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Biomedical subjects

H M Sharma

Publications and source records attributed to H M Sharma.

At least 37 records · Page 2Linked to original sources

Infectious hazards in the clinical laboratory: a program to protect laboratory personnel.

The increasing risk of exposure to blood-borne pathogens in the health care setting makes the development of effective infection control programs in the laboratory workplace critical. Central to such programs is the concept of universal precautions. The program described here relates the level of protection or precaution to the potential danger for infection, given the laboratory workstation and task which is to be performed. Four Levels of Protection are described. Implementation of this program requires that each workstation and procedure in each laboratory section be reviewed by the laboratory director and supervisory personnel for risk of exposure. Implementation additionally requires that provisions be made for both the initial and continuing education of laboratory employees. Laboratory directors and supervisors should also monitor the program to ensure compliance. There will certainly be situations unique to individual institutions or laboratory settings that may require precautions or policies over and above those described by universal precautions. Laboratory policies will not gain acceptance if they are developed and implemented without the advice and cooperation of the hospital medical staff. Employee acceptance of infection control policies will be greater if actual development and implementation actively involves the laboratory personnel who will practice them. The program described here is but one approach to the problem. Employers and laboratory directors must understand that it is their responsibility to develop a program that provides appropriate safeguards for workers who may be exposed to infectious agents in the laboratory workplace and to ensure that employees are properly trained and educated in the proper use and application of those safeguards.

Acquired Immunodeficiency Syndrome↗

Thyroid-stimulating immunoglobulin as a cause of recurrent intrauterine fetal death.

Hyperthyroidism is one of the numerous causes of infertility and recurrent abortion. Little mention has been made, however, of the specific role of thyroid-stimulating immunoglobulin (TSIg) as a potential etiology, especially in the clinically euthyroid mother. This report describes a case of intrauterine fetal death in a euthyroid woman with TSIg.

Adult↗

A unique familial lobular glomerulopathy.

Five members of a family (four brothers and their father) were found to have proteinuria and microhematuria. One of the affected brothers developed chronic renal failure. Although a renal biopsy was never performed, this brother has subsequently received a renal transplant from a clinically unaffected sister. Renal biopsy was performed on four of the siblings (three brothers and the sister). Renal tissue from all three brothers who underwent biopsy showed similar glomerular lesions, characterized by striking cloverleaf expansion of glomerular lobules by an acellular hyaline material and segmental mesangial cell proliferation. Electron microscopy showed massive mesangial and subendothelial deposits and occasional areas of glomerular basement membrane splitting with round inclusions. The renal biopsy specimen of the sister was normal on light and electron microscopy and negative for immunoglobulins and complement on immunofluorescent staining. Immunofluorescence microscopy on one of the male siblings was negative for immunoglobulins and complement. No other physical or serologic abnormalities could be established. To our knowledge, this is a unique form of familial glomerulopathy that has not been previously described.

Adult↗

Dissecting hematoma (aneurysm) of coronary arteries.

Isolated dissecting hematoma (aneurysm) of a coronary artery is a rare occurrence that often results in myocardial infarction and sudden death. A case of dissecting hematoma involving the left main, left anterior descending, and left circumflex coronary arteries is described in a patient who had received vigorous closed-chest cardiac resuscitation. This is believed to be the first reported case of coronary artery dissection caused by epicardial trauma from closed-chest cardiac resuscitation. This case demonstrates that dissecting hematoma of the coronary artery can be a complication of cardiac resuscitation.

Aged↗

Atheroembolic renal disease causes hypocomplementaemia.

7 patients with atheroembolic renal disease were found to have hypocomplementaemia. Evidence obtained in an experimental model of atheroembolic disease shows that the hypocomplementaemia is the result of complement activation by the atheromatous material in vivo. In addition to hypocomplementaemia, 6 patients had thrombocytopenia and 5 had eosinophilia. These observations indicate that atheroembolic disease should now be included in the differential diagnosis of hypocomplementaemia. In addition, atheroembolic disease should be considered in patients presenting with a combination of multisystem disease, hypocomplementaemia, thrombocytopenia, and eosinophilia--a syndrome which previously would have been regarded as diagnostic of immune-complex-mediated vasculitis.

