Long-term treatment of chronic schizophrenia with risperidone: a study with plasma levels.

Twenty-four chronic schizophrenic outpatients with a mean age of 37.21 years +/- 9.96 SD were treated with risperidone (RSP) at the dosage of 2-9 mg/die (mean 4.46 mg/die +/- 1.30 SD, mean 0.06 mg/kg +/- 0.01 SD) for a year. Clinical evaluation was assessed with the Brief Psychiatric Rating Scale (BPRS), Positive and Negative Symptoms Scale (PANSS), Extrapyramidal Side Effects Rating Scale (EPSE) and a checklist for Anticholinergic Side Effects (ACS) at T0, then after 1 (T1), 2 (T2), 3 (T3), 6 (T6), 9 (T9) and 12 (T12) months. RSP and 9-hydroxy-risperidone (9OH-RSP) plasma levels were determined at T12 by the HPLC method. BPRS and PANSS mean values showed a significant improvement during the study. No correlation between RSP dosage (mg/kg) and RSP, 9OH-RSP plasma levels or active moiety resulted. A positive correlation between age and active moiety was observed. A positive correlation between RSP and 9OH-RSP plasma levels was observed. A curvilinear relationship between active moiety and PANSS improvement (%) was observed. Patients with the higher PANSS amelioration showed RSP + 9OH-RSP plasma levels ranging from 15 to 30 ng/mL. RSP seems to be quite an effective drug. It seems, however, difficult to devise appropriate dose schedules and plasma level determination seems to be necessary in some cases.

Elastofibroma of the neck.

Elastofibromas are benign lesions of the chest wall. We describe the first reported case of elastofibroma in the neck. Imaging features as well as location of the lesion were atypical. On computed tomography and magnetic resonance imaging the lesion contained a marked preponderance of fat, because the lesion arose within fat.

MRI appearance of placenta percreta and placenta accreta.

The purpose of this paper is to describe the magnetic resonance imaging (MR) features of placenta accreta and percreta. We retrospectively reviewed MRI findings in four cases of placenta accreta/percreta to determine features which assist in identifying the presence and extent of placental implantation abnormality. All patients had ultrasound (US) examinations. Pathologic correlation was available in all cases. There were two cases of placenta percreta and two cases of placenta accreta. All cases were treated by hysterectomy. In the two cases of placenta percreta, the placenta demonstrated transmural extension through the uterus (percreta) on MRI. In the two cases of placenta accreta, the location of thinning in the uterine wall correlated with the location of placental invagination into the myometrium at pathology. US correlation was available in all four cases. Gray scale US did not demonstrate placental invasion in any of the four cases of placenta accreta/percreta, however, in two of three cases in which color Doppler was performed, there was flow at the uterine margin suspicious for implantation abnormality. In conclusion, MRI is useful for identifying the presence and extent of placenta accreta/percreta.

Symptomatic cervical macrocyst as a late complication of subtotal hysterectomy. A case report.

BACKGROUND: Ablation of the endocervical canal is sometimes performed as an adjunct to subtotal hysterectomy in an attempt to reduce mucous discharge and the risk of future neoplasia. Cystic accumulations within the canal of a partially obliterated cervical stump have not previously been reported to follow this practice. CASE REPORT: A 41-year-old woman presented with subacute cramping and cystic enlargement of the cervical stump on clinical, sonographic and magnetic resonance evaluation four years subsequent to a subtotal hysterectomy performed for menorrhagia. Cervical biopsies and cytology were benign, and vaginal trachelectomy was performed. Pathology demonstrated the fluid pocket to be a very large retention cyst (nabothian) that had occupied and distended the partially obliterated endocervical canal. CONCLUSION: Ablation of the cervical canal at subtotal hysterectomy may result in symptomatic entrapment of nabothian cysts. Internalization of the transformation zone and partial obliteration of the canal are postulated as predisposing factors.

Long term efficacy of paroxetine in major depression: A study with plasma levels.

Depressive disorders can be regarded as recurrent and chronic conditions that may reduce the quality of life and work output of patients. Data on the long-term efficacy of paroxetine appear to indicate that it is an effective maintenance treatment. Our aim was to measure paroxetine concentrations in plasma in order to optimize its clinical efficacy and tolerability during long-term treatment. We studied 35 patients aged 23-70 years, suffering from Major Depressive Disorder (recurrent). These patients received 10-50 mg of paroxetine once a day for one year; they were evaluated at baseline, after 2 weeks and then after 1,2,6,9 and 12 months by BPRS, HRS-D and HRS-A rating scales, and at the same time, any side-effects were assessed and samples for paroxetine plasma determination were also collected. Results confirmed the efficacy and tolerability of paroxetine for long-term treatment. We observed a curvilinear relationship between plasma paroxetine levels and improvement on the HRS-D with greater clinical amelioration at plasma levels between 20 and 70 ng/ml.

