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Injection pain of rocuronium and vecuronium is evoked by direct activation of nociceptive nerve endings.

BACKGROUND AND OBJECTIVE: Rocuronium and, to a lesser extent, vecuronium can induce burning sensations associated with withdrawal reactions during administration. Dermal microdialysis in human and electrophysiological recordings of nociceptors in mouse skin were used to elucidate the underlying mechanisms of pain induction. METHODS: Microdialysis catheters were inserted intradermally into the forearm of 10 volunteers and were perfused with two different concentrations of rocuronium and vecuronium (1 and 10 mg mL(-1)) or a control. Dialysis samples were taken every 15 min and analysed for protein, histamine, tryptase and bradykinin content. Pain intensity was rated on a numerical scale of 0-10. In a parallel design, activation of cutaneous nociceptors was assessed directly in a skin-nerve in vitro preparation of the mouse hind paw. The receptive fields of identified single C-nociceptors (n = 12) were superfused with rocuronium or vecuronium solutions (10 mg mL(-1)) at physiological pH. RESULTS: In accordance with clinical observations, microdialysis of rocuronium (10 mg mL(-1)) induced sharp burning pain (NRS 4.1 +/- 1.8), whereas vecuronium given in the usual clinical concentration (1 mg mL(-1)) induced only minor pain sensations (NRS 0.6 +/- 1.3). At equimolar concentrations, pain sensation and concomitant mediator release evoked by both drugs were similar. No correlations were found between pain rating and mediator release. In the in vitro preparation, C-fibres showed a consistent excitatory response with rapid onset after stimulation with vecuronium as well as rocuronium (differences not significant). CONCLUSIONS: The algogenic effect of aminosteroidal neuromuscular blocking drugs can be attributed to a direct activation of C-nociceptors.

Adult↗

PAR-2: structure, function and relevance to human diseases of the gastric mucosa.

PAR-2 (protease-activated receptor 2), a G-protein-coupled receptor activated by certain serine proteases such as trypsin and tryptase, is now considered a physiologically important molecule and also a novel target for drug development. PAR-2 is widely distributed in the mammalian body, especially throughout the alimentary system. PAR-2 plays various roles in the alimentary, circulatory, respiratory and neuronal systems. In the gastric mucosa, PAR-2 modulates multiple functions and exerts mucosal cytoprotection mainly by activating sensory neurons. Thus, PAR-2 would appear to be a therapeutic target for treatment of gastric mucosal injury. Agonists and/or antagonists for PAR-2 might also be applicable to the clinical treatment of patients with inflammatory diseases in other organs.

Animals↗

Human and murine cytotoxic T lymphocyte serine proteases: subsite mapping with peptide thioester substrates and inhibition of enzyme activity and cytolysis by isocoumarins.

The active site structures of human Q31 granzyme A, murine granzymes (A, B, C, D, E, and F), and human granzymes (A, B, and 3) isolated from cytotoxic T lymphocytes (CTL) were studied with peptide thioester substrates, peptide chloromethyl ketone, and isocoumarin inhibitors. Human Q31, murine, and human granzyme A hydrolyzed Arg- or Lys-containing thioesters very efficiently with kcat/KM of 10(4)-10(5) M-1 s-1. Murine granzyme B was found to have Asp-ase activity and hydrolyzed Boc-Ala-Ala-Asp-SBzl with a kcat/KM value of 2.3 X 10(5) M-1 s-1. The rate was accelerated 1.4-fold when the 0.05 M NaCl in the assay was replaced with CaCl2. The preparation of granzyme B also had significant activity toward Boc-Ala-Ala-AA-SBzl substrates, where AA was Asn, Met, or Ser [kcat/KM = (4-5) X 10(4) M-1 s-1]. Murine granzymes C, D, and E did not hydrolyze any thioester substrate but contained minor contaminating activity toward Arg- or Lys-containing thioesters. Murine granzyme F had small activity toward Suc-Phe-Leu-Phe-SBzl, along with some contaminating trypsin-like activity. Human Q31 granzyme A, murine, and human granzyme A were inhibited quite efficiently by mechanism-based isocoumarin inhibitors substituted with basic groups (guanidino or isothiureidopropoxy). Although the general serine protease inhibitor 3,4-dichloroisocoumarin (DCI) inactivated these tryptases poorly, it was the best isocoumarin inhibitor for murine granzyme B (kobs/[I] = 3700-4200 M-1 s-1). Murine and human granzyme B were also inhibited by Boc-Ala-Ala-Asp-CH2Cl; however, the inhibition was less potent than that with DCI. DCI, 3-(3-amino-propoxy)-4-chloroisocoumarin, 4-chloro-3-(3-isothiureidopropoxy)isocoumarin, and 7-amino-4-chloro-3-(3-isothiureidopropoxy)isocoumarin inhibited Q31 cytotoxic T lymphocyte mediated lysis of human JY lymphoblasts (ED50 = 0.5-5.0 microM).