Aged↗

Mitomycin-C induced improvement in superficial bladder tumors: a morphologic and immunohistochemical evaluation.

Twenty bladder biopsies from ten patients with superficial transitional cell carcinoma were obtained prior to and following therapy with intravesical mitomycin-C. Each biopsy was evaluated histologically and immunohistochemically for A, B, H blood group antigen (BGA) expression. A, B and H blood group antigens were identified using monoclonal anti-A, B and H antibody and were localized with the avidin-biotin-peroxidase complex (ABC) technique. Particular attention was directed toward flat urothelial lesions and the urothelium adjacent to papillary tumors. Routine histologic evaluation showed improvement in post-therapy biopsies compared to corresponding pre-therapy biopsies in 7/10 cases but was equivocal in 3/10 cases. Immunohistochemical evaluation, however, showed improvement in all 10 cases, as judged by increased urothelial BGA expression. This increase in urothelial BGA expression after intravesical mitomycin-C therapy suggests a therapy induced improvement in dysplastic urothelium which was not uniformly evident on routine histologic examination.

Biopsy↗

Cyclosporine-associated renal arteriopathy resulting in loss of allograft function.

Cyclosporine-associated arteriopathy was the cause of graft loss in 40 percent of all allografts that failed in a series of 200 consecutive cadaveric renal transplants. Arteriopathy was diagnosed by biopsy and renal uptake of indium 111m labeled platelets in the face of acute renal deterioration. A moderate thrombocytopenia and microangiopathic picture of hemolytic uremia was also present on peripheral blood smear. Immunofluorescence and histologic characteristics of the allograft biopsy specimens failed to show evidence for acute rejection: immunoglobulin M, immunoglobulin A, immunoglobulin G, C1q, C3, and C4 were not present, and there was no evidence of an interstitial or vascular mononuclear cellular infiltrate. Two clinical presentations have been described. In Group I (seven patients), anuria occurred rapidly within the first 2 weeks after transplantation. In Group II (nine patients) renal function gradually diminished 1 to 5 months after starting cyclosporine therapy. Fifteen of the 16 recipients had progressive and irreversible loss of renal function which was pathologically associated with fibrin deposition, intimal proliferation, and thrombotic occlusion of the cortical interlobular and arcuate arteries, with subsequent focal glomerular ischemia and cortical infarction. One recipient with rapid loss of renal function received an intraarterial allograft infusion of streptokinase and subsequent systemic heparinization, which resulted in return of normal allograft function. The syndrome of cyclosporine-associated arteriopathy has been linked to a lack of or reduced amounts of prostacyclin-stimulating factor or prostacyclin.

Arterial Occlusive Diseases↗

Alveolar soft part sarcoma of the vagina: an immunohistochemical and electron microscopic study.

Alveolar soft part sarcoma is a soft tissue neoplasm of unknown histogenesis which has a distinctive morphology. It is a relatively rare tumor with approximately 200 cases described in the literature. Only two cases have previously been reported as occurring in the vagina. The purpose of this paper is to report the third case of alveolar soft part sarcoma occurring in the vagina and to emphasize the role of electron microscopy in the differential diagnosis.

Adenocarcinoma↗

Glomerular basement membrane splitting and microaneurysm formation associated with nitrosourea therapy.

A patient who developed renal insufficiency following nitrosourea therapy is reported. Light, immunohistochemical, and electron microscopic studies of the renal biopsy disclosed an unusual glomerular basement membrane injury. Light microscopy showed extensive basement membrane splitting and capillary aneurysm formation. Electron microscopic examination revealed an extensive subendothelial accumulation of electron-lucent granular material. The glomerular basement membrane was separated from the mesangium and showed splitting of the lamina densa. Immunofluorescent and immunoperoxidase staining of the glomeruli was negative for immunoglobulin, complement, and fibrinogen. This form of nitrosourea-associated glomerular injury has not been described previously.