Groups of histopathologic abnormalities in brains of very low birthweight infants.

The neuropathologic changes in brains of very premature infants are well recognized but relatively few studies have attempted to identify if specific neuropathologic features cluster together. These data could assist in determining pathogenetic mechanisms of immature brain injury. The goal of this study is to identify which, if any, combinations of histologic features occur together. We identified the presence or absence of 19 histologic features in the brains of 67 infants from a multicenter study of 1,665 prematurely born infants whose birthweight was 500-1,500 grams. We used clustering algorithms and factor analysis to group pathologic features that occurred together. Our results indicate that certain histopathologic features do cluster. For example, telencephalic white matter astrocytosis occurs in 2 groups: 1) associated with amphophilic globules, and, 2) in an uncorrelated group, associated with focal macrophage deposits and coagulative necroses. Parenchymal hemorrhage was not found to be associated with any telencephalic leukoencephalopathy, regardless of whether characterized by rarefaction, astrocytosis, focal coagulative necroses, or foci of macrophages in the white matter. Intraventricular hemorrhage and germinal matrix hemorrhage were not seen together more often than by chance expectation. Intraventricular hemorrhage was only marginally associated with parenchymal hemorrhage. Our data indicate that specific histopathologic features tend to preferentially cluster with each other in groups. This clustering may represent the manifestation of a common mechanism for each. These data should be valuable indicators for future research attempting to establish pathogenesis.

Clozapine metabolism rate as a possible index of drug-induced granulocytopenia.

A possible relationship between haematological adverse reactions and clozapine (CLZ) metabolism rate was studied. Sixteen chronic schizophrenic outpatients (mean age 34.62 years +/- 7.56 SD) were treated with CLZ, 75-600 mg/daily for 9 weeks. CLZ and norclozapine (NCLZ) plasma levels were determined weekly, contemporarily with blood cell counts. CLZ plasma levels ranged from 25 to 1270 ng/ml (mean 266.27 ng/ml +/- 197.44 SD), while NCLZ plasma levels ranged from 25 to 1280 ng/ml (mean 169.0 ng/ml +/- 127.94 SD). NCLZ/CLZ ratio ranged from 0.13 to 1.72 (mean 0.72 +/- 0.28 SD). Leukocyte count ranged from 5.2 to 18.8 10(9)/l (mean 9.37 10(9)/l +/- 2.94 SD) and neutrophil count ranged from 1.8 to 13.4 10(9)/l (mean 5.73 +/- 2.57 SD). No correlation was found between CLZ dosage and NCLZ plasma levels. Both CLZ and NCLZ plasma levels correlated positively with neutrophil count (CLZ: P = 0.001, r = 0.26; NCLZ: P = 0.01, r = 0.20). The correlation between NCLZ/CLZ plasma level ratio and neutrophil count was significantly negative (P = 0.002, r = 0.25). These preliminary data suggest that the NCLZ/CLZ ratio, as an index of CLZ metabolism, might be a possible risk factor associated with CLZ treatment.

Cholecystokinin, beta-endorphin and vasoactive intestinal peptide in peripheral blood mononuclear cells of drug-naive schizophrenic patients treated with haloperidol compared to healthy controls.

Cholecystokinin (CCK), beta-endorphin (BE), and vasoactive intestinal peptide (VIP) in peripheral blood mononuclear cells from 30 drug-naive schizophrenics compared to 22 healthy controls were studied. Patients were evaluated with the Brief Psychiatric Rating Scale (BPRS), the Scale for the Assessment of Positive Symptoms (SAPS) and the Scale for the Assessment of the Negative Symptoms (SANS) at baseline (TO), and after four weeks (T4) in nine patients who were subsequently treated with haloperidol (HL). Neuropeptide concentrations in peripheral blood mononuclear cells (PBMC) were measured at TO and, for the treated patients, at T4. There was a negative correlation between CCK and SANS baseline scores and a trend for patients who responded poorly to HL (i.e. patients with a prevalence of negative symptomatology) to have lower CCK basal values.

