Clinical outcomes in patients with renal artery stenosis treated with stent placement with embolic protection compared with those treated with stent alone

Purpose: To compare the clinical outcomes in patients with chronic renal insufficiency (CRI) and renal artery stenosis (RAS) following renal artery (RA) stent placement with and without embolic protection device (EPD) usage. Materials and Methods: Eighteen patients who had RA stent placement with EPD were matched to control patients (RA stent only). Blood pressure, number of hypertensive medications, and estimated glomerular filtration rate (eGFR) at 3 months before the procedure and after 12 months were determined. An increase of ≥ 20% in eGFR at 12 months from baseline was defined as "improvement," decrease of ≥20% as "deterioration," and an eGFR change between those values as "stabilization" at 12 months. Results: At 12 months, stage 4 patients treated with EPD had significantly higher eGFR than controls (P = .01). There was no statistical difference in blood pressure outcomes between the 2 groups. Conclusions: Patients with stage 4 CRI did significantly better with EPD than those treated without it.     

Comparison of clinical and electrodiagnostic features in B12 deficiency neurological syndromes with and without antiparietal cell antibodies

Background and aims

This study was undertaken to compare the clinical and electrodiagnostic (Edx) features in autoimmune and nutritional vitamin B12 deficiency neurological syndromes.

Methods

Consecutive patients with vitamin B12 deficiency neurological syndromes were evaluated and blood counts, red blood cell indices, serum chemistry, thyroid function, HIV serology, antiparietal cell antibody (APCA), serum B12, bone marrow and spinal MRI assessed. EDx studies included nerve conduction, tibial somatosensory (SEP) and motor evoked potential (MEP) to the tibialis anterior, and visual evoked potential (VEP). The results were compared between APCA positive and negative groups.

Results

57 patients aged 17–80 years (mean 45.3) were studied; 48 were vegetarians. The presenting clinical syndromes were myeloneuropathy in 25, myelopathy in 14, myeloneuroencephalopathy in 13, myeloencephalopathy in four and behavioural abnormality only in one patient. Spinal MRI in 47 patients revealed posterior spinal cord hyperintensity in 21 and cord atrophy in six. Nerve conduction was abnormal in 15%, MEP in 56.6%, SEP in 87.3% and VEP in 63.6% of patients. At 3 months, 31 patients had complete, 11 partial and three poor recovery. APCA was positive in 49% of patients. There was no difference in clinical, MRI or Edx findings or outcome between the APCA positive and negative groups.

Conclusion

APCA was positive in 49% of patients with B12 deficiency neurological syndrome but their clinical, MRI and Edx changes were not different from the APCA negative group. Neurological manifestations may be caused by B12 deficiency itself rather than the underlying cause.Vitamin B12 deficiency is common in vegetarians, especially in Hindus and Jains who exclude animal protein from their diet for religious or social reasons. Lower levels of serum B12 have been reported in vegetarians compared with non‐vegetarians in India.¹ Vitamin B12 deficiency can also occur as a result of autoimmune diseases, parasitic diseases, drugs, gastrointestinal surgery, malabsorption and genetic defects, such as transcobalamin II polymorphism.² Pernicious anaemia is an autoimmune disorder in which the gastric mucosa is atrophic, with loss of parietal cells resulting in intrinsic factor deficiency. In the absence of intrinsic factor, less than 1% of dietary vitamin B12 is absorbed. In the nervous system, vitamin B12 acts as a coenzyme in the methyl melonyl CoA mutase reaction which is necessary for myelin synthesis. Vitamin B12 deficiency therefore results in defective myelin synthesis leading to diverse central and peripheral nervous system dysfunctions. Pernicious anaemia may be associated with a number of autoimmune disorders, such as myxoedema, thyrotoxicosis, Hashimoto''s thyroiditis, Addison''s disease and vitiligo. Untreated vitamin B12 deficiency due to autoimmune or nutritional causes results in macrocytic anaemia, subacute combined degeneration of the spinal cord, encephalopathy and neuropathy in various combinations and permutations.^3,4,5,6The different causes of B12 deficiency (that is, nutritional deficiency or autoimmunity) may have different clinical, laboratory and prognostic features because of the effect of autoimmune conditions or the effect of the associated antineuronal autoantibodies. A Medline search using the key words “pernicious anaemia”, “antiparietal cell antibody”, “nutritional deficiency” and “subacute combined degeneration” did not reveal any study comparing the clinical, laboratory findings and prognosis of vitamin B12 deficiency of autoimmune or nutritional aetiology. We have prospectively evaluated patients with B12 deficiency neurological syndrome and compared their clinical, radiological and electrodiagnostic (Edx) findings, and outcome, in terms of the presence or absence of antiparietal cell antibodies (APCA).     

