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PubMed2002

Impaired hair follicle morphogenesis and cycling with abnormal epidermal differentiation in nackt mice, a cathepsin L-deficient mutation.

We previously described an autosomal-recessive mutation named nackt (nkt) exhibiting partial alopecia associated with CD4(+) T-cell deficiency. Also, we recently reported that nkt (now Ctsl(nkt)) comprises a deletion in the cathepsin L (Ctsl) gene. Another recent study reported that Ctsl knockout mice have CD4(+) T-cell deficiency and periodic shedding of hair, which recapitulate the nkt mutation and the old furless (fs) mutation. The current study focuses on the dermatological aspects of the nkt mutation. Careful histological analysis of skin development of homozygous nkt mice revealed a delayed hair follicle morphogenesis and late onset of the first catagen stage. The skin of Ctsl(nkt)/Ctsl(nkt) mice showed mild epidermal hyperplasia and hyperkeratosis, severe hyperplasia of the sebaceous glands, and structural alterations of hair follicles. Epidermal differentiation seems to be affected in nkt skin, with overexpression of involucrin and profilaggrin/filaggrin along with focal areas of keratin 6 expression in the interfollicular epidermis. Severe epidermal hyperplasia, acanthosis, orthokeratosis, and hyperkeratosis were only observed in mice maintained in nonpathogen-free environments. The analysis of Rag2-/- Ctsl(nkt)/Ctsl(nkt) double-mutant mice indicates that the skin defect remains under the absence of T and B cells. This animal model provides in vivo evidence that cysteine protease cathepsin L plays a critical role in hair follicle morphogenesis and cycling, as well as epidermal differentiation.

Alopecia↗
PubMed2002

Cathepsin-L, a key molecule in the pathogenesis of drug-induced and I-cell disease-mediated gingival overgrowth: a study with cathepsin-L-deficient mice.

Drug-induced gingival overgrowth, the chronic side effect of calcium antagonists, is frequently seen due to the increase in patients with hypertension, although the etiology of the disease is largely unknown. I-cell disease, which accompanies gingival overgrowth, is characterized by a deficiency in UDP-N-acetyl-glucosamine and is classified as one of the lysosomal storage diseases. Here, we hypothesized that a common mechanism may underlie the etiology of gingival overgrowth seen in patients treated with calcium antagonist and in patients with I-cell disease. A calcium antagonist, nifedipine, specifically suppressed cathepsin-L activity and mRNA expression, but not that of cathepsin-B in cultured gingival fibroblasts. The activity of cathepsin-L was suppressed up to 50% at 24 hours after treatment of the cells with the reagent. The selective suppression of cathepsin-L activity appeared not to be dependent on Ca(2+), since treatment of the cells with thapsigargin suppressed both cathepsin-B and -L activity. Mice deficient in the cathepsin-L gene manifested enlarged gingivae. Histological observation of the gingivae demonstrated typical features of acanthosis, a phenotype very similar to that of experimentally induced gingival overgrowth. Since cathepsin-L deficiency was reported to be associated with thickening of the skin, impaired cathepsin-L activity may play a key role in the establishment of skin and gingival abnormalities seen in I-cell disease. In addition, reduced cathepsin-L activity may play an important role in inducing drug-induced gingival overgrowth.

Animals↗
PubMed2002

Mice lacking Smad3 are protected against cutaneous injury induced by ionizing radiation.

