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Very low-calorie ketogenic diet (VLCKD) in the management of hidradenitis suppurativa (Acne Inversa): an effective and safe tool for improvement of the clinical severity of disease. Results of a pilot study



Hidradenitis suppurativa (HS), an inflammatory-based dermatological condition often associated with obesity, poses significant challenges in management. The very low-calorie ketogenic diet (VLCKD) has shown efficacy in addressing obesity, related metabolic disorders, and reducing chronic inflammation. However, its effects on HS remain underexplored. In this prospective pilot study, we aimed to investigate the impact of a 28-day active phase of VLCKD on HS in a sample of treatment-naive women with HS and excess weight.


Twelve women with HS and overweight or obesity (BMI 27.03 to 50.14 kg/m2), aged 21 to 54 years, meeting inclusion/exclusion criteria and agreeing to adhere to VLCKD, were included. Baseline lifestyle habits were assessed. The Sartorius score was used to evaluate the clinical severity of HS. Anthropometric parameters (waist circumference, weight, height, and body mass index), body composition via bioelectrical impedance analysis, levels of trimethylamine N-oxide (TMAO), oxidized low-density lipoprotein (oxLDL), and derivatives of reactive oxygen metabolites (dROMs) were assessed at baseline and after 28 days of the active phase of VLCKD.


VLCKD led to general improvements in anthropometric parameters and body composition. Notably, a significant reduction in the Sartorius score was observed after the intervention (Δ%: − 24.37 ± 16.64, p < 0.001). This reduction coincided with significant decreases in TMAO (p < 0.001), dROMs (p = 0.001), and oxLDL (p < 0.001) levels. Changes in the Sartorius score exhibited positive correlations with changes in TMAO (p < 0.001), dROMs (p < 0.001), and oxLDL (p = 0.002).


The 28-day active phase of VLCKD demonstrated notable improvements in HS severity and associated metabolic markers, highlighting the potential utility of VLCKD in managing HS and its association with metabolic derangements in women with overweight or obesity.


Hidradenitis suppurativa (HS), also referred to as acne inversa, is a chronic inflammatory skin condition that primarily affects body areas with intertriginous sites and a high density of apocrine glands, such as the axillae, inframammary folds, and anogenital regions [1]. This condition typically emerges during adolescence and young adulthood and can persist throughout a person's life. HS is characterized by recurring inflammatory nodules and, in more severe cases, the development of abscesses accompanied by sinus tracts and extensive scarring. This leads to distressing symptoms, including pain, malodor, and physical disfigurement, resulting in significant psychological strain [1]. The prevalence of HS is likely underreported; however, current data estimate a global prevalence of 0.00033–4.1% [2]. Recent evidence has shifted away from apocrine glands as the primary origin of HS, highlighting defects in the follicular portion of the folliculopilosebaceous units as a key contributor to the disease's pathogenesis [3].

Patients with HS exhibit a higher obesity prevalence compared to the general population. In 2008, two case–control studies involving 67 and 302 patients with HS [4], respectively, highlighted these associations. In the first study, 16.4% of patients with HS suffered from obesity (BMI ≥ 30.0 kg/m2) versus 13.3% of controls. Overweight (BMI 25.0–29.0 kg/m2) was 26.9% in patients with HS versus 20.4% in controls. The second study reported 21.4% obesity in patients with HS versus 17.1% controls, with overweight percentages at 21.8% (HS) and 8.5% (controls). Cross-sectional design limits establishing causation. Other studies note that over 75.0% of patients with HS experience overweight or obesity [5, 6], correlating disease severity with a higher BMI [7,8,9].

The hormonal changes associated with obesity, androgen access, and dietary effects likely exacerbate HS, as do the larger areas of skin folds, sweat retention, and friction [10]. In contrast, exercise can be painful for HS patients, contributing to the vicious cycle of obesity and HS. The underlying inflammatory process is likely influenced by the increased levels of proinflammatory cytokines seen in patients with obesity [10]. Interestingly, a weight loss of 15% has been shown to significantly reduce HS severity [11].

However, several other factors may contribute to the development and clinical severity of HS, including altered microbial composition (microbiota dybiosis) and nutrition [12, 13]. In this context, we previously provided the first evidence that circulating levels of Trimethylamine N-Oxide (TMAO), a gut-derived metabolite associated with inflammation and cardiometabolic risk, were increased in patients with HS and were associated with the clinical severity of the disease [14].

