and included particles which appeared to be partially emptied. In addition to remnants of d less than 1.019 g/ml, iodinated lipoproteins derived from rat and human VLDL were recovered at d 1.019-1.063 and 1.063-1.21 g/ml. The former contained largely cholesterol and cholesteryl esters, while phospholipids were the dominant lipid in the latter. An average of 40% of the 125I-labelled apoprotein lost from the VLDL was associated with the perfused hearts. Very little d 1.019-1.063 g/ml lipoprotein was produced from low (physiological) concentrations of rat VLDL, most of the lipoprotein being removed by the heart. However, lipoproteins of density 1.019-1.063 g/ml were formed from human VLDL at all concentrations in the perfusate, as well as from higher concentrations of the rat VLDL. Agarose gel filtration of lipoproteins following heart perfusion with human VLDL revealed large aggregates containing particles which resemble low density lipoproteins (LDL) in electron microscopic appearance and apoprotein composition, since they contain largely apo-B. These data suggest that at normal concentrations rat VLDL are almost completely catabolised and taken up by the heart without the formation of LDL, while LDL is produced from human VLDL at all concentrations.

Restriction fragment length polymorphisms and single germline coding region sequence in VH18/2, a duplicated gene encoding autoantibody.

In this study, we analyze the restriction fragment length polymorphisms of VH18/2, a gene encoding the heavy chain of an anti-DNA antibody, and correlate that with the germline sequence of the gene's coding region. Oligonucleotides probes complementary to the CDR1 and to both the 5' and 3' halves of the CDR2 gene segments were hybridized under stringent conditions to genomic DNA digested with XbaI, and yielded polymorphic bands of 26, 24 and 18 kb with all three probes. Individuals had either one, two, or three bands in common in their genomic DNA, indicating duplication of VH18/2 genes at two sites within the IgH locus. While it is difficult to say which of the three polymorphic gene segments constitute an allelic pair, the 26 and 24 kb fragments were the most commonly seen (97% of individuals had one or both). VH18/2 is known to be over-represented in the expressed repertoire with very little nucleotide divergence from the germline sequence. In order to determine whether the observed RFLPs are due to sequence polymorphism of the VH18/2 coding region, and whether differences in the expressed genes arise from somatic mutation, size-selected genomic DNA containing the gene was cloned and sequenced. A single coding region sequence was found in the germline. The results of this study suggest that overexpression of VH18/2 may in part be due to its duplication. Like other genes encoding autoantibody, which are well conserved, nonpolymorphic and expressed early in programmed immunologic development, VH18/2 may be instrumental in the establishment or regulation of the immune repertoire.

Germline complexity, restriction fragment length polymorphism, and coding region sequences of the human VH7 gene family identified with family-specific FR3 segment oligonucleotides.

We have used the most family-specific gene segment, the 5'-end of framework 3 (FR3) to study the germline complexity and coding region sequences of the recently described human VH7 gene family. Because of the high degree of 5' sequence homology between members of the VH7 and VH1 families, full-length coding region probes are unable to distinguish between the two groups. Hybridization with a VH7 coding region probe to EcoRI digested genomic DNA revealed 12 fragments. Many of these hybridizing fragments were also identified with a full length VH1 coding sequence probe. However, examination of the same DNA samples with a VH7 family specific oligonucleotide, encompassing the 5'-end of the FR3 segment, greatly reduced hybridization complexity yielding only four fragments which included one polymorphic band of molecular weight 7.4 kb. The VH7 specific FR3 oligonucleotide was also used under conditions of moderate stringency to isolate VH7 clones from PCR-amplified genomic DNA libraries derived from six unrelated individuals. All clones isolated contained members of the VH7 family. Six sequences were obtained. Gene 7A.4, seen in all individuals, is identical to the previously described germline V1-4.1b gene other than G-C substitutions at nucleotides 253 and 254. Five distinct pseudogenes were also identified. Stop codons were confined to frameworks 2 and 3. Previously described expressed VH7 genes from cord blood, normal adults and two rheumatoid factors are > 96% homologous to gene 7A.4.

Anti-CD34+ Fabs generated against hematopoietic stem cells in HIV-derived combinatorial immunoglobulin library suggest antigen-selected autoantibodies.