Amino Acid Sequence↗

Solution structure of ascidian trypsin inhibitor determined by nuclear magnetic resonance spectroscopy.

The three-dimensional solution structure of ascidian trypsin inhibitor (ATI), a 55 amino acid residue protein with four disulfide bridges, was determined by means of two-dimensional nuclear magnetic resonance (2D NMR) spectroscopy. The resulting structure of ATI was characterized by an alpha-helical conformation in residues 35-42 and a three-stranded antiparallel beta-sheet in residues 22-26, 29-32, and 48-50. The presence of an alpha-helical conformation was predicted from the consensus sequences of the cystine-stabilized alpha-helical (CSH) motif, which is characterized by an alpha-helix structure in the Cys-X(1)-X(2)-X(3)-Cys portion (corresponding to residues 37-41), linking to the Cys-X-Cys portion (corresponding to residues 12-14) folded in an extended structure. The secondary structure and the overall folding of the main chain of ATI were very similar to those of the Kazal-type inhibitors, such as Japanese quail ovomucoid third domain (OMJPQ3) and leech-derived tryptase inhibitor form C (LDTI-C), although ATI does not show extensive sequence homology to these inhibitors except for a few amino acid residues and six of eight half-cystines. On the basis of these findings, we realign the amino acid sequences of representative Kazal-type inhibitors including ATI and discuss the unique structure of ATI with four disulfide bridges.

Amino Acid Sequence↗

Oxyanion-mediated inhibition of serine proteases.

Novel aryl derivatives of benzamidine were synthesized and tested for their inhibitory potency against bovine trypsin, rat skin tryptase, human recombinant granzyme A, human thrombin, and human plasma kallikrein. All compounds show competitive inhibition against these proteases with Ki values in the micromolar range. X-ray structures were determined to 1.8 A resolution for trypsin complexed with two of the para-substituted benzamidine derivatives, 1-(4-amidinophenyl)-3-(4-chlorophenyl)urea (ACPU) and 1-(4-amidinophenyl)-3-(4-phenoxyphenyl)urea (APPU). Although the inhibitors do not engage in direct and specific interactions outside the S1 pocket, they do form intimate indirect contacts with the active site of trypsin. The inhibitors are linked to the enzyme by a sulfate ion that forms an intricate network of three-centered hydrogen bonds. Comparison of these structures with other serine protease structures with noncovalently bound oxyanions reveals a pair of highly conserved oxyanion-binding sites in the active site. The positions of noncovalently bound oxyanions, such as the oxygen atoms of sulfate, are distinct from the positions of covalent oxyanions of tetrahedral intermediates. Noncovalent oxyanion positions are outside the "oxyanion hole." Kinetics data suggest that protonation stabilizes the ternary inhibitor/oxyanion/protease complex. In sum, both cations and anions can mediate Ki. Cation mediation of potency of competitive inhibitors of serine proteases was previously reported by Stroud and co-workers [Katz, B. A., Clark, J. M., Finer-Moore, J. S., Jenkins, T. E., Johnson, C. R., Ross, M. J., Luong, C., Moore, W. R., and Stroud, R. M. (1998) Nature 391, 608-612].

Amino Acid Sequence↗

Effects of coordinating metal ions on the mediated inhibition of trypsin by bis(benzimidazoles) and related compounds.

