Familial partial lipodystrophy (FPLD) is a rare inherited disorder characterized by limb adipose tissue atrophy and metabolic abnormalities, including severe insulin resistance. However, diagnosis is often delayed because the characteristic physique can be difficult to recognize without a high index of suspicion. We present the case of a 19-year-old Japanese woman diagnosed with FPLD type 2 (FPLD2). She had a history of irregular menses and hirsutism since adolescence. The FPLD2 diagnosis was prompted by her concerns about axillary and inguinal pigmentation. Her mother's online search first suggested acanthosis nigricans (AN). After including "muscular limb" as an additional search term, they suspected lipodystrophy, prompting a consultation with an endocrinologist. Clinical examination revealed impaired glucose tolerance, severe insulin resistance, dyslipidemia, fatty liver, and polycystic ovary syndrome. Genetic testing identified a heterozygous LMNA p.R482Q variant, confirming the diagnosis. This case demonstrates that AN, a skin manifestation of insulin resistance, is an important diagnostic clue for FPLD. Although women with FPLD frequently present with menstrual irregularities and hirsutism in their late teens, their insulin levels are rarely measured before diabetes onset. Consequently, the underlying severe insulin resistance is frequently overlooked. Although reported cases of FPLD2 in Japan are limited, many cases may remain undiagnosed. Therefore, clinicians should examine the friction-prone areas in non-severely obese individuals with metabolic or menstrual irregularities. The absence of AN does not rule out insulin resistance. Therefore, even without AN, the presence of other features of insulin resistance warrant consideration of FPLD and careful evaluation for limb fat loss, facilitating early diagnosis.

Morbid obesity is a chronic condition characterized by metabolic disorders and low-grade chronic inflammation, both of which are closely linked to insulin resistance and adipokine dysregulation. In addition to its systemic effects, obesity also leads to structural and functional changes in the skin, supporting its role as an active metabolic and immunological organ. This study analyzed skin lesions occurring in individuals with morbid obesity and explored their potential relevance in the context of metabolic risk and treatment response rather than establishing clinically validated tools. The focus was on how excess adipose tissue affects the skin through metabolic, hormonal and mechanical mechanisms. Although this review focuses on morbid obesity, many of the included studies examine general obesity without separating its severity. Therefore, the findings may not fully reflect patients with BMI ≥ 40 kg/m[2] and should be interpreted with caution. Three main areas were considered: the pathophysiological mechanisms underlying obesity-related skin lesions, selected dermatological manifestations as potential markers associated with metabolic risk, and changes in these manifestations during pharmacological, surgical, and lifestyle interventions. Available studies show that acanthosis nigricans and multiple acrochordons are consistently associated with insulin resistance, metabolic syndrome, and metabolic dysfunction-associated steatotic liver disease. An increase in BMI is also associated with impairment of the epidermal barrier, changes in the composition of skin lipids, and modifications of the skin microbiome, while biomechanical factors promote the development of chronic inflammation in the intertriginous areas. It has been shown that normalization of metabolic parameters achieved through GLP-1-based pharmacotherapy, bariatric surgery, or lifestyle changes can improve some skin manifestations, especially acanthosis nigricans. However, it should be emphasized that most available data are based on cross-sectional or observational studies, and validated composite dermatological indices are still unavailable. Skin changes in patients with morbid obesity often reflect underlying metabolic and hormonal disturbances. They may have potential as additional, non-invasive clinical clues, but they should not be treated as independent tools for risk assessment or treatment monitoring. At present, most evidence shows associations only, and it is unclear whether these findings add meaningful predictive value beyond standard metabolic markers. More prospective studies are needed to confirm their clinical usefulness and to define their role in assessing metabolic risk and monitoring treatment over time.