Transforming growth factor-beta (TGF-beta) plays a central role in the pathogenesis of inflammatory and fibrotic diseases, including radiation-induced fibrosis. We previously reported that mice null for Smad3, a key downstream mediator of TGF-beta, show accelerated healing of cutaneous incisional wounds with reduced inflammation and accumulation of matrix. To determine if loss of Smad3 decreases radiation-induced injury, skin of Smad3+/+ [wild-type (WT)] and -/- [knockout (KO)] mice was exposed to a single dose of 30 to 50 Gy of gamma-irradiation. Six weeks later, skin from KO mice showed significantly less epidermal acanthosis and dermal influx of mast cells, macrophages, and neutrophils than skin from WT littermates. Skin from irradiated KO mice exhibited less immunoreactive TGF-beta and fewer myofibroblasts, suggesting that these mice will have a significantly reduced fibrotic response. Although irradiation induced no change in the immunohistochemical expression of the TGF-beta type I receptor, the epidermal expression of the type II receptor was lost after irradiation whereas its dermal expression remained high. Primary keratinocytes and dermal fibroblasts prepared from WT and KO mice showed similar survival when irradiated, as did mice exposed to whole-body irradiation. These results suggest that inhibition of Smad3 might decrease tissue damage and reduce fibrosis after exposure to ionizing irradiation.

Animals↗
PubMedDate not supplied

Extensive papillomatosis of the bovine upper gastrointestinal tract.

Extensive papillomatosis was identified in a heifer born and raised in Scotland and a steer born and raised in England. In both cases, the papillomas extended from the mouth and tongue to the reticulum. Although cases of florid papillomatosis of the upper gastrointestinal tract occur relatively frequently in cattle grazing on bracken fern in the Scottish Highlands, no such cases have been reported previously in English cattle. Histopathological examination of the papillomas showed that the lesions were wholly epithelial, with acanthosis, hyperkeratosis and the pathognomonic koilocytes characteristic of papillomavirus infection. Bovine papillomavirus type 4 (BPV-4) was identified by molecular amplification and sequencing of the viral genome.

Animals↗
PubMed1978

Studies of insulin insensitivity in soleus muscles of obese mice.

The isolated mouse soleus muscle is a suitable system to measure specific insulin binding and insulin effects. Studies in obese mice have pointed to discrete sites of insulin resistance of skeletal muscle in obesity: (1) A decrease in the number of insulin receptors, which may result in diminished insulin sensitivity (i.e., impaired responses to submaximally stimulating doses of insulin); and (2) Alterations that lay apart from, or beyond, the insulin receptor: thus, glucose transport (and/or phosphorylation) appears to be intrinsically altered and the stimulation by insulin of glycogen synthesis is markedly depressed. These alterations are responsible for the marked resistance to maximally stimulating doses of insulin. The serum from a patient with the syndrome of insulin resistance and acanthosis nigricans contains antibodies that inhibit insulin binding and exert insulin-like effects in muscle; this serum is, however, less effective than insulin in maximally stimulating glycogen synthesis, which suggests some differences in their mechanisms of action.

Animals↗
PubMed1997

Insulin resistance in limb and trunk partial lipodystrophy (type 2 Köbberling-Dunnigan syndrome).

We studied insulin action in two patients with limb and trunk partial lipodystrophy with hirsutism and acanthosis nigricans. Glucose was normal in one of the patients and slightly above normal in the other during an oral glucose tolerance test (OGTT). An intravenous glucose tolerance test (IVGTT) was normal in both patients. Basal and glucose-stimulated insulin levels were elevated in both the OGTT and IVGTT in both patients. The response of plasma glucose to exogenously administered insulin was decreased. A euglycemic-hyperinsulinemic clamp performed in patient no. 2 indicated insulin resistance, which was not corrected by reducing the increased basal level of serum free fatty acids (FFAs). Binding of insulin to neck adipocytes was normal in both subjects, but glucose transport and oxidation in these cells was impaired. Insulin binding to abdominal adipocytes was increased in one patient whose adipocytes displayed higher glucose transport at low insulin concentrations. Glucose oxidation was decreased in abdominal adipocytes of both patients. We conclude that insulin resistance in Köbberling-Dunnigan type 2 partial lipodystrophy is not related to an alteration of the insulin molecule or to changes in insulin binding, but is more likely associated with a postreceptor defect, since glucose oxidation was impaired in adipocytes of the neck and abdomen.

Adult↗
PubMed2003

The evaluation and management of hirsutism.