Treatment of HS has been challenging, as it does not respond reliably to medical therapies. Given limited treatment options, dietary modifications have gained considerable interest as a possible treatment option for HS [15]. Although management through diet and lifestyle modifications is a primary interest of the patients with HS community, there is a lack of consensus on recommendations due to the paucity of evidence. In this regard, the British Association of Dermatologists noted in their 2018 guidelines that there were no high-quality studies supporting the beneficial effect of diet in HS [16]. The United States and Canadian Hidradenitis Suppurativa Foundations also published clinical management guidelines in 2019, concluding that there wasn't enough evidence to support the routine use of vitamin D, zinc, and dairy avoidance (recommendations classified as class C or level II/III evidence) [17]. Despite the interest in dietary modifications among the patients in the HS community, the lack of evidence has made it challenging to establish clear guidelines for its management.

Finally, among the exacerbating factors in HS, diet plays a key role [18]. Notably, recent studies have highlighted the potential impact of diet on HS, including the significance of the Mediterranean diet [19, 20]. However, there remains much to be studied in the pursuit of establishing the role of diet on disease outcomes. Dietary interventions should always be considered in addition to pharmacological therapy. Recently proposed as an obesity management nutritional strategy, the Very Low-Calorie Ketogenic Diet (VLCKD), through the production of ketone bodies, was associated with a significant reduction in body weight, inflammatory status, and gut microbiota composition [21,22,23]. While data on the efficacy of VLCKD in psoriasis is available, the efficacy of VLCKD in improving the clinical severity of HS has not been established in clinical studies, and there is no evidence in the literature [15, 18]. Dietary strategies for reducing inflammation and body weight represent a topic of great interest to both nutritionists and dermatologists. Recent research [24, 25] suggests a compelling anti-inflammatory role for VLCKD, potentially surpassing low-fat diets [26]. Although a comprehensive meta-analysis is lacking, emerging evidence highlights VLCKD's notable anti-inflammatory effects [26]. Thus, as HS is an inflammatory-based disease and often associated with obesity, in this prospective pilot study we aimed to investigate the effects of 28 days of the active phase of VLCKD in a sample of naive-treatment women with HS.


Design and setting

This prospective pilot study was conducted on women with HS at the Dermatology Unit of the Department of Clinical Medicine and Surgery of the University Federico II of Naples. The study ran from September 2021 to July 2023. Ethical authorization for the study was granted by the Local Ethics Committee (reference no. 50/20), and all procedures were conducted in strict compliance with the World Medical Association's Code of Ethics, in particular the Declaration of Helsinki, which defines the principles of human experimentation. The objectives and procedures of the study were fully communicated to all participants, ensuring complete clarity. Prior to involvement, written informed consent was obtained from each participant stating their willingness to take part in the study.

Population study

In order to enhance the uniformity of the patient groups, our attention was directed solely towards Caucasian women who had excess weight or obesity and were afflicted by HS. These women were specifically drawn from the geographical vicinity surrounding the Naples metropolitan area in Campania, Italy. Comprehensive medical information was collected from all women. The inclusion criteria for participation in the study were as follows:

  • Treatment-naive subjects;

  • BMI ≥ 25.0 kg/m2;

  • Fulfillment of all three diagnostic criteria for HS: presence of characteristic lesions, involvement of anatomical sites in typical regions, and an ongoing disease course marked by relapses and chronicity;

  • Women who had not previously received treatment for HS;

  • HS diagnosis was established at least 6 months before the study, with no medical therapy for a minimum of 3 months.

Women were excluded if they met any of the following exclusion criteria:

  • Occasional or current use of systemic treatments (such as anti-inflammatory, anti-obesity, biologics, cyclosporine A, rifampicin–moxifloxacin–metronidazole, clindamycin–rifampicin, dapsone, ertapenem, tetracycline, acitretin, and isotretinoin) or other medications for HS, including topical antibiotics;

  • Suffered from any other active skin condition (like psoriasis or acne) that might interfere with HS assessment;

  • Had one or more contraindications for VLCKD according to current guidelines from the European Association for the Study of Obesity (EASO);

  • Displayed symptoms or signs indicative of androgen excess or underlying endocrine disorders;

  • Adherence to hypocaloric diets, specific dietary patterns (including vegetarian or ketogenic diets), or use of antioxidants, vitamins, minerals, or probiotics within the past three months;

  • Presence of clinical conditions or use of medications affecting fluid balance, such as liver or renal failure, cancer, and other chronic or acute illnesses as determined by comprehensive medical examinations and laboratory tests;

  • Possess implanted pacemakers or defibrillators, considering the potential theoretical interference with the activity of the bioelectrical impedance analysis (BIA) device;

  • Had a history of clinical conditions that, in the judgment of the Dermatologist, Endocrinologist and Nutritionist could put the patient at risk if they participated in this study.

