Steroid Therapy In Patients Research Articles

Glycemic Crises in Patients with Hematologic Malignancies

Persons with hematologic malignancies such as leukemia, lymphoma, or myeloma often have coexisting medical conditions. Among these may be diabetes mellitus. The physiologic and psychologic stress of diagnosis and treatment may precipitate the life-threatening complications of DKA or HHNS in this group of patients. People with personal risk factors may develop diabetes mellitus secondary to diagnosis and treatment and present with either DKA or HHNS. It is essential that the health care team have a heightened awareness of potential complications. These are complex syndromes involving severe hyperglycemia, metabolic acidosis, fluid and electrolyte imbalances, and neurologic and cardiovascular collapse. Working collaboratively with the critical care team to provide optimal care, nurses play an essential role in the management of these challenging complications of diabetes mellitus.

Increased non-articular tenderness in patients on steroid therapy

Increased non-articular tenderness and tender shins have been suggested to be associated with steroid therapy in patients with lupus. The aim of the present study was to extend this observation in a different disease, inflammatory bowel disease (IBD), and to examine the relationship between tenderness, dosage and duration of steroid therapy. Eighty-seven patients with 11313, 23 of them on steroid therapy, were assessed for disease activity and nonarticular tenderness. A count of 18 tender points was conducted by thumb palpation, and tenderness thresholds were assessed by dolorimetry at four shin sites, nine tender point sites and four control point sites. Patients on steroids were significantly more tender than subjects not on steroids: their mean tender point counts were 13.3 and 6.7 ( p<0.001), respectively, and the dolorimetry thresholds at all three sites were significantly lower in the steroid group ( p<0.001). Increased tenderness was also associated with increased steroid dosage. However, tenderness was not related to duration of steroid therapy, to gender, or to previous steroid therapy being discontinued at least a year ago. Disease activity was neither related to tenderness nor to steroid treatment. The demonstration of increased tenderness in IBD patients on steroid therapy, in addition to earlier observations in lupus, may suggest that such a relationship is not disease specific. The recognition of this association is important to physicians treating patients with steroids and will prevent misinterpretations of complaints about tender shins and diffuse tenderness as part of the disease entity itself.

A new scoring system to predict the efficacy of steroid therapy for patients with active myocarditis--a retrospective study.

The efficacy of steroid therapy for active myocarditis is controversial, so a new scoring system was constructed based on 6 clinical parameters: (1) the mode of onset of the disease; (2) complications of immune-related systemic disorders; (3) evidence of viral infection; (4) the population of infiltrating inflammatory cells; (5) the appearance of multinucleated giant cells in endomyocardial biopsy specimens; and (6) the duration of active myocarditis. Points from -2 to +2 were assigned to each parameter and the total score was calculated from the 6 parameters. Twenty-one patients with clinically suspected myocarditis, who had been admitted to hospital from 1987, were retrospectively analyzed by this scoring system. Sixteen patients were treated without corticosteroids at presentation, and 5 patients were treated by conventional methods with adjunctive use of corticosteroids. In 10 patients of the non-steroid group myocarditis improved and their mean score was -4.8 at presentation. In 6 patients of the non-steroid group, myocarditis and cardiac symptoms persisted after initial therapy, and their score at presentation was -0.8. In 2 patients of the steroid group myocarditis improved after initial therapy and their score was +2. In 2 other patients of the steroid group, myocarditis and cardiac symptoms persisted and their score was +3. Another patient of the steroid group died from congestive heart failure and his score was -5 at presentation. In 8 of 9 patients with persistent myocarditis, the secondary phase therapy was challenged. Seven patients were treated with corticosteroids and 6 patients improved. Their score at the secondary phase was +2.5. Overall, non-steroid conventional treatment was successful in patients with the scores from -5 to -4, and steroid therapy succeeded in patients with scores from 0 to +6. Although this is a retrospective study, this scoring system is able to predict the efficacy of steroid therapy in patients with clinically suspected active myocarditis.

Are corticosteroids salvage therapy for refractory acute respiratory distress syndrome?