Frequency of neuropathological abnormalities in very low birth weight infants.

The occurrences of histologic changes in the central nervous system of very low birth weight infants (500 to 1500 grams) according to gestational age and postnatal age are incompletely reported. In order to better understand the abnormalities present in this patient population, the brains of 67 very low birth weight infants who died after having had at least one cranial ultrasound scan were studied. More than half the infants were born at gestational ages of 24 to 26 weeks, and only 28% died within 24 hours (h) of birth. The slides of the brains of all 67 infants were reviewed simultaneously by 3 neuropathologists who had to agree on the presence and/or absence of each histologic characteristic. Among infants who died within 24 h of birth, fully one quarter had parenchymal hemorrhage, 42% had petechial hemorrhages in the white matter, and more than 20% had hypertrophic astrocytes. These data indicate that in utero, prepartum, injury to the nervous system was common. Compared with infants who died before the sixth day, those who survived at least 6 days were twice as likely to have moderate/severe ventriculomegaly, rarefaction, amphophilic globules, hypertrophic astrocytes, macrophage foci, coagulative necrosis, and hemorrhagic necrosis than those who died before the 7th postnatal day. Parenchymal hemorrhage and moderate/severe ventriculomegaly decreased in frequency with increasing gestational age. On the other hand, the older the gestational age, the higher the likelihood of finding amphophilic globules, hypertrophic astrocytes, macrophage foci, and zones of coagulative necrosis upon neuropathologic examination. Our data indicate that several central nervous system abnormalities appear to increase with both older gestational age and older postnatal age for infants born weighing less than 1500 grams. We were unable, however, to determine the relative contribution of gestational age and postnatal age to the specific neuropathologic findings in this study.

Oral aluminum administration during pregnancy and lactation produces gastric and renal lesions in rat mothers and delay in CNS development of their pups.

The expression of the neurofilament protein of the highest molecular weight (NF-H) is developmentally and spatially regulated. For example, the MAb RMO24.9, directed against a phosphorylated epitope in the tail domain of NF-H, immunohistochemically labels specific tracts within the rat brainstem prenatally, but does not label diencephalic tracts until after postnatal day 10 (P10). A diet providing 300 mg/kg/d Al (as Al lactate) to rat dams throughout gestation causes behavioral deficits in their offspring (Bernuzzi et al., 1989). We repeated this regimen by substituting 120 mM Al lactate (pH 6.5) for drinking water during gestation and lactation, and examined the distribution of immunolabeling by RMO 24.9 after exposure to Al. Tracts within the diencephalon that bind RMO 24.9 on P11 in control pups did not bind the MAb until P14 in Al-treated pups. In these preliminary experiments, Al seemed to have caused a developmental delay in the expression of phosphorylated NF-H in the pups of mothers that received Al during gestation. However, subsequent experiments showed that the neuropathology observed--and that reported by other investigators using similar Al levels--may not be the result of the direct effects of Al on the pups. Throughout lactation, treated dams appeared progressively more cachexic. Unlike the normal viscera of pair-watered controls, the stomachs of treated dams were ulcerated, and their kidneys had decreased cortical thickness and contained stones. Lesions such as these compromise a rat's ability to absorb nutrients, to excrete toxins, and to regulate water and electrolytes. In a lactating dam, these alterations could compromise the dam's ability to nourish her pups. Our experiments point out that the mechanisms of Al toxicity-- already complex in the adult--are further complicated in a system in which the pup is dependent on the mother for delivery of both nutrients and toxins. It is therefore impossible to determine the cause of any neuropathology in the pup in a system where Al delivery overlies a background of multisystem defect and altered maternal homeostasis.

A risk-benefit assessment of sulpiride in the treatment of schizophrenia.

