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Biomedical subjects

M C Heng

Publications and source records attributed to M C Heng.

At least 37 records · Page 2Linked to original sources
PubMed1991

Focal endothelial cell degeneration and proliferative endarteritis in trauma-induced early lesions of necrobiosis lipoidica diabeticorum.

Microangiopathy is an essential component in diabetic vascular pathology. We report ultrastructural observations of ballooning degeneration involving isolated endothelial cells of cutaneous capillaries, while leaving adjacent endothelial cells relatively intact in six diabetic patients with early lesions of necrobiosis lipoidica induced by trauma. Focal proliferation of endothelial cells encroaching upon the vascular lumina (obliterative endarteritis) was also observed. Lectin studies on biopsy specimens of older lesions of necrobiosis lipoidica revealed paucity of dermal blood vessels. These observations enable us to gain further insight into the pathophysiological mechanisms that underlie diabetic microvascular disease.

Aged↗
PubMed1991

Electron microscopic and immunocytochemical studies of the sequence of events in psoriatic plaque formation following tape-stripping.

Electron microscopic and immunocytochemical studies were performed on sequential biopsies following the tape-stripping of the uninvolved skin in 12 patients with psoriasis. In the biopsies taken after 5 min for up to 7 days during the pre-psoriatic phase, there were initial lymphocyte-Langerhans cell interactions as well as interactions between lymphocytes and keratinocytes. In biopsies taken after 6-8 weeks during the proliferative phase there were lymphocyte-macrophage interactions. In the 24-h and 7-day biopsies there were close contacts between epidermal lymphocytes and keratinocytes via microvilli, with blebbing of the keratinocyte plasma membranes and granular cytoplasmic changes around these microvilli. Few basal keratinocyte herniations were noted during this phase. The 6-8-week biopsies of Köbner-positive patients were characterized by a marked increase in lymphocyte-macrophage interactions via similar microvillous processes with associated electronlucent areas suggestive of cytotoxicity.

Adult↗
PubMed1991

Predominance of CD8 subset in id eruption of poison oak-induced dermatitis.

The pathophysiology and immune mechanisms involved in the clinical syndrome of autoeczematization remain a mystery. In this study of nickel dermatitis without autoeczematization and poison oak dermatitis with autoeczematization, it was noted that the process of autoeczematization was associated with the presence of CD8+ lymphocytes within the epidermis and the expression of HLA-DR antigens on epidermal keratinocytes. It is surmised that since CD8+ clones are induced by poison oak antigen but not by nickel, the inability of nickel to induce CD8+ lymphocytes may explain why uncomplicated nickel dermatitis does not autoeczematize. Since the selective adherence of CD8+ lymphocytes to keratinocytes, probably via the expression of adhesion molecules such as ICAM-1, the generation of antigens on endothelial cells of high endothelial venules involved in lymphocyte trafficking, and the expression of HLA-DR antigens on epidermal keratinocytes are all due to the activity of interferon-8, it is deduced that this lymphokine may play a key role in id eruptions induced by contact allergens.

CD8 Antigens↗
PubMed1991

Alpha-1 antitrypsin deficiency in a patient with widespread prurigo nodularis.

Skin lesions associated with alpha 1-antitrypsin deficiency are becoming better defined and understood. Deficiency in this major antiproteinase, which neutralizes multiple proteolytic enzymes ranging from collagenases and elastases to trypsin and chymotrypsin, thus results in significant tissue autodigestion. This anti-proteinase is secreted by activated lymphocytes and macrophages, suggesting the existence of homeostasis which titrates the release of proteolytic enzymes by these cells, and the adequate neutralization of these proteases in order to prevent excessive tissue autodigestion each time these inflammatory cells are activated. We report a patient with alpha 1-antitrypsin deficiency who, following insect bites and cellulitis developed widespread itching and scratching, leading to widespread lesions of prurigo nodularis. The colonization of his multiple skin lesions with Staphylococcus aureus and the release of potent T cell mitogens, such as Protein A and enterotoxin A from the bacterial cell membrane may have resulted in the release of additional proteolytic enzymes by the activated lymphocytes and macrophages, without the concomitant secretion of alpha 1-antitrypsin with subsequent aggravation of his pruritus. These concepts are supported by electron microscopic evidence of excessive tissue autodigestion, and by immunocytochemical data identifying the presence of T helper and T cytotoxic/suppressor lymphocytes as well as macrophages within the upper dermis.