Hirsutism is the presence of terminal (coarse) hairs in females in a male-like pattern, affecting between 5% and 15% of women, depending on definition. Hirsutism has a significant negative impact on psychosocial development and is usually a sign of an underlying endocrine abnormality-namely, androgen excess. The most common cause of androgen excess is the polycystic ovary syndrome (PCOS), with 21-hydroxylase-deficient nonclassic adrenal hyperplasia, the hyperandrogenic insulin-resistant acanthosis nigricans syndrome, androgen-secreting tumors, and androgenic drug intake occurring less frequently. However, although 70-80% of patients with androgen excess demonstrate hirsutism, this sign may be less prevalent among women of Asian extraction. Conversely, not all hirsute patients have evidence of detectable androgen excess, as 5-15% of these women have "idiopathic hirsutism," with normal ovulatory function and androgen levels. There is a strong familial predilection for hirsutism, primarily because the underlying endocrine disorders (eg, PCOS) and the factors regulating the development of hair growth (eg, androgen receptor activity, 5alpha-reductase activity) have a strong genetic component. The diagnostic evaluation of the potentially hirsute patient first involves confirming the presence of hirsutism and then excluding associated or etiological abnormalities and disorders (eg, ovulatory dysfunction, adrenal hyperplasia, diabetes, thyroid hormone abnormalities). Treatment should be undertaken using combination therapy, to possibly include 1) hormonal suppression (oral contraceptives, long-acting gonadotropin-releasing hormone analogues, and insulin sensitizers), 2) peripheral androgen blockade (spironolactone, flutamide, cyproterone acetate, or finasteride), and 3) mechanical/cosmetic amelioration and destruction of the unwanted hairs (electrology and, potentially, laser hair removal). The application of eflornithine hydrochloride 13.9% topical cream may also be useful to ameliorate unwanted facial hair growth. Overall, although hirsutism is a frequent and distressing abnormality often signaling an underlying endocrine disorder, a systematic approach to evaluation will uncover the etiology, and combination therapy will provide satisfactory treatment for most patients.

Androgen Antagonists↗
PubMed1997

Non-insulin-dependent diabetes mellitus in childhood and adolescence.

NIDDM in children and adolescents represents a heterogeneous group of disorders with different underlying pathophysiologic mechanisms. Most subtypes of NIDDM that occur in childhood are uncommon, but some, such as early onset of "classic" NIDDM, seem to be increasing in prevalence. This observed increase is thought to be caused by societal factors that lead to sedentary lifestyles and an increased prevalence of obesity. In adults, hyperglycemia frequently exists for years before a diagnosis of NIDDM is made and treatment is begun. Microvascular complications, such as retinopathy, are often already present at the time of diagnosis. Children are frequently asymptomatic at the time of diagnosis, so screening for this disorder in high-risk populations is important. Screening should be considered for children of high-risk ethnic populations with a strong family history of NIDDM with obesity or signs of hyperinsulinism, such as acanthosis nigricans. Even for children in these high-risk groups who do not yet manifest hyperglycemia, primary care providers can have an important role in encouraging lifestyle modifications that might delay or prevent onset of NIDDM.

Adolescent↗
PubMed2001

Leishmaniasis in Sudan. Post kala-azar dermal leishmaniasis.