Figure 1 shows the flow chart of women included in the analysis.

Fig. 1
figure 1

Flow chart of study participants. HS, hidradenitis suppurativa; BMI, body mass index

Study protocol

The study protocol encompassed a series of five visits (T0, T1, T2, T3, T4), each occurring every 7 days over a total span of 28 days, constituting the active phase of VLCKD, as depicted in Fig. 2. At baseline (T0), a comprehensive assessment carried out by a team of Dermatologist, Endocrinologist, and Nutritionist was conducted to ascertain the eligibility of women. Those meeting the criteria for inclusion and exclusion were enrolled in the study and provided their written informed consent. At this point, a Nutritionist undertook lifestyle, anthropometric, and body composition assessments. Women were then provided with personalized instructions for adhering to the VLCKD. This included receiving individualized dietary plans and scheduled replacement meals for the week. Simultaneously, with the support of nursing staff, blood samples were collected for general biochemical tests, oxidative stress evaluation, and TMAO levels. Finally, women were advised to maintain their existing level of physical activity throughout the study duration. During the subsequent follow-up visits (T1, T2, and T3), women underwent assessments of adherence to VLCKD by the Nutritionist via telephone interview. Adherence was gauged through ketone body measurements extracted from capillary blood samples, and the Nutritionist recorded whether the patient exhibited ketosis (YES/NO). The Nutritionist also documented any deviations in physical activity levels or deviations from the food and beverage consumption patterns outlined in the VLCKD protocol. In the last visit (T4, day 28), a final round of dermatological, endocrinological, and nutritional assessments was conducted in the presence of the doctors (Dermatologist and Endocrinologist) and the Nutritionist. Blood samples were collected once more for the repetition of biochemical, oxidative stress, and TMAO analyses.

Fig. 2
figure 2

Study protocol. VLCKD, very low-calorie ketogenic diet

Hidradenitis suppurativa assessment

Since there is no established benchmark for this purpose, the evaluation of HS was conducted using the Sartorius HS score [1]. The Sartorius HS score is a clinical classification system that involves the enumeration of individual fistulas and nodules in seven anatomical regions. It also entails measuring the greatest distance between two similar lesions within each of these anatomical areas, namely the axilla, gluteal, groin, genital, and other inflammatory sites on the left and/or right sides [9]. The clinical severity of HS was determined by two unbiased Dermatologists who were unaware of the study's design, thus minimizing any potential biases. In addition, we evaluated the Dermatology Life Quality Index (DLQI), a standardized instrument used to assess the impact of dermatitis and other skin conditions on patients' quality of life. It is a self-assessment questionnaire that measures different aspects of daily life influenced by the presence of dermatological symptoms. The DLQI consists of ten questions divided into six categories: symptoms and feelings, embarrassment, daily activities, clothing, leisure, and interpersonal relationships. Each question is rated on a four-point scale, with scores ranging from 0 to 3, representing 'no impact', 'minor impact', 'moderate impact' and 'major impact', respectively. To calculate the total DLQI score, the scores obtained from the ten questions are added together, with a total possible score ranging from 0 (no impact on quality of life) to 30 (maximum impact on quality of life).

Lifestyle habits

As previously reported [27,28,29], we defined current smokers as women smoking at least one cigarette per day, former smokers as women who had stopped smoking at least one year before the interview, and non-current smokers as the remaining women. Women habitually engaging in at least 30 min per day of aerobic exercise (YES/NO) were defined as physically active.

Anthropometric assessment

The same Nutritionist performed the anthropometric assessment. All women were assessed between 8 and 10 a.m. after an overnight fast, wearing light clothing and no shoes. Body weight was measured to the nearest 0.1 kg using a calibrated balance beam scale, and height was measured to the nearest 0.5 cm using a wall-mounted stadiometer. BMI was calculated by dividing weight (in kg) by height squared (in meters). BMI was classified according to the World Health Organization's criteria for normal weight, overweight, and I, II and III grades of obesity. Waist circumference (WC) was measured to the nearest 0.1 cm with a no-stretch tape measure at the natural indentation or halfway between the lower edge of the rib cage and the iliac crest if no natural indentation was visible.

Bioelectrical impedance analysis

Body composition was evaluated using a BIA phase-sensitive system, administered by an experienced nutritionist, as previously documented [22, 30,31,32]. The system applied an 800-µA current at a signal frequency of 50 kHz, using the BIA 101 RJL instrument from Akern Bioresearch in Florence, Italy. The examination was conducted in accordance with the guidelines provided by the European Society of Parenteral and Enteral Nutrition (ESPEN) [33]. Electrodes were positioned on the hand and the corresponding foot, following the protocol established by Kushner in 1992 [34]. The PhA was calculated based on conditions under 50 kHz using the following formula: PhA (°, degrees) = arctangent of reactance (Xc) divided by resistance (R) multiplied by (180/π).