Humans↗
PubMed1990

Correlation of Pityosporum ovale density with clinical severity of seborrheic dermatitis as assessed by a simplified technique.

One hundred patients with facial seborrheic dermatitis and 42 control subjects were studied. The number of periodic acid-Schiff-positive Pityosporum ovale yeast cells in skin scrapings per high-power field were counted and designated 1 + to 4 +. Our data indicate a correlation between the density of P. ovale and the clinical severity of seborrheic dermatitis, both before and after therapy with a precipitated sulfur/salicyclic acid shampoo. The data support the concept that yeast contributes to the pathogenesis of seborrheic dermatitis.

Administration, Cutaneous↗
PubMed1990

Basement membrane changes in psoriatic patients on long-term topical corticosteroid therapy.

It has been observed that the beneficial anti-inflammatory effects of topical steroids in psoriasis are counteracted by increasing instability of the disease, with rebound phenomena associated with the cessation of these drugs. We report the occurrence of multi-layered fragmentation and disorganization of the basal laminae in active, untreated psoriatic lesions, resolving and uninvolved, inadvertently steroid-treated psoriatic skin, as well as in a variety of non-psoriatic dermatoses treated with fluorinated topical steroids for prolonged periods. These changes, which were associated with a moderate to severe loss of dermal collagen, were not found in untreated and treated psoriatic controls, with or without concomitant alpha 1-antitrypsin deficiency, who had not received steroids, suggesting that they were probably the consequence of prolonged fluorinated steroid use. This conclusion is supported by the observation that the largest number of layers (10-15) of fragmented basal laminae was noted in the patients who had received fluorinated steroids for 6 years or more, while those on 4 years or less of fluorinated steroid therapy exhibited only three to seven layers of fragmented basal laminae. In psoriatic lesions, the fragmentation of the basal lamina was associated with the presence of basal keratinocyte herniations (BKH), the frequency of which has been shown to parallel clinical psoriatic activity. The persistence of these electron-microscopic markers of psoriatic activity (i.e. BKH) in psoriatic plaques treated with prolonged fluorinated steroids suggests that loss of integrity of the basement membrane, as indicated by the presence of multi-layered fragmentation of the basal lamina, may account for the instability of the psoriatic lesions treated with prolonged topical fluorinated steroids.

Administration, Topical↗
PubMed1990

Tannic-acid staining material on high endothelial venules and lymphocytes in skin and peripheral lymph nodes in Staphylococcus aureus-associated erythroderma.

The recognition and binding of glycoprotein receptors on lymphocytes to specific antigens present on high endothelial venules (HEV) precedes the egress of lymphocytes from the blood stream into the tissues. In this paper, we report the presence of HEVs with tannic-acid staining material (TASM+ HEVs) in Staphylococcus aureus-associated erythroderma, which allow the migration of CD8+ lymphocytes from the bloodstream into the epidermis. TASM positivity is also expressed on lymphocytes within the regional lymph nodes, and by intravascular lymphocytes prior to leaving the TASM+ HEV. It is proposed that TASM positivity may represent a molecule, which may function in binding lymphocytes to HEVs prior to egress from the HEV. (TASM is lost from lymphocytes after leaving the HEVs). The expression of TASM positivity may form an essential part of the CD8+ lymphocyte-HEV recognition system, and may be the means whereby CD8+ lymphocytes generated in the regional lymph nodes by various mitogens (in this case by staphylococcal mitogens) may 'home' to specific sites within the epidermis. TASM positivity on both the HEVs and lymphocytes may serve as a convenient marker of such a system.