Background: Late acute respiratory distress syndrome (ARDS), characterized by progressive pulmonary interstitial fibroproliferation, is associated with mortality >80%. Although previous large prospective trials failed to show a benefit of steroids in early ARDS, recent small reports describe improved survival in patients with late ARDS. Recognizing the pathogenetic differences between early and late ARDS, we employed steroid therapy in patients with refractory late ARDS. Patients and methods: Over a 5-year period, we treated 6 patients who were dying of isolated refractory ARDS with methylprednisolone sodium succinate (1 to 2 mg/kg every 6 hours). Ventilatory parameters and lung injury scores were serially recorded, and steroids were weaned based on clinical response. Results: Steroids were instituted after 16 days of advanced mechanical ventilatory support. By day 7 of steroid therapy, there was clinically significant improvement in PaO 2 FiO 2 ratios (84 to 172) and lung injury scores (3.6 to 2.9); 5 patients (83%) survived. Conclusions: Steroid therapy appears to be effective in patients with refractory late ARDS. Prospective trials are needed to define the indications, timing of intervention, dose and duration, and precautions of steroid therapy.

Drug-induced Immune Thrombocytopenia

SUMMARY. Immune thrombocytopenia is a relatively common problem associated with the clinical usage of drugs. Drugs frequently implicated include quinine, quinidine, heparin, penicillins, cephalosporins, co-trimoxazole, gold and D-penicillamine. Bleeding including bruising and purpura is the usual clinical manifestation except in immune heparin-induced thrombocytopenia in which thrombosis occurs more frequently than bleeding. Cessation of the offending drug is the important step in the treatment but other measures may also be required such as platelet transfusion and steroid therapy for patients with clinical bleeding or antithrombotic therapy with warfarin and dextran or low molecular weight heparin/heparinoid for patients with heparin-induced thrombocytopenia and thrombosis. Idiosyncratic drug-induced thrombocytopenia is mediated by an antibody which binds to platelets only in the presence of the drug resulting in the clearance of sensitised platelets by the reticuloendothelial system. In quinine/quinidine-induced thrombocytopenia, the antibodies recognise drug-dependent epitopes on platelet membrane glycoproteins Ib-IX and/or glycoproteins IIb-IIIa. In immune heparin-induced thrombocytopenia the current data suggest a mechanism which probably involves the binding of heparin-antibody complexes to the platelet Fc receptors but the precise mechanism is yet to be fully characterised. The associated thrombosis in this condition is likely to be due to platelet activation and possibly endothelial cell damage induced by the heparin-related antibody.

Corticosteroid-induced Myopathy and the Respiratory Muscles: Report of Two Cases

Two women with connective tissue disease developed a characteristic steroid-induced myopathy. Reduced maximal transrespiratory pressures indicated reduced respiratory muscle strength. Gradual steroid dosage tapering resulted in prompt clinical improvement and marked increases in respiratory muscle strength, maximal inspiratory pressure increasing by 33 percent in one patient and by 70 percent in the other. This reversible steroid-induced respiratory muscle weakness may be of great significance in reconsidering long-term steroid therapy in patients with underlying lung disease.

Growth and sexual development before and after sex steroid therapy in patients with thalassemia major

Growth and sexual development before and after sex steroid therapy in patients with thalassemia major

Growth and Sexual Development Before and After Sex Steroid Therapy in Patients With Thalassemia Major

Growth, sexual development, and hypothalamic-pituitary-gonadal function were evaluated in 23 patients with thalassemia major (14 female and nine male) aged 13 to 29 years. Five women (group 1) with hemoglobin levels of less than 7 g/dL, which were maintained by transfusions during childhood, did not spontaneously enter puberty. They had evidence of severe hypothalamic-pituitary dysfunction. Maintaining hemoglobin levels of about 8 g/dL resulted in spontaneous onset of puberty in seven of nine female patients (group 2), but had no such ameliorative effect on the nine male patients. In the latter, peak luteinizing hormone (LH) responses to gonadotropin releasing hormone correlated with bone age. Treatment with testosterone produced inconsistent partial inhibition of LH and follicle-stimulating hormone (FSH) responses to stimulation. After discontinuation of testosterone treatment, a rebound of basal testosterone, LH, and FSH levels was observed, but this was not sustained. These findings are compatible either with dysfunction of hypothalamic maturation or with partial pituitary dysfunction. Four of the group 1 females and six of the males treated with appropriate sex hormones showed satisfactory pubertal progression. Acceleration in linear growth was observed in four of the male patients whose epiphyses were still open. Treatment was well tolerated in all patients.