The presence of the Zn2+ ion dramatically enhances the inhibition of trypsin and tryptase by amidine-modified benzimidazole inhibitors via coordination to both the catalytically active Ser195 hydroxyl and His57 imidazole residues of the enzyme and the nitrogens of the amidine-modified benzimidazole inhibitor (Janc, J. W.; Clark, J. M.; Warne, R. L.; Elrod, K. C.; Katz, B. A.; Moore, W. R. Biochemistry 2000, 39, 4792-4800). Some new 5-amidino-2-substituted benzimidazoles were synthesized and compared to known related molecules to explore systematically the metal-mediated inhibition of bovine trypsin as a function of coordinating groups and metal ions. These compounds take advantage of the favorable interaction between the amidine group on one side of the inhibitor and the Asp189 carboxylate in the binding pocket of the enzyme. The 5-amidino-2-substituted benzimidazoles all demonstrated similar inhibition constants (Ki) of 20-50 microM in the absence of metal ions. In the presence of Zn2+, inhibition increased to varying extents, depending upon the group substituted at the 2 position of the benzimidazole. The largest increase in inhibition in the presence of Zn2+ was seen with (5-amidino-2-benzimidazolyl)-2-benzimidazolylmethane with an apparent inhibition constant (Ki') of 0.37 +/- 0.06 nM, giving a 59,000-fold increase in inhibition when Zn2+ is present. Other metal ions, including Mn2+, Sc3+, and Hg2+, also increased the inhibition by several of the benzimidazole derivatives synthesized. The compound bis(2-benzimidazolyl)methane (BBIM) was also examined because it lacks the amidine group that provides a favorable hydrogen-bonding interaction with Asp189 in the binding pocket of trypsin. In the absence of metal ions, BBIM did not have a detectable affinity for trypsin; however, in the presence of Zn2+, a Ki' of 127 +/- 3 nM was observed. This result demonstrates that an affinity for the enzyme in the absence of metal ions is not required for potent metal-mediated inhibition, greatly expanding the possibilities for metal mediation of nonmetalloenzymes.

Animals↗

Histochemical and morphological characteristics of canine cardiac mast cells.

Cardiac mast cells have been recently isolated and characterized in humans, however canine cardiac mast cells have not been investigated. The objective of this study is to describe the histological and morphological characteristics of canine cardiac mast cells and examine the potential usefulness of canine models in investigating the role of mast cells in cardiovascular pathology. Canine cardiac mast cells could be easily identified by staining with Toluidine Blue or FITC-avidin. Using Toluidine Blue staining, we demonstrated fewer mast cells in formalin-fixed samples than in specimens fixed in Carnoy's, thus identifying a formalin-sensitive mast cell population in the canine heart. Mast cells were equally distributed in atria and ventricles with approximately 50% showing a perivascular location. Using enzyme-histochemical techniques, we detected tryptase and chymase activity in canine cardiac mast cells. Ultrastructural studies identified mast cells as granular cells with an eccentric non-segmented nucleus. Immunohistochemistry with the macrophage specific antibody AM-3K demonstrated that resident cardiac macrophages were 1.9 times more numerous than mast cells, also showing a predominantly perivascular (60%) location. Perivascular macrophages were more often periarteriolar, whereas perivascular mast cells were more often located along small veins and capillaries. Due to their ability to release cytokines and growth factors and their strategic perivascular location, resident cardiac inflammatory cells, such as mast cells and macrophages, may be important in pathological processes causing myocardial inflammation and fibrosis. Furthermore, mast cell-derived chymase, an important angiotensin II-forming enzyme may have a significant role in regulating the cardiac renin-angiotensin system.

Animals↗

Immunological similarities between primary sclerosing cholangitis and chronic sclerosing sialadenitis: report of the overlapping of these two autoimmune diseases.

Primary sclerosing cholangitis (PSC) is characterized by destructive inflammation and fibrosis affecting the bile ducts. The etiology of PSC is still unknown, although lymphocytic infiltration in the portal areas suggests an immune-mediated destruction of the bile ducts. Patients with one autoimmune disease often suffer from one or more other autoimmune diseases. It is well known that there is a close relationship between PSC and inflammatory bowel disease, particularly ulcerative colitis(UC). However, the pathological findings in UC and other overlap diseases do not resemble those of PSC. In the present study, we report a patient with chronic sclerosing sialadenitis (Kuttner's tumor) and PSC. It is compared the sclerosing changes in both salivary glands and bile ducts histologically. In addition, the expression pattern of mast cell tryptase, b-FGF, and HLA-DR were examined in both tissues immunohistochemically. Histological features of sclerosing change in both salivary and bile ducts were quite similar. Marked mast cell infiltration and b-FGF expression were seen in the sclerosing areas in both tissues. In active inflammatory areas of the salivary glands, HLA-DR expression was also seen. We hypothesized that similar immune reactions occur in both the salivary gland and bile ducts and are responsible for the fibrosis that follows.