Dermatitis, Exfoliative↗
PubMed1990

Proliferation of HIV in lymphocyte--associated macrophages with cytopathic changes in AIDS erythroderma.

Latency of the Human Immunodeficiency Virus (HIV) has been demonstrated in both helper T-Lymphocytes and cells of the macrophage/monocyte series. Although mitogen-dependent amplification of HIV infection within lymphocytes and monocytes/macrophages has been demonstrated to occur in vitro, in vivo evidence of such a phenomenon has been lacking. We have performed electron microscopic and immunocytochemical evaluation of skin biopsies from a patient with the Acquired Immunodeficiency Syndrome (AIDS) with chronic erythroderma. These biopsies provided evidence of proliferation of HIV in macrophages interacting with activated lymphocytes (CD3+). These macrophages were undergoing morphologic changes characteristic of cytopathicity and contained numerous viral particles, many of which were actively budding from plasma membranes. Cutaneous macrophages which were not interacting with lymphocytes did not demonstrate cytopathicity or evidence of viral multiplication. These in vivo data substantiate the concept that activation of cells which harbour latent HIV promotes viral replication as well as subsequent cytopathicity.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Lack of host cellular immune response in eruptive molluscum contagiosum.

A lack of cellular immunity on the part of the host has been incriminated as the cause of the persistence of the cutaneous lesions of molluscum contagiosum. We present a patient in the eruptive phase of the disease, confirming the absence of T-lymphocyte and natural killer cell subsets in the base of these typical lesions, using a panel of monoclonal antibodies. We also report the observation of lipid material ultrastructurally (confirmed by osmium staining on fresh-frozen tissue), as well as cross-reactivity immunocytochemically of the antigens on these molluscum bodies with antigens normally present on macrophages, as defined by DAKO-macrophage monoclonal antibodies. We have considered the possible role of these findings in the lack of host cellular responsiveness in the eruptive phase of the disease.

Adult↗
PubMed1989

An electron microscopic study of the epidermal infiltrate in recurrent herpes simplex.

Host immunity has been suspected of playing a role in recurrent herpes simplex. In this preliminary ultrastructural study of two patients with acute herpetic eruption, it was noted that the keratinocytes exhibiting the most severe damage are those adjacent to large granular lymphocytes. In contrast, many keratinocytes filled with viral particles of herpes simplex show little or no signs of keratinocyte damage. These observations suggest that in recurrent herpes simplex the epidermal damage may be due, at least in part, to cell-mediated host immunity as well as to the viral infection.

Adult↗
PubMed1989

Healing of necrobiotic ulcers with antiplatelet therapy. Correlation with plasma thromboxane levels.

Necrobiosis lipoidica in diabetics has been considered to be a cutaneous manifestation of diabetic microangiopathy. Seven diabetic patients with necrobiotic ulcers of recent onset that healed after administration of acetylsalicylic acid and dipyridamole had elevated thromboxane levels. Healing was associated with depression of the elevated thromboxane levels in all seven patients.

Adult↗
PubMed1988

Linear seborrheic keratoses associated with underlying malignancy.

A clinical syndrome, consisting of eruptive linear seborrheic keratoses associated with adenomatous colonic polyps (malignant but without invasion of the stalk) and/or frankly invasive colonic adenocarcinomas, is described in five patients. Partial to almost complete regression of the cutaneous lesions over the succeeding months to years was noted after removal of the internal malignant tumors in all five patients. Resolving lesions were characterized by an accentuation of chronic inflammatory infiltrate both within the epidermis and dermis, suggesting perhaps that the regression of the skin lesions may be related to enhanced immunologic response concomitant with the removal of the underlying malignancy.