Post kala-azar dermal leishmaniasis (PKDL) is increasingly recognized in Sudan as a complication of visceral leishmaniasis (VL), occurring in c. 55% of patients after, or during treatment of, VL. The development of PKDL seems to be restricted to parasites of the Leishmania donovani sensu stricto cluster; no particular zymodeme has been found to be associated with it. In contrast to PKDL in India, PKDL in Sudan occurs within 0-6 months after treatment for VL. The rash may be macular, maculo-papular or nodular, and spreads from the perioral area to other parts of the body, depending on grade of severity. Young children are particularly at risk of developing more severe disease. In 16% of PKDL patients, parasites can be demonstrated by microscopy in lymph node or bone marrow aspirates and, with the aid of the polymerase chain reaction (PCR), in lymph nodes of 81% of patients, possibly indicating persistent visceralized infection. Diagnosis can be made by demonstration of parasites in skin smears or biopsies in 20-30% of cases; newer techniques, using PCR with skin smears, have higher sensitivity (83%). Monoclonal antibodies against L. donovani can detect parasites in 88% of biopsies. Serological tests are of limited value. The leishmanin skin test is positive in 50-60% of cases; there is an inverse relationship between the skin test result and severity of PKDL. In differential diagnosis, miliaria rubra is the most common problem; differentiation from leprosy is the most difficult. In biopsies, hyperkeratosis, parakeratosis, acanthosis, follicular plugging and liquefaction degeneration of the basal layer may be found in the epidermis; in the dermis there are varying intensities of inflammation with scanty parasites and mainly lymphocytes; macrophages and epithelioid cells may also be found. In 20% of cases discrete granulomas may be found. After VL, the immune response shifts from a Th2-type to a mixed Th1/Th2-type. High levels of interleukin-10 in skin biopsies as well as in peripheral blood mononuclear cells and plasma in patients with VL predict the development of PKDL. Treatment is needed only for those who have severe and prolonged disease; sodium stibogluconate (20 mg/kg/d for 2 months) is usually sufficient. (Liposomal) amphotericin B is effective, whereas ketoconazole, terbinafine and itraconazole are not.

Age Distribution↗
PubMed1999

Vitamin D and calcium dysregulation in the polycystic ovarian syndrome.

Over the past 30 years, numerous studies in invertebrates and vertebrates have established a role of calcium in oocyte maturation as well as in the resumption and progression of follicular development. Polycystic ovarian syndrome (PCO) is characterized by hyperandrogenic chronic anovulation, theca cell hyperplasia, and arrested follicular development. The aim of this observational study was to determine whether vitamin D and calcium dysregulation contribute to the development of follicular arrest in women with PCO, resulting in reproductive and menstrual dysfunction. Thirteen premenopausal women (mean age 31 +/- 7.9 years) with documented chronic anovulation and hyperandrogenism were evaluated. Four women were amenorrheic and nine had a history oligomenorrhea, two of whom had dysfunctional bleeding. Nine had abnormal pelvic sonograms with multiple ovarian follicular cysts. All were hirsute, two had alopecia, and five had acanthosis nigricans. The mean 25 hydrovitamin D was 11.2 +/- 6.9 ng/ml [normal (nl): 9-52], and the mean 1,25 dihydroxyvitamin D was 45.8 +/- 18 pg/ml. with one woman with a 1,25 dihydroxyvitamin D <5 pg/ml (nl: 15-60). The mean intact parathyroid hormone level was 47 +/- 19 pg/ml (nl: 10-65), with five women with abnormally elevated parathyroid hormone levels. All were normocalcemic (9.3 +/- 0.4 mg/dl). Vitamin D repletion with calcium therapy resulted in normalized menstrual cycles within 2 months for seven women, with two experiencing resolution of their dysfunctional bleeding. Two became pregnant, and the other four patients maintained normal menstrual cycles. These data suggest that abnormalities in calcium homeostasis may be responsible, in part, for the arrested follicular development in women with PCO and may contribute to the pathogenesis of PCO.

Adult↗
PubMedDate not supplied

[Inguinal pseudotumor: relapse of a pemphigus after 15 years' remission].

INTRODUCTION: Pemphigus vegetans (PV) is a rare type of pemphigus vulgaris. We report a patient with pemphigus vulgaris relapsing as an isolated vegetative tumour. CASE REPORT: A 59-year-old man was seen in February 2001 for a tumour on the right groin. He had received systemic corticosteroids and cyclophosphamide for pemphigus vulgaris from 1974 to 1985, and he had been in complete remission since 1985. At the time of evaluation, a 10 x 5 x 5 cm, smooth vegetative tumour was seen on the right groin. Biopsies showed spongiosis, acanthosis and some acantholysis. Direct immunofluorescence showed strong deposition of immunoglobulin G within the intercellular substance of the epidermis. Indirect immunofluorescence revealed anti-intercellular antibodies at a titer of 1/800. Immunoblot analysis showed reactivity with the 130 kD pemphigus vulgaris antigen. PVg was diagnosed. Local corticosteroid treatment was initiated. The patient was disease-free at follow-up three years later. DISCUSSION: Localised forms of pemphigus are very rare. Twenty four other cases have been reported among them just one case of localised PV. Our case report is very unusual because of the variability of the expression of the disease, the high antibody level, the absence of trigger factors, and the efficacy of the local corticosteroid treatment.