Laryngeal Complications in a Patient With Inactive Systemic Lupus Erythematosus

Laryngeal complications in systemic lupus erythematosus (SLE) are rarely described. They range from hoarseness to life-threatening respiratory distress. To our knowledge, previous reports describe laryngeal involvement with SLE occurring only during periods of active disease. We saw a patient with inactive SLE in whom hoarseness and exertional dyspnea developed as a result of arytenoiditis and vocal cord paresis during steroid tapering. The condition responded dramatically to readjustment of her steroid dosage. Involvement of the larynx with SLE is a potentially life-threatening complication and may occur in patients with either active or inactive disease. It is an indication for close observation and steroid therapy in patients with SLE.

Minimal Change Nephrotic Syndrome in Children: Deaths During the First 5 to 15 years’ Observation. Report of the International Study of Kidney Disease in Children

Of 521 children with a previously untreated nephrotic syndrome, as defined by proteinuria greater than or equal to 40 mg/h/m2 and serum albumin less than or equal to 2.5 g/dL, entering the International Study of Kidney Disease in Children between January 1967 and April 1976, 389 showed minimal changes on renal biopsy. Of these, seven boys and three girls died, all before July 1972. Infection was the cause of death in six patients. One child died of dural sinus thrombosis, one died as a result of cardiorespiratory failure following salt-poor albumin infusion, and another died from chronic renal failure due to focal and segmental glomerulosclerosis not apparent on initial biopsy. The mode of death in the remaining child was uncertain. Analysis according to histopathologic subgroups of minimal change disease showed no statistically significant differences in the incidence of deaths, although mesangial abnormalities and tubular atrophy were associated with higher mortality than nil disease or focal glomerular obsolescence. Nine of the ten children who died had either failed to respond to initial prednisone therapy (initial nonresponders, n = 5), or responded but relapsed during the initial 8 weeks of treatment (early relapser, n = 4), even though only one quarter of the total sample were nonresponders or early relapsers (P less than .0005). Nearly one fifth of all initial nonresponders with minimal change nephrotic syndrome died. Thus the pattern of response to initial steroid therapy in patients with minimal change nephrotic syndrome may have prognostic significance.

Minimal Change Nephrotic Syndrome in Children: Deaths During the First 5 to 15 Years' Observation

Of 521 children with a previously untreated nephrotic syndrome, as defined by proteinuria ≥40 mg/h/m2 and serum albumin ≤2.5 g/dL, entering the International Study of Kidney Disease in Children between January 1967 and April 1976, 389 showed minimal changes on renal biopsy. Of these, seven boys and three girls died, all before July 1972. Infection was the cause of death in six patients. One child died of dural sinus thrombosis, one died as a result of cardiorespiratory failure following salt-poor albumin infusion, and another died from chronic renal failure due to focal and segmental glomerulosclerosis not apparent on initial biopsy. The mode of death in the remaining child was uncertain. Analysis according to histopathologic subgroups of minimal change disease showed no statistically significant differences in the incidence of deaths, although mesangial abnormalities and tubular atrophy were associated with higher mortality than nil disease or focal glomerular obsolescence. Nine of the ten children who died had either failed to respond to initial prednisone therapy (initial nonresponders, n = 5), or responded but relapsed during the initial 8 weeks of treatment (early relapser, n = 4), even though only one quarter of the total sample were nonresponders or early relapsers (P &amp;lt; .0005). Nearly one fifth of all initial nonresponders with minimal change nephrotic syndrome died. Thus the pattern of response to initial steroid therapy in patients with minimal change nephrotic syndrome may have prognostic significance.