Sulpiride is a substituted benzamide with a selective action on receptors of the dopamine D2-like family, and clinical and pharmacological data suggest that it could be considered to be an atypical antipsychotic. Sulpiride penetrates the blood-brain barrier poorly because of its low lipid solubility. It is mainly excreted unchanged in the urine, and accumulation of the drug could occur in patients with renal dysfunction and possibly in elderly patients with declining glomerular filtration rate. At low dosages (50 to 150 mg/day), sulpiride produces a disinhibiting and antidepressant effect, which is probably related to its action on D2 presynaptic autoreceptors, thus facilitating dopaminergic neurotransmission. Data have confirmed the efficacy of sulpiride in patients with acute or chronic schizophrenia during both short and long term treatment, but long term, placebo-controlled trials are still lacking. It is still doubtful whether sulpiride is more effective than typical antipsychotics for the treatment of negative symptoms. Data from clinical studies are controversial; the majority of authors indicate that sulpiride produces a better recovery rate from negative than from positive symptoms at low doses, but it shows a similar efficacy either on negative and positive symptoms at higher doses. The safety profile of sulpiride is similar to that of typical antipsychotics, although the frequency of adverse effects seems to be globally lower. Extrapyramidal reactions appear generally to be mild. Autonomic effects occur less frequently with sulpiride than with typical antipsychotics, showing no clinically relevant influence on cardiovascular parameters and, on the whole, good tolerability in elderly patients. Sulpiride is known to induce prolactin elevation in both serum and CSF, which may be associated with impotence in men and diminished gonadal function in women; these effects appear to be dosage-dependent. Sulpiride can be considered to be an atypical antipsychotic, considering its action on negative, defective symptoms, its partial activity against positive symptoms, and its low incidence of extrapyramidal adverse effects. Sulpiride could find its specific therapeutic role in elderly patients with schizophrenia, as it shows a good margin of safety between therapeutic dosages and toxic concentrations.

Neurobiological and psychopharmacological basis in the therapy of bulimia and anorexia.

1. Eating disorders can be found in several psychiatric pathologies: schizophrenia, delusional disorder (somatic type), bipolar disorders, major depressive disorder, borderline personality disorder, generalized anxiety disorder, body dysmorphic disorder, somatization disorder and conversion disorder. 2. Although their clinical features have been defined, relatively little is known about the role of neurobiological patterns in the pathogenesis of these disorders. Several CNS neurotransmitters and neuromodulators are involved in the regulation of eating behavior in animals and have been implicated in symptoms such as depression and anxiety often observed in patients with eating disorders. The authors will review some studies on NA, DA, 5-HT, beta-endorphins, CRH, VP, OT, CCK, NPY and PYY involved in eating disorders. Furthermore, we will highlight some of the studies on drug therapy of eating disorders taking into account the effects of these agents on neurotransmitters and neuromodulators. 3. Antidepressant drugs have long been used for anorexia nervosa and bulimia, these disorders been claimed to be affective equivalent. Antidepressant agents seem to be effective in reducing the frequency of binge-eating episodes, purging behavior and depressive symptomatology. It is notable that antidepressant agents have been proved to be effective in patients with chronic bulimic symptoms, even in cases persisting for many years and in patients who had repeatedly failed courses of alternative therapeutic approaches. In all of the positive studies, antidepressant agents appeared effective even in bulimic subjects who did not display concomitant depression. 4. Few controlled studies on use of medications for anorexia nervosa have been published. Central serotonergic receptor-blocking compounds such as cyproheptadine cause marked increase in appetite and body weight. Zinc supplementation or cisapride could be a therapeutic option in addition to psychological and other approaches in anorexia nervosa. 5. There is no therapy as yet which is fully effective in alimentary disorders. Psychotropic drugs give some relief from symptoms, but they cannot cure the disorders. An integrated approach, either pharmacological or psychological, is still recommendable.

Prevalence of intestinal parasite infections among individuals with mental retardation in New York State.

The prevalence of intestinal parasite infection among program participants of the New York State Office of Mental Retardation and Developmental Disabilities for the period 1986-1987 was estimated, and demographic factors associated with increased risk for infection were identified. The overall prevalence of infection was 7.3%. The two most prevalent infections were Enterobius vermicularis (4.5%) and strongyloides stercoralis (1.2%). Males and individuals with severe or profound mental retardation were twice as likely to be positive for the presence of intestinal parasites as females and individuals with mild/moderate retardation. The relatively low prevalence found in this study compared with previous surveys suggests that management of parasitic infection is improving in conjunction with developments in delivery of medical and habilitative services.

Sonographic diagnosis of cisternal subarachnoid hemorrhage in the premature infant.