Facial melanoses (FMs) encompass a diverse group of disorders characterised by altered facial pigmentation, particularly prevalent in individuals with darker skin types, such as the Indian population. While common causes like melasma, post-inflammatory hyperpigmentation, and lichen planus pigmentosus are well documented in the literature, this review emphasises the lesser-known and uncommon causes of FM. These include facial acanthosis nigricans, maturational hyperpigmentation, frictional facial melanosis, and seborrheic melanosis, which are frequently observed in Indian populations but remain underrecognised and understudied. The aetiology of FM is multifactorial, involving genetic predisposition, racial factors, ultraviolet radiation, and exposure to photosensitising chemicals and allergens. Uncommon causes often present unique diagnostic challenges and are frequently misdiagnosed due to their overlapping clinical features. Diagnosis relies on clinical evaluation, supported by Wood's lamp examination, dermoscopy, and, in some cases, skin biopsy. FM can be classified into brown, blue, or mixed hypermelanosis based on the location and nature of melanin deposition. Management of these uncommon conditions is complex and requires a nuanced approach. Photoprotection remains a cornerstone of therapy, alongside topical depigmenting agents, chemical peels, and laser or light-based interventions. However, the risk of post-inflammatory hyperpigmentation in richly pigmented skin necessitates cautious and individualised treatment strategies. The lack of standardised guidelines for these uncommon causes further complicates management, underscoring the need for tailored therapeutic approaches. This review highlights the clinical significance of recognising and addressing uncommon causes of FM, which significantly impact patients' quality of life and psychosocial well-being. Enhanced awareness, further research, and the development of evidence-based treatment protocols are essential to improve outcomes for patients with these understudied conditions. By focussing on these uncommon causes, this review aims to fill a critical gap in the literature and provide a comprehensive resource for clinicians managing facial melanoses in skin of colour. Such comprehensive articles are lacking in literature.

This observational study was designed to establish and validate a stigma prediction model for patients with polycystic ovary syndrome (PCOS). The stigma risk scoring table for overweight and obese patients with PCOS has good predictive ability. When an overweight or obese patient with PCOS presents, the prediction model allows clinic staff to rapidly grade hirsutism, acne, and acanthosis, determine fertility desire, and quantify anxiety. Low-risk patients then receive standard care, whereas high-risk patients receive precision interventions. Unlike the traditional approach, this clinical prediction model incorporates not only laboratory values but also body-image concerns and psychological well-being, providing more comprehensive management for women with PCOS. To preliminarily explore the associations among stigma, PCOS signs, anxiety, and depression. A total of 124 overweight and obese patients with PCOS were selected using convenience sampling. The patients in the order of clinic visit time were divided into a modeling set and a validation set at a ratio of 3:1. Univariate analysis was first performed, normally distributed continuous variables were compared using t-tests, non-normally distributed continuous variables with nonparametric rank-sum tests, and categorical variables with χ2 tests. Independent risk factors for stigma were identified using multivariable logistic regression, and a nomogram was constructed. The model's discrimination and calibration were evaluated with the receiver operating characteristic curve and calibration curve. Internal validation was subsequently conducted on the validation data set to assess model performance comprehensively. Hirsutism (odds ratio [OR]=0.075, 95%Cl: 0.015-0.368) , acne (OR=0.210, 95%Cl: 0.050-0.878) , acanthosis nigricans (OR=0.184, 95%Cl: 0.044-0.073) , fertility requirements (OR=0.212, 95%Cl: 0.051-0.890) , and anxiety (OR=1.217, 95%Cl: 1.074-1.378) were independent influencing factors for stigma in these patients (P < .05). The constructed prediction model also demonstrated good predictive ability, with area under the curve values of 0.941 and 0.803 for the modeling and validation sets, respectively. Internal validation using 1000 bootstrap resamples revealed a mean area under the receiver operating characteristic curve area under the curve of 0.941.

Acral acanthotic anomaly (AAA), also referred to as acral acanthosis nigricans (AAN), is a variant of acanthosis nigricans characterized by hyperpigmented, hyperkeratotic plaques localized to acral surfaces, particularly the knuckles, toes, and dorsal aspects of the hands and feet. Unlike other common forms, AAA is not typically associated with obesity, insulin resistance, or endocrinopathy. Its pathogenesis remains poorly understood. The aim of this article is to provide a comprehensive synthesis of the literature on AAA, including its epidemiology, clinical features, histopathologic findings, reported cases, and associated systemic associations. A narrative review of the literature was conducted using PubMed to identify articles discussing AAA. Relevant case reports and reviews were examined to extract data on presentation, histology, differential diagnosis, and potential clinical associations. Existing literature consistently describes a characteristic acral distribution and histologic features such as papillomatosis, hyperkeratosis, and basal pigmentation. Although often observed in otherwise healthy individuals, the literature demonstrates the potential for association with malignancy or autoimmune disease. Due to the rarity of AAA, available data are limited to case reports and small series, with no large-scale studies or longitudinal follow-up. Accurate recognition of AAA is essential to guide clinical evaluation, avoid unnecessary testing, and identify potential systemic associations when present.