Bone marrow suppression associated with HIV infection does not appear to be solely due to direct viral cytopathic effects. Autoantibodies may play a role in myelosuppression, however it is unclear whether autoantibodies produced in HIV infection represent a primary pathogenic process or merely reflect polyclonal B cell activation. To address these questions, we generated combinatorial immunoglobulin libraries using the pComb3 phagemid from an HIV+ individual with evidence of circulating autoantibodies. From one library, three anti-CD34 Fabs were identified using fresh CD34+ cells as antigenic targets by a method of phage subtraction. The anti-CD34 Fabs are specific by immunoblotting and Elisa and are of high affinity, with calculated Kds in the range of 10(-7) -10(-8) M. Nucleic acid sequencing revealed all three to be of the VH3 family and to have lambda light chains with some gene segments expressing little somatic mutation, while other segments were somatically mutated in patterns suggestive of antigen selection. These findings indicate that (1) A subset of HIV-associated anti-CD34 autoantibodies are monospecific and antigen-selected and are not merely a consequence of polyclonal B cell activation and elevated Ig levels in HIV. Autoreactivity in HIV therefore includes both polyspecific, low affinity antibodies as well as monospecific antigen-selected high affinity antibodies. (2) Although bone marrow suppression in HIV is likely to be multifactorial, autoantibodies to hematopoietic stem cells may contribute to its pathogenesis. (3) Library sampling of VH gene family rearrangements shows no evidence for under-representation of the VH3 family in the immune dysregulation of HIV infection. Phage subtraction is corroborated to be an effective means of identifying, cloning, and characterizing antibodies to hematopoietic differentiation antigens.

Targeting retroviral vectors to CD34-expressing cells: binding to CD34 does not catalyze virus-cell fusion.

We have attempted to engineer murine leukemia virus (MuLV)-based retroviral vectors to specifically transduce cells expressing human CD34, an antigen present on the surface of undifferentiated hematopoietic stem cells. A number of chimeric ecotropic MuLV envelope (Env) proteins were constructed that contained anti-CD34 single-chain antibody variable fragments (scFvs). The scFv-Env proteins were generated either by replacing the receptor-binding domain of Env with the scFv or by inserting the scFv into the N terminus of the Env protein. Only chimeric Env proteins with scFv insertions between amino acids 6 and 7 were incorporated into viral particles, and coexpression of native MuLV Env did not rescue incorporation-defective proteins. In addition, the efficiency of incorporation varied with the specific anti-CD34 scFv that was used. Retroviral vectors containing the scFv-Env proteins bound to CD34+ cells and transduced NIH 3T3 cells expressing human CD34 (3T3-CD34 cells) at approximately twice the efficiency of the parental NIH 3T3 cells. However, the introduction of the mutation D84K, which prevents binding to the ecotropic MuLV receptor mcat-1, prevented transduction of both NIH 3T3 and 3T3-CD34 cells. Complementation cell-cell fusion assays [Zhao et al. (1997). J. Virol. 71, 6967-6972] in 3T3-CD34 cells revealed that although the scFv-Env proteins could contribute postbinding entry functions when bound to mcat-1, they were unable to do so when bound to CD34. Taken together, these data suggest that although the interaction with CD34 effectively increased the concentration of virus on 3T3-CD34 cells, entry could occur only through an interaction with mcat-1; CD34 alone was not capable of triggering the appropriate postbinding changes that lead to viral entry.

Varicella-zoster virus myelitis: an expanding spectrum.

We report four cases of varicella-zoster virus (VZV)-associated myelopathy in adults. Myelopathy was remitting-exacerbating in two remarkable instances, once acute and once chronic. VZV myelopathy was diagnosed based on the close temporal relationship between rash and onset of myelopathy, and for the first time, by polymerase chain reaction, which revealed VZV DNA in the cerebral spinal fluid of three patients with pleocytosis weeks to months later. Magnetic resonance imaging was abnormal in three of four patients. Although all four patients were treated at some time with intravenous acyclovir, concomitant treatment with steroids and the presence of acquired immunodeficiency syndrome in one patient prevented conclusions about a favorable response to therapy. Myelopathy after VZV infection may be remitting-exacerbating in addition to acute or chronic. Detection of VZV DNA in cerebral spinal fluid months after rash was useful for diagnosis and suggests a role for virus in the pathogenesis of myelopathy.

Turnover of apoE in normal and hypercholesterolemic rats.