Adenocarcinoma↗
PubMed1988

High endothelial venules in involved and uninvolved psoriatic skin: recognition by homing receptors on cytotoxic T lymphocytes.

We report the presence of tannic acid staining material in the intercellular spaces between adjacent endothelial cells of the high endothelial venules (HEVs) in psoriatic skin, which appears to be recognized by T8 (cytotoxic/suppressor) lymphocytes, as the presence of HEVs was found to be related to the presence of T8 lymphocytes in the epidermis. As HEVs with similar tannic acid staining material were also observed in peripheral lymph nodes, we suggest that this material may serve as a marker for HEVs recognized by the T8 lymphocyte subset. T8 + lymphocytes were found in the epidermis at 5 min and I h after tape-stripping of uninvolved skin of psoriatic patients with active disease, but not until 24 h in a psoriatic patient in remission. The prior existence of HEVs in uninvolved psoriatic skin could account for the rapid egress of T8 lymphocytes from the vasculature to the epidermis in response to trauma.

Antibodies, Monoclonal↗
PubMed1988

Beta-adrenoceptor antagonist-induced psoriasiform eruption. Clinical and pathogenetic aspects.

A number of beta-adrenoceptor blocking drugs have been reported to induce a papulosquamous eruption which resembles psoriasis. We report distinctive clinical, histopathologic, immunocytochemical, and electron microscopic features in beta-blocker-induced psoriasiform eruptions that differentiate this syndrome from psoriasis. Preliminary data suggest that biopsy specimens from eruptions caused by beta 1-selective adrenoceptor blocking agents (metoprolol and atenolol) were characterized by excessive degranulation of the neutrophils in the dermis, while the nonselective beta blockers (propranolol, nadolol, and sotalol) were marked by excessive release of proteolytic enzymes from macrophages, which are thought to possess beta 2-adrenergic receptors. Surprisingly, excessive release of enzymes by lymphocytes were noted in both the beta 1-selective and in the nonselective induced syndromes. It is believed that excessive lysosomal enzyme release by neutrophils, lymphocytes, and macrophages is responsible for the presence of basal keratinocyte herniations, which have previously been shown to correlate with hyperproliferation and psoriasiform changes, as well as with the presence of excessive proteolytic enzymes in the skin. It is postulated that the beta-blocker-induced syndrome may result from enhanced proliferation, motility, and activity of lymphocytes, neutrophils, and cells of the macrophage-Langerhans cell series, stemming from depressed intracellular cyclic adenosine monophosphate levels caused by the beta blockade.

Adrenergic beta-Antagonists↗
PubMed1987

Thrombotic phenomena associated with intravenous cocaine.

A patient with infarctive skin lesions and associated involvement of the kidney and liver caused by an intravenous overdose of cocaine is described. The thrombotic tendency may possibly be related to endothelial cell damage from prolonged vasoconstriction or cocaine toxicity, with disturbance of prostacyclin-thromboxane balance and enhancement of platelet aggregation and thrombotic tendency.

Adult↗
PubMed1987

Electron microscopic features in generalized pustular psoriasis.

Basal keratinocyte herniations (BKH) have been used as markers of psoriatic activity. Abnormal multipolypoid forms herniating through large gaps in the basal lamina have been found to characterize biopsies from psoriatic patients with concomitant alpha 1-antitrypsin deficiency, and appear to be a marker of excessive proteolytic activity. The finding of similar multipolypoid BKH in patients with generalized pustular psoriasis of the von Zumbusch variety (but not in patients with psoriasis vulgaris), in the absence of concomitant alpha 1-antitrypsin deficiency, would support the concept of the presence of large amounts of proteolytic enzymes in the dermis of patients with this syndrome. The large proportion of BKH directly associated with dermal neutrophils, and the presence of clusters of high-density BKH overlying collections of dermal neutrophils, suggests that neutrophilic proteases are largely responsible for BKH formation in patients with this syndrome.

Adult↗