PURPOSE: To evaluate sonographic criteria for the diagnosis of subarachnoid, and particularly cisternal, hemorrhage in the preterm infant. METHODS: The subarachnoid cisterns were studied on cadaveric anatomic sections and on postmortem ultrasonograms, as well as on in vivo ultrasonograms of healthy neonates. Based on the normal ultrasound appearances of these cisterns, criteria were developed for the recognition of abnormal cisternal fluid collections, which strongly suggest the presence of subarachnoid hemorrhage in the premature infant. These criteria were evaluated prospectively in a group of 63 preterm infants who underwent subsequent autopsy. RESULTS: In the 63 infants with neuropathologic verification, increased echogenicity and/or increased echo-free content of the subarachnoid cisterns correctly predicted subarachnoid hemorrhage with an accuracy of 75%, sensitivity of 69%, and specificity of 93%. The positive and negative predictive values were 97% and 46%, respectively. In 47% of the cases, ultrasound correctly detected cisternal subarachnoid hemorrhage before intraventricular hemorrhage could be diagnosed. CONCLUSION: A highly specific, although somewhat insensitive, sonographic diagnosis of subarachnoid hemorrhage can be made from the appearance of the subarachnoid cisterns. The diagnosis of subarachnoid hemorrhage may predate the ultrasound diagnosis of intraventricular hemorrhage and may alert the neonatologist to the need for follow-up sonograms in the absence of ultrasound evidence of intraventricular hemorrhage.

Presence of non-fibrillar amyloid beta protein in skin biopsies of Alzheimer's disease (AD), Down's syndrome and non-AD normal persons.

A total of 66 skin biopsies from persons with Alzheimer's disease (AD) or Down's syndrome (DS) and from persons without AD were used in this study. The age range was from 7 to 89 years. Positive immunoreactivity of skin biopsies to monoclonal antibody 4G8, which is reactive to amino acid residue 17-24 of synthetic amyloid beta protein (A beta), and 4G8-Fab (the antigen-binding fragment of 4G8 IgG, reactive only to amyloid plaque) was observed in the epidermis-dermis junction or the basement membrane of the epidermis and in some blood vessels of the biopsy skins of 13/18 (72%) AD, 9/10 (90%) DS, and 14/38 (37%) non-AD control cases. The Fisher exact probability test revealed a significant difference (P = 0.0415 one-tailed) in immunoreactivity between AD and age-matched controls. There was also a significant difference (P = 0.0152 one-tailed; P = 0.0200 two-tailed) between DS and age-matched control in the same test. Immuno-gold electron microscopy examination of these cases with positive immunoreactivity revealed that the gold particles were deposited along the basement membrane of the epidermis. Amyloid fibrils were not observed in the regions with gold particles. Results of this study suggest that A beta is associated with the basement membrane of skin and is present in amorphous, non-fibrillar form as soluble A beta.

Nearly ubiquitous tissue distribution of the scrapie agent precursor protein.

The "modified host protein" model of scrapie proposes that the transmissible agent is composed of the degradation-resistant protein, Sp33-37, and that clinical and pathologic signs result from neurotoxic accumulations of this protein. Sp33-37 is an abnormal, amyloidogenic isoform of the normally occurring cellular protein Cp33-37. This study investigated the tissue distribution of Cp33-37 in hamster. In brain, Cp33-37 was most concentrated in the hippocampal formation. Immunohistochemical studies localized Cp33-37 to neurons and surrounding neuropil in hippocampus; septal, caudate, and thalamic nuclei; dorsal root ganglia cells; and large-diameter dorsal root axons. In non-neuronal hamster tissues, Cp33-37 was detected in circulating leukocytes, heart, skeletal muscle, lung, intestinal tract, spleen, testis, ovary, and some other organs. The presence of Cp33-37 in extracerebral tissues indicates that its function is not unique to brain. These results indicate that the molecular substrate for the production of Sp33-37, the scrapie agent, and scrapie amyloid is present in a variety of cerebral and extracerebral sites.

Analysis of neocortex in three males with the fragile X syndrome.

Fragile X [fraX] syndrome is a common hereditary disorder associated with a fragile site marker at Xq27.3 which clinically presents as a form of mental retardation (MR). Postmortem investigation of 3 fraX positive males with mild to moderate MR did not document any gross neuropathological changes. Golgi analysis of neocortical dendritic spine morphology extended our previous observations of immature, long, tortuous spines in one adult case of fraX (Rudelli, et al., Acta Neuropathologica 67:289-295, 1985) to 2 new cases. Evidence for similar dendritic spine abnormalities was found, although Golgi analysis was less than optimal because of incomplete dendritic stain impregnation. Neocortical intra-layer cell density was also investigated in all 3 cases. Cresyl violet stained neurons were counted in 10 randomly selected fields in neocortical layers II-VI of cingulate and temporal association areas (Brodmann's areas 23 and 38). Neuron counts in fraX and control neocortex showed no significant differences. Thus, abnormal dendritic spine morphology with preservation of neuronal density appears to characterize the neocortex in individuals with this common form of mental retardation.