Adenoma, Islet Cell↗

Adverse effect of exercise on immune complex-mediated glomerulonephritis.

To assess the effect of strenuous daily exercise on immune complex-mediated glomerulonephritis (GN), rabbits were randomly assigned to one of three experimental groups: Group I (n = 12): treadmill exercise for 28 days plus twice weekly intravenous injections of saline. Group II (n = 10): treadmill exercise for 28 days plus twice weekly intravenous bovine serum albumin (BSA) injection. Group III (n = 9): intravenous doses of BSA, as in group II, but no exercise. Blood and urine samples were collected from each animal periodically during the 28-day experimental period. On the 29th day of the study all animals were sacrificed and tissue taken for renal histopathologic studies. We found that in group II (exercise + GN) abnormal albuminuria was more frequent (p less than 0.001), blood urea nitrogen (BUN) levels rose significantly with time (p less than 0.02) and hematuria (blood in renal tubules) was more common (p less than 0.05), compared to group III (GN only). The differences between groups II and III could not be explained by the effect of exercise alone since group I (exercise only) developed no abnormal albuminuria, BUN levels or hematuria during the course of the study. These findings suggest that strenuous exercise superimposed on active immune complex-mediated GN results in worsening of the abnormal glomerular function.

Animals↗

Responses of the ischemic acute renal failure kidney to additional ischemic events.

To test whether the ischemic acute renal failure (IARF) kidney has increased susceptibility to additional ischemic events, IARF was induced in female Sprague-Dawley rats [40 min of bilateral renal artery occlusion (RAO)] and either 18 or 48 hr later, at the height of morphologic injury, they were rechallenged with either 25 or 40 min of RAO. Changes in renal function (GFR, blood flow), morphology, and adenine nucleotide (AN) concentrations in response to these second ischemic challenges were compared to those of normal kidneys subjected to a single ischemic event. In additional experiments, rates of recovery from IARF were compared between rats subjected to one or two bouts of RAO (40 min, 24 hr apart). IARF kidneys retained a significantly greater percent of their baseline GFR and had comparable or higher absolute GFRs after 25 or 40 min of RAO than control rats. IARF rats showed no significant exacerbation of their underlying morphologic injury by superimposing a second ischemic event. IARF kidneys (24 hr post RAO) had normal AN concentrations, and by 30 min of reflow from a second 40 min of RAO, they re-established their AN energy charge and retained AN pools as well as control kidneys. A second 40-min bout of RAO did not significantly prolong recovery rates from the first 40-min ischemic event. In additional experiments, intraperitoneal injection of normal urine or solute matched artificial urine (urea, creatinine, NaCl) into normal rats to mimic the degree of azotemia seen in the IARF rats induced significant and comparable protection against 40 min of RAO. We conclude that the IARF kidney, at or near the height of its functional and morphologic injury, does not have increased susceptibility to additional ischemic insults. Rather a modicum of protection appears to exist, possibly due to renal-failure-induced increments in solute loads per nephron.

Acute Kidney Injury↗

Glomerulopathy does not increase renal susceptibility to acute ischemic injury.