Antibodies, Monoclonal↗

Direct activation of mast cells by prosthetic biomaterial particles.

IL-4 is a mast cell and T cell produced immune cytokine that is important in the regulation of macrophage function. IL-4 has also been implicated in the induction of foreign body giant cell formation. In patients with long-term joint prostheses, a localized granulomatous inflammation develops in periarticular tissues and other organs where phagocytosis of particulate material from various prosthetic components takes place. In this study we used the inflammatory lesions of the bone-implant interface as a model to investigate the possible production, the frequency and the cellular source of IL-4. 40 samples of the interface membrane obtained from 25 patients undergoing revision of clinically failed implants were analyzed by immunohistochemistry. Cryostat sections were labeled with specific monoclonal antibodies to mast cell products: IL-4, tryptase and the receptor c-kit (CD117). The study has identified a significant level of production of IL-4 by mast cells in all the cases analyzed. There was an apparent difference in the number of mast cells in relation to the histological variants of the interface. The increase in the number of mast cells and IL-4 production was more pronounced in cases with heavy macrophage infiltrate than those exhibiting a predominance of giant cells. The findings imply that the recruitment of mast cell and IL-4 expression precede the granulomatous reaction and may have a role in the induction of a number of immunopathological changes related to mast cell activation by biomaterial particles.

Journal Article↗

Immunological modulation of human cardiac mast cells.

Human mast cells, by elaborating various cytokines, chemokines and proinflammatory mediators play a complex role in several allergic and inflammatory disorders. Mast cells have been identified in human heart tissue in close proximity to the sarcolemma, in perivascular and adventitial locations and in the shoulder region of coronary atheroma. Human heart mast cells (HHMC) can be isolated from patients undergoing heart transplantation and can be immunologically activated in vitro to induce the release of tryptase, chymase, cysteinyl leukotriene C4 and prostaglandin D2. Several cytokines (e.g., stem cell factor and TNF-alpha) reside in secretory granules of HHMC. Mast cell density is increased in the hearts of patients with ischemic and idiopathic dilated cardiomyopathy. Cardiac mast cells might contribute to the evolution of atherosclerosis, dilated cardiomyopathy, cardiac and systemic anaphylaxis through the release of cytokines and vasoactive and proinflammatory mediators.

Arteriosclerosis↗

Distribution, histochemical and enzyme histochemical characterization of mast cells in dogs.

This study describes the distribution, proteoglycan properties and protease activity of mast cells from 15 different dog organs. In beagles and mixed breed dogs, staining with Alcian Blue-Safranin O revealed mast cells in all the organs examined. However, their numbers varied and they demonstrated unique localization patterns within some of these organs. Berberine sulphate fluorescence-positive mast cells were observed in the submucosa, muscularis and serosa of the intestines, as well as the tongue and liver (within the connective tissue). Mast cells within the intestinal mucosa were negative for, or demonstrated weak, berberine sulphate staining. Heterogeneity of mast cells in terms of the proteoglycans contained within their granules was further confirmed by determination of critical electrolyte concentrations (CECs). The CECs of mast cells within the connective tissue of several organs, including the intestines (submucosal and muscularis-serosal layers) were all greater than 1.0 M. The results from CEC experiments together with berberine staining indicate that heparin was contained within their granules. Relative to the CECs of mast cells in other organs, mast cells in the intestinal mucosa exhibited lower CECs, suggesting that the proteoglycans within their granules were of lower charge density and/or molecular weight. Although mast cells were classified into two groups by proteoglycans within the granules, enzyme histochemical analysis in beagles revealed three subtypes of mast cells: chymase (MC(C)), tryptase (MC(T)) and dual positive (MC(TC)) cells. There was no correlation between the proteoglycan content and enzyme properties of the mast cell granules.

Alcian Blue↗

Cellular infiltration and cytokine mRNA expression in perennial allergic rhinitis.