VLCKD intervention

According to EASO guidelines, VLCKD consists of three phases (active, re-education, and maintenance) [35]. The active phase of VLCKD was collaboratively devised by a Nutritionist and endorsed by an Endocrinologist. The dietary composition adhered to specific parameters, with a total energy intake of less than 800 kcal per day. This energy was derived from a distribution of 13% from carbohydrates (less than 30 g per day), 43% from protein (1.3 g per kilogram of ideal body weight), and 44% from fat. The ideal body weight (kg) was calculated using the Lorentz equation: ideal body weight = height (cm) – 100 − [(height − 150)/2] [36]. Throughout VLCKD, meals with high biological value were provided as replacements, and the protein content originated from sources such as whey, soy, eggs, and peas. To ensure nutritional adequacy during the VLCKD, supplementation was introduced. This included B-complex vitamins, vitamins C and E, essential minerals like potassium, sodium, magnesium, and calcium, as well as omega-3 fatty acids. An example of a VLCKD with meal replacements is reported in Additional file 1.

Biochemical assessment

Blood samples were obtained through venipuncture between 8 and 10 in the morning, following an overnight period of fasting, with the procedure conducted by the nursing staff. Subsequently, the samples were transported to the local laboratory and processed in accordance with the established local standards and protocols. The measurements included assessments of glucose and lipid profiles, electrolyte levels, uric acid concentrations, liver enzyme activities, and indicators of kidney function. The intra- and inter-assay CVs were below 3% for all the samples. Additionally, the Homeostatic Model Assessment for Insulin Resistance (HoMA-IR) was computed for each woman using the formula [fasting glucose (mmol/l) × fasting insulin (mU/ml)/22.5] [37]; the intra-assay CV for insulin was < 5.5%.

Evaluation of the oxidized low-density lipoprotein levels

Blood samples were obtained using the brachial puncture method and placed into heparin vacuum tubes with a 5-mL capacity. After being centrifuged at 3000 rpm for 10 min at room temperature, the sera were isolated and stored at a temperature of − 80 °C for subsequent analysis within a maximum period of 6 months. The measurement of plasma levels of oxidized low-density lipoprotein (ox-LDL) was conducted through the employment of the LP-CHOLOX test on an automated analyzer known as Free Carpe Diem, provided by Diacron International, Grosseto, Italy. This test employed a commercial kit from the same manufacturer and was executed following the provided instructions. The LP-CHOLOX test assesses a category of hydroperoxides originating from lipid peroxidation, primarily comprising oxidized cholesterol. These hydroperoxides have the capability to induce the conversion of ferrous iron (Fe2+) to ferric iron (Fe3+), thereby promoting oxidation. The LP-CHOLOX test is reliant on a spectrophotometric assessment conducted at a wavelength of 505 nm, measuring the development of a colored complex formed by the interaction of Fe3 + and thiocyanate. The resulting absorbance values exhibit a direct correlation to the concentration of lipoperoxides present, and these values are standardized against a specific solution (400 μEq/L). For all the analyzed samples, the calculated intra- and inter-assay CV% values were below t2.8% indicating the high reliability and precision of the used method. The outcomes are expressed in μEq/L units, with reference ranges established as follows: normal (≤ 599 μEq/L), minor alteration (600 to 799 μEq/L), moderate alteration (800 to 999 μEq/L), and significant alteration (≥ 1000 μEq/L) [19].

Evaluation of dROMS

The assessment of oxidant ability in the plasma was conducted using the d-ROM Lab test developed by Innovatics Laboratories Inc. This analytical method indirectly gauges the presence of organic hydroperoxides (ROOH) in a sample, which are the primary contributors to oxidant ability. The methodology is centered around the oxidation of iron (or copper) through Fenton's reaction. The resulting change in color, induced by the addition of the oxidizable chromogen substrate N,N-diethyl-paraphenylendiamine, is quantified through photometric measurements. The outcomes are reported in "Carratelli units" (U Carr), with 1 U Carr being equivalent to 0.08 mg of hydrogen peroxide (H2O2) per 100 mL [38]. The reliability of the performed analysis was assessed by the calculation of CV% at the intra- and inter-assay levels for all collected samples, which resulted in an estimated CV% below 3.72% for both parameters.