Acromegaly is a chronic multisystem disorder driven by persistent hypersecretion of growth hormone (GH) and consequent elevation of insulin-like growth factor 1 (IGF-1). Beyond its hallmark acral and craniofacial alterations, it manifests with a broad spectrum of systemic complications that substantially contribute to morbidity and mortality. Skeletal and soft tissue overgrowth cause characteristic disfigurement, while musculoskeletal involvement-including degenerative arthropathy, vertebral fractures, myopathy, and neuropathies-remains a major determinant of long-term disability despite biochemical remission. Cutaneous changes such as skin thickening, hyperhidrosis, seborrhea, and acanthosis nigricans are common and may partially regress after treatment. Cardiovascular sequelae, particularly hypertension, cardiomyopathy, valvular disease, and arrhythmias, represent leading causes of morbidity and mortality. Respiratory involvement, especially obstructive sleep apnea, is frequent and often persists after disease control. Metabolic disturbances, including impaired glucose tolerance, diabetes, and dyslipidemia, are highly prevalent and significantly raise cardiovascular risk. Gastrointestinal manifestations include motility disorders, hepatobiliary involvement, and increased incidence of colonic polyps and colorectal cancer, with emerging evidence of elevated risk for other malignancies. Additional endocrine and neuropsychiatric complications, such as hypopituitarism, thyroid abnormalities, cognitive dysfunction, and depression, further aggravate disease burden and impair quality of life. Despite advances in surgery, medical therapy, and radiotherapy, residual morbidity and irreversible sequelae frequently persist. Early diagnosis and multidisciplinary care are crucial not only for achieving biochemical remission but also for mitigating comorbidities, improving quality of life, and enhancing survival outcomes in acromegaly.

The AKT2-related hypoinsulinemic hypoglycemia and overgrowth syndrome was initially described over 30 years ago as MORFAN syndrome which was an acronym for Mental retardation, pre- and post-natal Overgrowth, Remarkable Face, and Acanthosis Nigricans. Despite the limited possibility of confirming a diagnosis on the molecular level at that time, a comprehensive 30-year follow-up of a patient facilitated a detailed exploration of the syndrome's clinical trajectory. This article presents a case report spanning three decades, highlighting the significance of detailed clinical follow-up in understanding and studying this unique syndrome. Although initially associated with intellectual deficiency, the patient's intellectual abilities remain largely within the normal range. Neuropsychological examinations revealed selective neurocognitive impairment, with a predominant disruption in psychomotor speed and executive functions. Molecular genetic examination confirmed a pathogenic variant in the AKT2 gene, associated with impaired insulin metabolism and increased tumorigenesis risk. Neurooncological assessments revealed intracranial meningiomatosis, emphasizing the syndrome's potential oncological implications. Surgical interventions addressed various complications, including meningiomas and renal hamartomas. The presented case offers valuable insights into the long-term natural history of AKT2-related hypoinsulinemic hypoglycemia and overgrowth syndrome, suggesting the importance of regular oncological surveillance due to its predisposition to tumorigenesis, thereby providing clinical considerations for future cases based on long-term follow-up experience.

Facial hyperpigmentation disorders (FHD) are common in dermatology, particularly in people with skin of color (SOC). They include melasma, post-inflammatory hyperpigmentation, and less frequent conditions such as exogenous ochronosis, lichen planus pigmentosus, Riehl's melanosis, acanthosis nigricans, seborrheic melanosis, pigmentary demarcation lines, drug-induced pigmentation, and nevus of Ota, among others. These conditions may significantly affect quality of life. They can present similar clinical and dermoscopic features, making diagnosis challenging. A thorough medical history, physical examination, and careful dermoscopic evaluation are essential to achieve an accurate diagnosis. In this article, we present a narrative review of the clinical and dermoscopic characteristics of FHD in SOC and provide diagnostic clues for the early diagnosis of these conditions.