Adrenal Cortex Hormones↗
PubMed1979

Alteration of specific binding of prostaglandin F2 alpha by hyperproliferative skin membrane fractions from essential fatty acid-deficient rats.

Specific binding of [3H] PGE2 and [3H] PGF2 alpha to smooth endoplasmic reticulum (SER) membranes prepared from rat skin at various stages of the development of essential fatty acid (EFA)-deficiency syndrome was demonstrated in these studies. The normal SER-binding capacity for [3H] PGE2 per mg of membrane protein was approximately two-fold that for [3H] PGF2 alpha in control rats fed a diet rich in essential fatty acids (EFA). Two weeks following the feeding of the animals with the EFA-deficient diet: histological evaluation revealed hyperplasia and acanthosis of the epidermal layer; a two-fold increase in labeling index (a marker for DNA synthesis) and no alteration in the SER-binding capacity for [3H] PGE2 or [3H] PGF2 alpha. By the 12th week however, labeling index had increased six-fold, accompanied by a five-fold increase in SER-binding capacity for [3H] PGF2 alpha. SER-binding for [3H] PGE2 was relatively unaltered. These results have demonstrated a relationship between marked alteration of skin SER-binding capacity for PGF2 alpha and the increase in epidermal hyperplasia and proliferation characteristic of the skin of the EFA-deficient rat. Refeeding of the animals with EFA-rich diet restored the epidermal proliferation and the SER-binding capacity to PGF2 alpha to normal conditions.

Animals↗
PubMed1981

Hereditary benign intraepithelial dyskeratosis. A report of two cases from Texas.

Hereditary benign intraepithelial dyskeratosis (HBID) is a rare disorder characterized by autosomal dominant inheritance, onset in childhood, bilateral limbal conjunctival plaques, chronic relapsing course of ocular irritation and photophobia, and oral lesions resistant to medical and surgical therapy. The lesions are characterized histologically by dyskeratosis, acanthosis, parakeratosis, and a variable amount of subepithelial inflammation. The patients in all previously reported cases have been descendants of Halowar Indians from North Carolina. This report illustrates the typical clinical and histologic findings of HBID in two siblings who, along with their parents and grandparents, were born in Texas.

Adult↗
PubMed1987

Inverted mucoepidermoid papillomas of the epibulbar conjunctiva.

Juxtalimbal epibulbar inverted papillomas that were locally excised without recurrence developed in two women, aged 42 and 51 at the time of initial presentation. There is only one previous report of this unusual conjunctival neoplasm, which documented involvement of the plical, caruncular, or tarsal conjunctiva. The tumor grew by acanthosis of the surface nonkeratinizing squamous epithelium, with invagination into the underlying connective tissue in the absence of inflammation or a tendency toward keratinization. The initial invaginations may be cystic in character, but solid lobules secondarily originated from their walls to push into the connective tissue. Mucus-producing goblet cells were scattered throughout the lesions; highly distinctive eosinophilic globoid bodies, probably reflecting inspissated mucoid material, were found in the walls of the cysts and entrapped within their secretions. Conjunctival inverted papilloma does not exhibit locally aggressive behavior, does not involve extensive segments of the conjunctival epithelium, and does not display diffuse spread or multicentricity. The authors therefore believe that it should be clearly separated from inverted squamous (Schneiderian) papillomas of the nasal cavity and sinuses.

Adult↗
PubMed2003

Involvement of the peripheral benzodiazepine receptor in the development of cutaneous pathology in Mrl/Lpr mice.