The use of the 12 minute walking test in assessing the effect of oral steroid therapy in patients with chronic airways obstruction

The reproducibility of the 12 minute walking distance (12MD) was assessed in ten men with chronic airways obstruction, and the 12MD was used, together with spirometry, transfer factor and three subjective assessments of breathlessness to evaluate the effects on respiratory function of prednisone 30 mg daily given orally in double-blind placebo-controlled fashion for two weeks. Like others, we found the 12MD reproducible on a single day with a mean variation of 3.1%. Tests performed two weeks apart showed greater variability ranging from 0.2% to 30.9%, (mean 9.1%). During placebo and prednisone therapy the 12MD and assessments of breathlessness correlated significantly with each other and with TLCO, but not with spirometry. Following steroid therapy there was a significant increase in mean TLCO but no significant change in 12MD, spirometry or subjective assessments. Changes in 12MD and TLCO correlated significantly with each other and with changes in subjective assessments. Changes in FEV 1 correlated with changes in breathlessness, and also with variability in FEV 1 while receiving placebo. Individuals with the greatest changes in 12MD and FEV 1 were those with the greatest variability on placebo. The variability of the 12MD and FEV 1 should be measured in individuals before using these tests to assess response to steroid therapy.

In vitro steroid sensitivity testing: a possible means to predict response to therapy in primary hypoproliferative anemia.

We investigated the effects of various steroids on erythroid colony formation by normal human bone marrow and peripheral blood, and by marrow and peripheral blood from 18 patients with primary hypoproliferative anemia. These agents were variously found to enhance both CFU-E and BFU-E derived colony growth by normal human cells. Fluoxymesterone and dexamethasone were the most active inducers of CFU-E proliferation, and etiocholanolone and dexamethasone were the most potent burst augmenters. Androsterone did not significantly influence BFU-E proliferation in 66% of the marrow cultures from hematologically normal donors. Colony formation by erythroid progenitor cells of the patients with hypoproliferative anemia was reduce (20 +/- 10 CFU-E derived colonies/6 X 10(4) marrow cells; 12 +/- 5 BFU-E derived colonies/1 X 10(5) blood cells) when compared to growth by normal cells (65 +/- 14 CFU-E derived colonies/6 X 10(4) marrow cells; 21 +/- 9 BFU-E derived colonies/1 X 10(5) blood cells). Colony formation by marrow or peripheral blood cells of eight patients with steroid-responsive anemia was only moderately reduced (26 +/- 11 CFU-E derived colonies/6 +/- 10(4) marrow cells; 17 +/- 3 BFU-E derived colonies/1 X 10(5) blood cells) when compared to growth by marrow cells of three steroid-unresponsive patients (3 +/- 1.5 CFU-E derived colonies/6 X 10(4) cells). Whereas the addition of steroids of the same class to marrow and peripheral blood cultures of the steroid-responsive patients enhanced colony growth by 60-300%, their addition to marrow cultures of the steroid-unresponsive patients increased colony growth by less than 60%. It appears that further investigations using in vitro culture techniques as predictors of response to steroid therapy in patients with hypoproliferative anemia may be warranted.

The effect of vitamin A on the immunosuppressive action of cortisone on skin homografts in mice.

The use of immunosuppressive steroid therapy in patients having transplant operations is associated with increasing numbers of patients with wound healing problems. Vitamin A is known to prevent some biological effects of steroids, including impaired gain in strength of healing wounds and impaired epithelialization of open wounds. Other effects of steroids are not affected by vitamin A. Before vitamin A can be safely used to promote wound healing in transplant patients having steroid immunosuppressive therapy, it is essential to determine whether the immunosupprressive action could be impaired by vitamin A. A study was designed using skin homografts in mice to determine whether vitamin A administration affected the prolongation of homograft survival resulting from cortisone therapy. Although in these experiments vitamin A was not found to influence significantly the immunosuppressive action of cortisone, further experiments are required entailing the use of different doses of vitamin A and also a different homograft model, before any conclusions can be made concerning the likely effect of the use of vitamin A in transplant patients having immunosuppressive steroid therapy.