Dapsone hypersensitivity syndrome: a clinico-epidemiological review

Diaminodiphenyl sulphone (dapsone) is a drug of choice in the treatment of leprosy. It is also useful for the treatment of many neutrophilic and other dermatoses. Dapsone hypersensitivity syndrome is a rare but well recognized serious adverse effect characterized by fever, skin rashes, generalized lymphadenopathy, hepatitis, and hepato-splenomegaly. Twenty-six patients with dapsone hypersensitivity syndrome were studied for clinical profile, outcome, and prognosis. The male:female ratio was 2.2:1, and the mean age was 33.19 years (range 13 to 64 years). The interval between start of dapsone therapy and appearance of symptoms varied from 2-7 weeks (mean 29.82 days). Twenty-four patients received dapsone as a part of multi-drug therapy for leprosy; the other two patients received dapsone for lichen planus and acne vulgaris. Exfoliative dermatitis was the most common cutaneous manifestation followed by erythematous maculo-papular eruption and Stevens-Johnson syndrome-like lesion. The other common systemic manifestations were: fever (26 cases), itching (22 cases), lymphadenopathy (21 cases), jaundice (21 cases), pallor (20 cases), hepatomegaly (19 cases), and pedal edema (14 cases). Investigation profile revealed elevated levels of serum liver enzymes in 100% of patients, elevated erythrocyte sedimentation rate in 92.3%, raised bilirubin in 84.6%, leucocytosis in 69.23%, low hemoglobin (<9 gm/dl) in 46.15% and hypoproteinemia in 42.3%. Eosinophilia, hemolytic anemia, and reticulocytosis count were found in 4 patients each. All the patients had favorable outcomes except three who died due to hepatic failure. Medical personnel must be aware of this potentially fatal syndrome, because it can cause considerable morbidity and mortality.     

Secondary Tuberculosis of the Skin

One hundred patients with secondary skin tuberculosis--59 with lupus vulgaris (LV), 27 with scrofuloderma (SD), and 14 with tuberculosis verrucosa cutis (TVC)-were included in this study. The buttocks and lower limbs were seen to be important sites of involvement in LV, besides the occurrence over the face. An active focus of tuberculosis was present in 18, a past history of pulmonary tuberculosis in 8, and intrafamilial tuberculous infections in 21. Histopathology and culture for Mycobacterium tuberculosis were done in all the cases. Guinea pig inoculation was done in 11. The poor results of these investigations have been highlighted and discussed with reference to studies done in the past by other workers. The need for improvement in laboratory techniques is suggested.     

Neurological and developmental outcomes of prenatally cocaine-exposed offspring from 12 to 36 months

Second generation studies of prenatal cocaine exposure failed to find gross deficits after controlling for confounders. Concern remained that exposure could cause subtle deficits. This prospective, cohort study evaluated effects of cocaine on development at 12, 18, 24, and 36 months. From 1991-1993, 361 mother-infant pairs were recruited from the Children's Hospital of New York, Presbyterian Medical Center's prenatal clinic or delivery room suite. Mothers were assigned to the cocaine group based on report of prenatal cocaine use or positive urine toxicology. Control mothers were enrolled from the same clinic and matched for age and socioeconomic status (SES). Women with serious medical problems were excluded from either group. Of the retained cohort, at 12 months, 147 infants were exposed and 89 were unexposed case controls. Both groups were raised in impoverished environments with few supports. Developmental evaluations were conducted blinded to group. Cross-sectional analysis revealed cocaine-related deficits in neurological exams and speech across all time periods, in spite of catch up in weight, length, and head circumference. Overall analysis of development was evaluated using Generalized Estimating Equations regression analysis. Bayley Mental [Badj = -6.5 (CI--9.4, -3.5, p < or = 0.001)] and Psychomotor [Badj = -3.9 (CI--7.4, -0.5, p = 0.02)] Developmental Indices showed deficits after controlling for confounders. Males were more vulnerable to cocaine exposure for height, motor development, and emotional regulation. Dose-response relationships existed for abnormal neurological exams (Ptrends < 0.08), Mental Development Index (MDI) (Ptrend < 0.001), and Psychomotor Development Index (PDI) (Ptrend < 0.001) deficits. Although nonexposed children performed poorly, cocaine-exposed children showed worse performance. Both groups showed declines at 18 months in mental and psychomotor development from which only nonexposed children rebounded. Overall, cocaine exposure adds an additional risk to disadvantaged children's development. Cocaine-exposed children are less resilient to effects of these multiple risks.     

New norms for a new generation: cognitive performance in the framingham offspring cohort

A previous publication presented normative data on neuropsychological tests stratified by age, gender, and education based on the Original Cohort of the Framingham Heart Study. Many contemporary investigations include subject samples with higher levels of education, a factor known to affect cognitive performance. Secular change in education prompted the reexamination of norms in the children of the Original Cohort. The study population consisted of 853 men and 988 women from the Offspring Study, free of clinical neurological disease, who underwent a neuropsychological examination, which included tests given to their parents in 1974 to 1976 as well as additional newer tests to provide a more comprehensive battery. The Offspring population overall was more evenly distributed by gender and better educated. Their performance on cognitive tests was superior to that of the Original Cohort. Multivariable analyses revealed that more years of education explained only a part of the cohort differences. These findings suggest that continued surveillance of each generation is necessary to document the impact that unique social and economic variables have on cognitive function. Here, the authors provide updated normative data.