Mrl/Lpr mice develop inflammatory pathologies similar to human lupus erythematosus (LE). In that model, we showed a protective effect of different peripheral benzodiazepine receptor (PBR) ligands: PK 11195, Ro5-4864 and the newly described SSR180575 on the development of the cutaneous lesions. Specifically, we evidenced that a chronic treatment at 3 mg/kg per i.p. for 30 days prevented acanthosis, hyperkeratosis and generation of dermal infiltrates as compared with control untreated mice. In addition, using a specific polyclonal anti mouse PBR antibody, we characterized PBR expression in the skin lesions, and we observed that PBR expression in the epidermal component was increased when Mrl/Lpr mice developed the pathology and diminished upon PBR ligand treatment. PBR expression modulation together with the protective effects of its ligands further reinforce the role that PBR may play in the regulation of inflammation processes. Provided the exact mechanism of action that accounts for PBR action in that process is elucidated, these data support new therapeutic applications for specific potent PBR ligands.

Animals↗
PubMed2003

Confluent and reticulated papillomatosis without papillomatosis.

Confluent and reticulated papillomatosis is a papulosquamous disorder that affects young individuals. There are several hypotheses regarding the cause, including genetic keratinization disorder, reaction to pityrosporum, and reaction to UV light. Multiple therapeutic agents have been used with variable success. The histologic findings include papillomatosis, hyperkeratosis, and minimal or no acanthosis. We present a patient with the clinical findings of confluent and reticulated papillomatosis who responded dramatically to minocycline, and in whom histologic examination did not reveal papillomatosis.

Adult↗
PubMed1982

Perturbations of membrane glycosylation in retinoid-treated epidermis.

Differentiation of keratinizing epithelial results in the formation of an exterior cornified layer that is both sufficiently cohesive to provide a protective barrier and dyshesive enough to permit orderly, apical desquamation. Membrane glycoconjugates, which are of presumed importance for intercellular adhesion and growth control, have recently been visualized in mouse, rat, and human epidermis. Because retinoids are known to profoundly influence epidermal differentiation, the lectin-staining pattern in normal mouse epidermis was compared to that observed in mice treated with etretinate (Ro 10-9359, 50 mg/kg/day). Within 2 days of treatment with 50 mg/kg/day of etretinate, abnormal transepidermal water loss began, followed by mild acanthosis after 4 to 6 days, and focal loss of stratification by 10 days. Despite these dramatic alterations in structure and function, abnormalities in lectin staining first appeared only after 15 days. Both wheat germ agglutinin and succinyl wheat germ agglutinin stained an etretinate-dependent product localized in the granular layer in samples treated for 21 to 38 days. Both the intensity and the distribution of PNA (galactose-N-acetyl-galactosamine) and Ulex ( alpha -L-fucose) staining were affected by retinoid treatment, but the staining pattern with other lectins was not altered until 40 to 45 days, at which time the sugars in some samples were either restricted to isolated nests of cells or greatly diminished. Although etretinate appeared to provoke selective changes in keratinocyte membrane glycoconjugates, these alterations became apparent only after the retinoid had profoundly perturbed epidermal differentiation. These altered patterns may not only reflect retinoid-induced aberrations in cohesion and barrier function, but also may provide clues about the role of certain membrane sugars in the control of normal epidermal differentiation.

Animals↗
PubMed1983

Verruciform xanthoma. Occurrence in eroded skin in a patient with recessive dystrophic epidermolysis bullosa.

Verruciform xanthoma is a rare, granular, plaque-like lesion which occurs on mucosal surfaces and is characterized by acanthosis with xanthoma cells in the dermis between rete pegs. A case of verruciform xanthoma is reported which occurred on the sacral region in a patient with recessive dystrophic epidermolysis bullosa (RDEB). Electron microscopic studies suggested that many of the xanthoma cells were fibroblasts whose vacuolated appearance was expressed in cell culture and persisted for several passages. The occurrence of a verruciform xanthoma in a patient with severe recessive dystrophic epidermolysis bullosa suggests that repeated epidermal and/or dermal damage gave rise to a reactive process involving the formation of lipid-laden cells.

Adolescent↗