BACKGROUND: Allergen challenge in allergic rhinitis patients leads to local eosinophilia and Th2-type cytokine expression. Natural exposure to grass pollen is additionally characterized by epithelial mast-cell infiltration. We hypothesized that perennial allergic rhinitis is also associated with T-cell and eosinophil infiltration of the nasal mucosa, local Th2-type cytokine expression, and increased numbers of nasal epithelial mast cells. METHODS: Nasal biopsies from perennial allergic rhinitis patients and controls were analysed by immunocytochemistry for different cell populations and in situ hybridization for cytokine mRNA-expressing cells. RESULTS: Perennial allergic rhinitis was associated with increased numbers of submucosal CD3+ T cells (P=0.05), EG2+ activated eosinophils (P=0.01), and CD68+ macrophages (P=0.01) compared to controls. Epithelial, but not submucosal, tryptase-positive mast cells were also elevated in rhinitics compared to controls (P=0.01). The numbers of cells expressing interleukin (IL)-5 were higher (P=0.01) and the numbers of cells expressing IL-2 were lower (P=0.04) in rhinitic patients than controls. There were no significant differences for either IL-4 or interferon-gamma between the groups. CONCLUSIONS: Perennial allergic rhinitis is characterized by mast-cell migration into the epithelium; submucosal infiltration by T cells, eosinophils, and macrophages; and an imbalance in local T-cell cytokine production in favour of enhanced IL-5 and reduced IL-2 expression.

Adult↗

Allergic rhinitis: not purely a histamine-related disease.

Allergic rhinitis is an inflammatory disorder of the nasal mucosa typified by the symptoms of nasal itch, sneeze, anterior nasal secretions, and nasal blockage. These symptoms arise from the interaction between mediators and neural, vascular, and glandular structures within the nose. Nasal itch, sneezes, and rhinorrhoea are predominantly neural in origin, while nasal obstruction is predominantly vascular. Nasal biopsy studies show accumulation of eosinophils within the lamina propria and epithelium and an increase in tissue and cell surface basophils in both seasonal and perennial allergic rhinitis. These cells are in an activated state. Within the epithelium, increased numbers of mast cells, T cells and Langerhans' cells, which induce T-cell activation, are found. The accumulation of these cells can be linked to chemokine and cytokine generation by the epithelial cells themselves. Thus, the tissue cell recruitment is orchestrated by activated mast cells, T cells, and epithelial cells, with the recruited tissue eosinophils also contributing to their persistence at this site through autocrine mechanisms. Mast cells generate an array of mediators including histamine, tryptase, leukotrienes, and prostaglandins. Histamine is also generated by basophils. Eosinophils and basophils contribute to the leukotriene synthesis within the tissue. Histamine nasal insufflation induces nasal itch, sneeze, and rhinorrhoea as well as nasal blockage, thereby reproducing all the symptoms of allergic rhinitis. These effects are primarily mediated by H1-receptors, and H1-receptor antagonists are a prominent treatment. Antagonism of histamine at these receptors reduces symptoms by about 40-50%, with the greatest effect on the neurally mediated responses. Thus, histamine is a major mediator of allergic rhinitis, but not the sole contributor. Nasal insufflation with leukotrienes, prostaglandins, or kinins is associated with the development of nasal blockage. These mediators act primarily on the nasal vasculature and, in this respect, leukotrienes are potent mediators. Leukotrienes also induce plasma protein exudation, which contributes to the anterior nasal secretions. Studies with combination products have suggested that modifying the effects of both leukotrienes and histamine has complementary effects in relieving nasal symptoms, indicating that both these mediators are relevant to disease expression.

Eosinophils↗

Serum inhibitors for human mast cell growth: possible role of retinol.

BACKGROUND: In vitro culture systems have been used to study the physiological and pathological characteristics of human mast cells. However, there are some differences in proliferation and maturation of mast cells between fetal bovine serum (FBS)-containing and serum-deprived cultures. Accordingly, we attempted to identify circulating factor(s) affecting the development of human mast cells. METHODS: We measured the serum levels of retinol and several cytokines. To elucidate the antiproliferative effects of the serum, a retinoic acid receptor (RARalpha) antagonist and neutralizing antibodies against cytokines were used. RESULTS: Similar to FBS, human serum dose-dependently suppressed the growth of tryptase+ cells from CD34+ cord blood cells or 20-week cultured mast cells under stimulation with stem cell factor (SCF). The serum-mediated inhibition might be based on a decline in proliferation rate. Among inhibitors for mast cell growth, retinol and transforming growth factor (TGF)-beta1 were present at high levels in human serum. In contrast with anti-TGF-beta1 antibody, an RARalpha antagonist counteracted the serum-induced suppression of human mast cell proliferation. CONCLUSIONS: Our results suggest that retinol and its derivatives act as a circulating regulator for human mast cell growth. The RARalpha antagonist may be a useful tool to obtain higher numbers of mast cells in FBS-containing cultures.