Copurification of Sp33-37 and scrapie agent from hamster brain prior to detectable histopathology and clinical disease.

Studies were conducted to determine whether accumulation of the scrapie agent protein Sp33-37 in brain correlated with the appearance of the scrapie agent or with pathology. The concentrations of the scrapie agent and Sp33-37 were measured in purified fraction P5 isolated from hamster brains at weekly intervals after inoculation. The scrapie agent concentration in fraction P5 was approximately 10(-1) LD50/g brain 1 day post-inoculation and increased to 10(9.4) LD50/g at day 77. Sp33-37 was first detected in P5 at day 21, when the agent titre was 10(3.9) LD50/g. Sp33-37 concentration increased in concert with the scrapie agent concentration, although the apparent rate of increase was somewhat lower for the protein than for the agent. The histopathological evidence of disease, consisting of mild vacuolation and gliosis, was first seen at 35 days, but was not conspicuous until 49 to 56 days post-inoculation. Vacuolation and gliosis increased until termination of the experiment at day 77. Amyloid plaques were first detected at 56 days and were widespread at day 77. Clinical disease was first seen in these animals at day 66, with an average onset at day 71. Control animals inoculated with buffer alone showed some mild gliosis, but were otherwise normal. The fact that Sp33-37 purified with the scrapie agent isolated from brain 14 days prior to detectable (light microscopic) pathology supports the theory that Sp33-37 is the major structural component of the scrapie agent and not solely a product of the pathology.

The Fra(X) syndrome: neurological, electrophysiological, and neuropathological abnormalities.

We have evaluated 62 fragile X syndrome [fra(X)] individuals (55 males and 7 females) with different degrees of developmental disabilities that were clinically non-progressive and non-focal in character. The mean age for the 55 males was 23.1 years +/- 14.3 SD with a range of 2-70: for the 7 females, the mean age was 15.7 years +/- 3.5 SD with a range of 10-20 years. Mental retardation (MR) was found in 53 males (8/53 [15.1%] mild, 26/53 [49.1%] moderate, 14/53 [26.4%] severe, and 5/53 [9.4%] profound). Learning disabilities were found in 2/55 (3.6%) of males. One of the 7 females had mild and one had moderate MR: the other 5 were learning disabled. Autistic stigmata were present in 10/62 (16%) of the patients. Only 14/62 (23%) had a history of seizures, all of which were controlled with anticonvulsants. In 36/62 cases, an electroencephalogram (EEG) was performed. We compared these data with that of others. Brain stem auditory evoked response (BAER) was performed in 12 cases. Abnormalities were found in only 5/12. Neuroimaging and computerized cranial transaxial tomography (CT scan) were performed on 21/62 (34%) of the patients. Only 8 of these 21 (38%) studies were abnormal. One patient died; neuropathological studies showed mild brain atrophy, with light microscopic and ultrastructural abnormalities. Rapid Golgi dendritic spine patterns showed that the proximal apical segments were abnormally developed. Very thin, long tortuous spines with prominent terminal heads and irregular dilatations were present. Marked reductions in the length of the synapses, as determined on EPTA-postfixed tissue where noted.(ABSTRACT TRUNCATED AT 250 WORDS)

Alterations in the immune system in cats fed diets with excess cystine.

As part of an ongoing biochemical study in nutrition we examined blood profiles, serum chemistry, lymphocyte transformation and lymphoid pathology in cats fed a diet containing 5% cystine with and without taurine. Automated blood counts of whole blood samples showed a decrease in red blood cell counts accompanied by a significant decrease in hemoglobin and hematocrit in cats fed 5% cystine in the absence of taurine compared to cats fed 0.05% taurine (control). A significant increase was noted in serum cholesterol in cats fed cystine and cystine/taurine compared to cats fed control diets. There were no significant differences in lymphocyte transformation using leukocytes isolated from the spleen and blood with the mitogens, phytohemagglutinin and pokeweed. However, lymphocyte transformation of both spleen and blood without mitogen from the excess cystine group were significantly higher than leukocytes from the 0.05% taurine group (control). Pathological examination of regional lymph nodes, livers, and spleens showed histological abnormalities in cats fed the excess cystine diet. These results indicate that there are alterations in the immune system of cats fed a diet containing 5% cystine with and without dietary taurine.