The turnover of apoE in the total lipoprotein fraction (p less than 1.21 g/ml) of normolipemic and hypercholesterolemic rats was compared. The specific activity of 125I-labelled apoE in the lipoproteins was determined after isolation of the apoprotein by immunoaffinity chromatography. The serum apoE decay curves showed rapid first and slower second phases. The first phase of the curve of hypercholesterolemic animals suggests some sequestration of the apoprotein. The half-lives of apoE in the second phase were approximately 7 and 23 h in the normal and hypercholesterolemic sera, respectively. Elevated apoE levels and moderate hypercholesterolemia persisted one week after restoration of the normal diet, indicating that the increased apoprotein level seen in hypercholesterolemic rats was not solely to VLDL or chylomicron remnants. However, due to the elevated apoE levels in the hypercholesterolemic rats, the total replacement rates of the apoprotein appeared to be greater than that in normolipemic animals, consistent with the concept that in the steady state there is an increase in apoE secretion in hypercholesterolemic animals rather than a decrease in catabolism.

Peripheral destruction of platelets in chronic lymphocytic leukemia: recognition, prognosis and therapeutic implications.

In patients with chronic lymphocytic leukemia and depressed platelet counts, it is important to discriminate between the thrombocytopenia due to bone marrow replacement with abnormal lymphocytes and that caused by increased peripheral destruction of platelets. The former is due to progressive chronic lymphocytic leukemia and, as a Rai Stage IV, carries a poor prognosis. The latter, as illustrated in four patients seen at the National Cancer Institute, may be remediable by either splenectomy alone or splenectomy followed by immunosuppressive and antitumor therapy. In all four patients, survival was substantially longer than for patients whose condition was classified as Rai Stage IV. The importance of identifying the subgroup of patients with chronic lymphocytic leukemia with reversible thrombocytopenia is emphasized by these examples.

Peripheral blood mononuclear cells from autologous hematopoietic stem cell transplantation recipients produce and respond to IL-12.

Autologous hematopoietic stem cell transplantation effectively results in restoration of hematopoiesis, but induces an often prolonged period of T cell dysfunction including redistribution of T cell subsets and defective T cell proliferation. Because IL-2 production is markedly decreased following autologous stem cell engraftment, and because IL-12 has direct stimulatory effects on TH1 cells, a major source of IL-2, we investigated the production and responsiveness of IL-12 of peripheral blood mononuclear cells (PBMC) of autologous stem cell recipients in the first 6 months following engraftment. When stimulated with S. aureus Cowan I (SAC), PBMC from autologous hematopoietic transplant recipients in the early months following engraftment show no decrease in production of IL-12 as compared to control PBMC. Furthermore, transplant-derived PBMC appear to be functionally responsive to exogenously provided IL-12 as indicated by several criteria. In vitro proliferation of total PBMC and of isolated CD4+ T cells from transplanted recipients to PHA (1 microgram/ml) + IL-12 (20 U/ml) was comparable to controls, excluding the possibility that only NK or CD8+ cells respond to IL-12. Culture of both control and transplant-derived PBMC in PHA + IL-12 (20 U/ml) or IL-2 (100 U/ml) + IL-12 (20 U/ml) combinations yielded comparable production of IFN-gamma, one of the major biological effects of IL-12 in vivo, as well as equal production of TNF-alpha, a costimulatory factor of IL-12-mediated induction of IFN-gamma by NK cells. Taken together, this in vitro evidence suggests that following autologous transplantation, PBMC do not appear to have either decreased production of endogenous IL-12 or defective functional responsiveness to exogenously provided IL-12.

Inhibition of actions of glucagon in adipocytes by gastric inhibitory polypeptide.

Possible interactions between gastric inhibitory polypeptide (GIP) and glucagon were investigated in rat adipocytes. GIP was nonlipolytic and inhibited lipolysis stimulated by glucagon but not that stimulated by secretin or vasoactive intestinal polypeptide (VIP). GIP competed with 125I-glucagon for binding to adipocyte receptors, and at physiologic concentrations inhibited the stimulation of AMP produced by glucagon. Thus GIP acts as an inhibitor of actions of glucagon on adipocytes and may be a physiologic modulator of effects of glucagon.

Histologic chorioamnionitis and preterm delivery in different patient populations.