Evaluation of Corticosteroid and Exchange-Transfusion Treatment of Acute Yellow-Phosphorus Intoxication

To evaluate steroid therapy in patients acutely intoxicated with yellow phosphorus, 49 patients were sequentially assigned to one of three groups. Group A did not receive steroids at any time, Group B received steroids from the time of admission, and steroids were used in Group C only when liver coma developed. Two out of four patients in coma recovered in Group A, none out of five in Group B, and four out of seven in Group C. Thus, steroids did not appear to prevent onset of coma in this type of liver injury and did not increase survival after development of coma. In another group of 44 patients similarly intoxicated, deep hepatic encephalopathy developed in 15. Five of these were given exchange transfusions, with two deaths and three survivals. Of the 10 not given exchange transfusions, seven died, and three survived.

An overview of idiopathic optic neuritis in eastern Nepal

Inflammation of the optic nerve is a common cause of visual loss due to optic nerve pathology. To report the clinical features, demographic pattern and response to pulse steroid therapy in patients with idiopathic optic neuritis in eastern Nepal. The hospital data of patients with idiopathic optic neuritis admitted to the department of ophthalmology in a tertiary level center in eastern Nepal between Jan 2000 to Dec 2006 were retrospectively analyzed. The parameters studied were demographic pattern, clinical features, visual acuity and field defects. Thirty-six patients (52 eyes) were found to have optic neuritis (papillits in 36 and retrobulbar optic neuritis in 16 eyes). The male to female ratio was 1.25:1. The mean age of the patients was 33.56 +/- 17.88 years (95% CI = 24.66-42.45). The most common modes of presentation were loss of visual acuity and color vision defect. One patient had features suggestive of multiple sclerosis. Vision improved in 42 eyes at discharge from the hospital. Response to pulse methylprednisolone therapy was good in most (42 eyes) of the cases except for the patients having initial visual acuity of no light perception. Response to pulse methylprednisolone therapy is good in patients with initial visual acuity of at least perception of light. Demographic and clinical features of our patients were different from those reported from the western world. Some similarity was observed between studies reported from the oriental countries.

Effects of steroids on cerebral edema in cats.

ALTHOUGH clinically the beneficial effect of steroid therapy in patients with cerebral edema is well established, 1,2 only recently has experimental evidence indicated that dexamethasone treatment may diminish cerebral edema associated with traumatic lesions. Poor parameters for assessing the extent of edema, insufficient experimental time interval, and lack of control regarding the biological activity of the drugs in the species used are some of the reasons why the studies reported to date have been contradictory or inconclusive. 3-11 Thus, previously we could not demonstrate any effect of cortisone on water and electrolyte content of edematous cerebral tissues of the cat. 3 These earlier experiments, however, did not rule out the possibility that the volume of the tissue which became edematous was diminished in treated animals nor was there any assurance that the cat responds to cortisone in the same way as the human. The present study was designed

AVASCULAR NECROSIS OF BONE COMPLICATING STEROID THERAPY.

The effects of steroids on the skeleton have been described extensively, and it is not surprising that most of the information regarding joint changes in this context has been obtained from the study of the effects of steroids on rheumatoid disease or osteoarthritis. In these conditions it is of some interest that cortisone and its analogues may sometimes appear to hasten a destructive process, especially in weight-bearing joints such as the hip (Ansell, 1958; Chandler and Wright, 1958; Chandler, Jones, Wright and Hartfall, 1959; Murray, 1960; 1961; Sweetnam, 1960). It is felt that this type of joint lesion must be distinguished clearly from avascular necrosis of bone occurring in association with steroid therapy in patients without evidence of previous arthropathy. Prior to 1963 few examples of such a condition were recorded. Four cases were described by Heimann and Freiberger (1960), two of their patients showing changes in both the femoral and humeral heads. One case, also with hips and shoulders affec...

Steroid Therapy in Patients with Polymyositis and Dermatomyositis

Excerpt Polymyositis and dermatomyositis cause weakness and atrophy (1, 2) of muscle. Eaton in a classic paper delineated the clinical syndrome of polymyositis and noted that the muscular componen...