Animals↗

Differences in nasal cellular infiltrates between allergic children and age-matched controls.

Little is known about the cellular infiltrates in the nasal mucosa of children. This study was set up to compare the nasal cellular infiltrates in biopsy specimens from allergic children and controls. Atopic children were distinguished from controls on the basis of symptoms of allergic rhinitis and/or asthma, total serum immunoglobulin (Ig)E, family history and specific serum IgE to food and aeroallergens. Fifteen allergic patients (median age 4.3 yrs) and 15 age-matched nonallergic control subjects were evaluated. The number of cells positive for CD1a, CD4, CD8, CD19, CD68, chymase, tryptase, IgE and major basic protein was determined in the mucosa of the inferior turbinate. A significantly higher number of IgE-positive cells and mast cells was found in the epithelia of the allergic group. In the lamina propria, higher numbers of IgE-positive cells and eosinophils were found. Langerhans' cells positive for IgE were only seen in allergic children with specific serum IgE against aeroallergens. These children also had a higher number of IgE-positive mast cells compared to controls and atopic children without specific serum IgE. These results show that the nasal cellular infiltrates of allergic children differ from nonallergic control subjects. Prior to the detection of specific serum immunoglobulin E, cellular changes can be found in the nasal mucosa of atopic children.

Biopsy↗

Anaphylactic reactions during induction of anaesthesia using rocuronium for muscle relaxation: a report including 3 cases.

Anaphylaxis during induction of anaesthesia is a dreaded complication with a mortality rate of 3-6%, most frequently associated with the use of muscle relaxants. Current knowledge on this matter is reviewed in relation to the presentation of 3 cases of anaphylaxis and bronchospasm associated with the use of the recently released nondepolarizing muscle relaxant rocuronium. Bronchospasm may be the sole sign of a serious drug reaction, triggered by precipitation of insoluble thiopental crystals when mixed with a muscle relaxant in the intravenous (iv) line. It is recommended that these drugs are administered via different injection ports. The hypotension requires immediate treatment with oxygen, epinephrine and large amounts of iv fluids. Epinephrine infusion may be needed for hours. It is recommended that serum tryptase is measured approximately 2 h after debut of the serious drug reaction. Allergy testing should be performed for all the drugs the patient was exposed to, 4-8 weeks after the incident, and due to cross-reactivity, including all available muscle relaxants. Doctors are urged to inform their patients, and systematically register adverse drug reactions.

Adult↗

An anaphylactic reaction to blood supplied from patient's mother.

We present the case of a 4-year-old girl who developed anaphylactic shock during general anesthesia. Symptoms appeared 80 min into the operation and may have been an immediate allergic reaction to the transfused blood supplied from the child's mother based on the clinical signs, the decrease of components of complements and the elevated concentrations of histamine and tryptase. The blood type was the same and antibody screening test and crossmatch was negative. The blood was irradiated and we used a white cell-reduction filter. This patient possibly has antibodies to her mother's plasma and this type of reaction cannot be prevented by these routine methods. It is reported that the risk of transfusion associated graft-vs.-host disease is high when a patient receives blood from a closely related donor. However, there are, no reports of anaphylactic reactions to blood supplied from mother to child. We suggest that there is a potential for anaphylactic reaction as well as transfusion associated graft-vs.-host disease when a child patient receives blood from the mother.

Anaphylaxis↗

Scarring alopecia associated with mastocytosis.

BACKGROUND: Mastocytosis is comprised of a group of heterogeneous diseases involving various organs. Urticaria pigmentosa is the most common manifestation of cutaneous mastocytosis; others include mastocytoma, diffuse mastocytosis, and telangiectasia macularis eruptiva perstans. METHODS: We describe a case of indolent mastocytosis presenting as scarring alopecia. The scalp biopsy revealed a perifollicular and dermal inflammatory infiltrate composed predominantly of mast cells, which was confirmed by tryptase and Giemsa stains. RESULTS: The preponderance of mast cells in the biopsy prompted testing for urine N-methylhistamine levels, which were elevated and confirmed the diagnosis of mastocytosis. This is the first report of mastocytosis presenting as scarring alopecia. CONCLUSIONS: This case suggests that the diagnosis of mastocytosis should be entertained in patients presenting with scarring alopecia accompanied by an intense mast cell infiltrate on scalp biopsy and also supports the notion that mast cells may be involved in the pathogenesis of alopecia.

Alopecia↗