To determine whether preexistent glomerular injury and the nephrotic syndrome increase renal susceptibility to ischemic renal injury, normal rats and rats with either experimental minimal-change disease (Adriamycin nephropathy) (AN) or membranous nephropathy (passive Heymann nephritis) (PHN) underwent renal functional and histologic studies under either basal conditions or 18 h after bilateral renal artery occlusion (over 30 min). Prior to renal ischemia AN and PHN rats had minimally depressed glomerular filtration rate (GFR), normal (AN) or increased (PHN) renal blood flow (RBF), heavy proteinuria, hypoalbuminemia, decreased urine sodium excretion, extensive glomerular foot process fusion, and intratubular hyalin cast formation. Losses of GFR in response to ischemia were comparable among the three groups of rats (controls, 0.29; AN, 0.28; PHN, 0.25 ml X min-1 X 100 g body wt-1) despite prevailing differences in postischemic hemodynamics. Neither light nor transmission electron microscopy showed any differences in the degree of ischemic renal injury. These results suggest that 1) glomerulopathy and the nephrotic syndrome do not significantly increase renal susceptibility to ischemic renal injury; 2) the syndrome of acute renal failure that occurs in patients with minimal-change glomerulopathy is not due to a marked susceptibility of these kidneys to clinically occult ischemic events; and 3) foot process fusion is probably not a pathophysiologically significant lesion in ischemic acute renal failure, as previously suggested.

Acute Disease↗

Primary carcinoma of the renal pelvis and ureter. Evaluation of clinical and pathologic features.

Thirty-eight cases of carcinoma of the renal pelvis and ureter were evaluated for stage, grade, histologic type, location, presence or absence of vascular invasion, abnormalities in the urothelium adjacent to the tumors, clinical appearance, patient survival, and therapeutic intervention. A good correlation between tumor grade and stage was found in the transitional cell carcinomas. Squamous cell carcinomas were high-stage tumors and transitional cell carcinomas with prominent squamous components were of a higher stage than "pure" transitional cell carcinomas of the same grade. Vascular invasion was present in only high-grade tumors and the squamous cell carcinomas. The degree of atypia present in the urothelium adjacent to the tumors corresponded with the grade of the tumors. Hematuria, with or without associated flank pain, was the most common initial symptom in patients with these neoplasms. Survival was good in stage A neoplasms but poor in higher-stage neoplasms. Appropriate treatment for these tumors remains controversial.

Adult↗

ABO (H) cell surface antigens in benign and malignant parotid neoplasms.

Twenty-two inflammatory, benign, or malignant parotid lesions were studied by means of the specific red cell adherence test (SRCA), a modification of the Coombs' mixed cell agglutination reaction. In 22 normal parotid tissues the acinar structures were devoid of red cell agglutination, but it was present in ductal epithelium. Findings were similar in 2 cases of parotitis, 11 benign mixed tumors, and 1 malignant mixed tumor. All lacked red cell agglutination in areas of neoplastic change. Benign Warthin's tumors (4 cases) demonstrated antigenicity in the columnar epithelial component of the tumor, but lacked red cell agglutination in areas of the lymphoid component. One malignant Warthin's tumor showed agglutination in areas of normal columnar epithelium but not in areas of malignant dedifferentiation. Undifferentiated carcinoma (1 case) and adenoid cystic carcinoma (2 cases) did not possess detectable ABO (H) antigens in neoplastic areas of the gland. The absence of ABO antigens in normal acinar glands supports their suggested myoepithelial or mesenchymal derivation, as the absence of antigen in benign and malignant mixed tumors supports their proposed mesenchymal derivation. Ductular epithelium and the epithelial components of benign Warthin's tumors have ABO (H) antigens, while the loss of antigen in the epithelial portion of the malignant Warthin's tumor is characteristic of epithelial neoplastic dedifferentiation. Loss of antigen in adenoid cystic and undifferentiated carcinomas of the parotid supports the concept that antigen is absent in epithelially derived malignant neoplasms.

ABO Blood-Group System↗

Supradiaphragmatic accessory lobe of the liver in BB Wistar rats.

Supradiaphragmatic accessory livers were observed in two closely related rats in a series of 172 necropsies on BB Wistar rats. The gross and histological appearance of both accessory lobes are described. This abnormality has been reported in only one other inbred strain of rats where it also arose with a very low incidence. As in the previous report, the pattern of occurrence of these accessory lobes suggests a mode of inheritance that is either polygenic or autosomal recessive with low penetrance.

Animals↗