The placentas of 1843 deliveries were examined for the presence of histologic chorioamnionitis, which was classified as mild, moderate, or severe. Chorioamnionitis was present in 7.5% of patients who underwent cesarean before labor and in 18 and 32% of those delivering at term and preterm, respectively. Chorioamnionitis was severe in 74% of preterm but in only 15% of term deliveries. Premature rupture of membranes (PROM) was more frequent with preterm than with term delivery, with chorioamnionitis present in 42 and 15% of patients, respectively. Although chorioamnionitis was equally frequent in women with intact membranes delivering preterm and term, chorioamnionitis was severe in 63% of preterm and 14% of term deliveries (P less than .001). The frequency and severity of chorioamnionitis were related inversely to gestational age at preterm birth. Preterm delivery was more frequent in black than in white patients (19 versus 9%) and in indigent clinic versus private patients (13 versus 7.5%). However, there was no significant difference in frequency and severity of chorioamnionitis between black and white or between indigent clinic and private patients who delivered preterm. Among term births, chorioamnionitis was more often severe in black than in white patients. Chorioamnionitis in term deliveries was more frequent in clinic than in private patients; however, this was not true when only severe chorioamnionitis was considered. There were no differences in PROM between these patient populations. Thus, higher preterm birth rates in black and indigent clinic populations are not due to the more frequent occurrence of chorioamnionitis.

Gas in the cavernous sinus.

PURPOSE: To evaluate the significance of cavernous sinus gas identified on head CT scans. METHODS: Head CT scans were viewed prospectively for a period of 3 years. The charts of patients who demonstrated cavernous sinus gas were reviewed. RESULTS: Seventeen patients without head trauma and 10 patients with head trauma demonstrated gas in the cavernous sinus. None of the patients had symptoms or developed symptoms originating in the cavernous sinus. All of the patients without trauma had an intravenous line in place. Sphenoid fractures or basilar skull fractures were not a constant finding in trauma patients with cavernous sinus gas. CONCLUSIONS: In patients without symptoms referable to the cavernous sinus, gas in the cavernous sinus does not appear to be a significant finding. The gas is most likely the result of venous air emboli from intravenous lines or penetrating trauma.

The anatomy of the inferior petrosal sinus, glossopharyngeal nerve, vagus nerve, and accessory nerve in the jugular foramen.

PURPOSE: To define the variations of the courses of the cranial nerves and the inferior petrosal sinuses as they enter and traverse the jugular foramen. METHODS: Thirty-nine cadaveric specimens containing the jugular foramen were scanned with 1-mm contiguous axial and coronal CT sections. Each specimen was dissected to evaluate the position of the cranial nerves and inferior petrosal sinus as they entered the jugular foramen. RESULTS: The glossopharyngeal nerve entered the most superior, anterior, and medial aspect of the jugular foramen and descended in the anterior portion of the jugular foramen, often within a groove. The vagus and accessory nerves could not be separated by CT. They entered the jugular foramen most often anterior or anterior and inferior to the jugular spine of the temporal bone and descended in a position ranging from medial to anterior to the jugular vein. The inferior petrosal sinus most often coursed inferior to the horizontal portion of the glossopharyngeal nerve and entered the jugular system in the jugular foramen, at the exocranial opening or below the skull base. A pars nervosa and pars venosa could be identified only at the endocranial opening, where the jugular spine separated the pars nervosa containing the inferior petrosal sinus and three cranial nerves from the pars venosa containing the jugular vein. CONCLUSION: Our evaluation demonstrated anatomic variation in the area of the jugular foramen.

Methanol intoxication with putaminal and white matter necrosis: MR and CT findings.

We report a case of methanol intoxication in which the initial CT scans appeared normal. MR at 4 days showed the typical putaminal lesions of methanol intoxication and, in addition, peripheral white matter lesions that spared a thin rim of subcortical white matter. A CT scan at 17 days showed the putaminal and white matter lesions. The white matter lesions correspond well to lesions previously described in pathologic specimens.

Gasserian ganglion: appearance on contrast-enhanced MR.

PURPOSE: To characterize the appearance of the gasserian ganglion on contrast-enhanced MR images. METHODS: We retrospectively reviewed the MR images from 57 patients with suspected pituitary disease. These patients had undergone unenhanced and contrast-enhanced MR imaging of the sella, including evaluation of Meckel's cave. None of the patients had clinical signs or symptoms referable to the fifth cranial nerve or ganglion. Correlation was made with a previous study that compared gross anatomy with high-resolution CT scans of cadaveric specimens. RESULTS: A discrete semilunar enhancing structure within the inferolateral aspect of Meckel's cave was identified in 100 of the 114 caves examined; the other 14 caves had a thickened area of enhancement that blended with the dura inferolaterally. A small semilunar structure within the inferolateral aspect of Meckel's cave was also identified on CT scans of the cadaveric specimens. CONCLUSION: The gasserian ganglion enhances on MR images and should not be confused with a pathologic process.