Trimethylamine-N-oxide assessment

Blood samples aimed at determining TMAO levels in the serum were stored at a temperature of -80° C. This preservation approach was selected due to evidence indicating that TMAO remains stable over extended durations under these specific conditions [39]. The quantification of TMAO levels in the serum was conducted using the procedure delinelated by Beale and Airs [40], which was detailed in our previous studies [14, 41]. For chromatographic separation, a guard column (HILIC) was employed in conjunction with a Luna HILIC column (measuring 150 mm × 3 mm, with 5 µm particles), both provided by Phenomenex (located in Torrance, CA, USA). The sensitivity of the analytical method was described by the determination of a Limit of Detection (LOD) of 2 ng/ml and a Limit of Quantification (LOQ) of 6 ng/ml. In order to evaluate the precision of the method used, the CV% at intra- and inter-day levels were calculated at three different TMAO levels (0.3, 3, and 13 µM), resulting in a calculated intra-day CV% of 8.12, 1.54, and 1.52 µM and of an inter-day CV% of 9.2, 2.2, and 3.3 µM, respectively. Similarly, over the same TMAO levels, the accuracy of the method was calculated by the evaluation of the accuracy (% bias) both intraday and intraday, leading to an estimation of % bias ranging from − 3.52 to 0.66, indicating the high reliability of the used LC/MS method.

Statistical Analysis

G* Power was used to conduct an a priori sample size calculation. In the absence of preliminary data on the efficacy of this intervention and considering an effect size of 0.8 (clinically meaningful, according to Cohen), the sample size sufficient to have a power of 80% with a 1-tailed type-I error of 5% was 12 patients. The data analysis was conducted using the MedCalc® package (Version 12.3.0, 1993–2012 MedCalc Software bvba—MedCalc Software, Mariakerke, Belgium) and IBM SPSS Statistics Software (PASW Version 21.0, SPSS Inc., Chicago, IL, USA). The statistical analysis included only women who had measurements at both the baseline and after 28 days of the active phase of VLCKD. Results were presented in the form of mean ± standard deviation (SD) for continuous variables and as a number and percentage (n, %) for categorical variables. To assess data distribution, the Kolmogorov–Smirnov test was employed. The differences between baseline and measurements after 28 days of the active phase of VLCKD were compared using the paired Student’s t-test. Spearman’s correlation was utilized to investigate the association between baseline and measurements after 28 days of the active VLCKD phase in terms of percentage changes (delta ∆%). Furthermore, a multiple linear regression analysis model employing the stepwise method used the Δ% Sartorius score as a dependent variable to estimate the predictive value of changes in PhA, TMAO, dROMs, and ox-LDL after 28 days of the active phase of VLCKD, expressed as R2, beta (β), and t.


The average ideal weight calculated (Lorentz equation) in the study population was 59.21 ± 4.48 kg. Based on ideal body weight, the protein intake of the VLCKD was calculated (1.3 g of protein per ideal body weight). The average protein content of the diet was 76.97 ± 5.82 g.

The study population included 12 women participants with overweight or obesity (BMI 27.03 to 50.14 kg/m2), aged 21 to 54 years. The preponderance of women was characterized as sedentary (83.3%) and non-smokers (58.3%). None of the patients changed their physical activity levels or cigarette smoking habits during the 28 days of treatment. Furthermore, of interest, no patient reported adverse effects important to suspending the VLCKD protocol, as stated during the three telephone interviews. All patients also declared the presence of a state of ketosis.

Anthropometric characteristics and body composition of the study population at baseline and after 28 days of the active phase of VLCKD are reported in Table 1. After 28 days of the active phase of the VLCKD, in the entire study population, both BMI (Δ%: − 7.94 ± 1.95, p < 0.001) and WC (Δ%: − 7.56 ± 6.34, p = 0.002) were significantly reduced compared to baseline. After 28 days of the active phase of VLCKD, FM (%) (Δ%: − 14.26 ± 14.32, p = 0.004) was significantly reduced while FFM (%) (Δ%: 10.72 ± 9.87, p = 0.004) slightly increased. A significant increase in PhA (Δ%: 15.54 ± 10.43, p < 0.001) compared to the baseline was also detected.

Table 1 Anthropometric characteristics and body composition of the study population at baseline and after 28 days of the active phase of VLCKD

Biochemical parameters of the study population at baseline and after 28 days of the active phase of VLCKD are reported in Table 2. Noticeable shifts were evident in the lipid profile. In particular, at the end of the 28-day active phase of the VLCKD total (Δ %: -19.41 ± 15.19, p = 0.002), HDL cholesterol (Δ %: − 14.02 ± 12.23, p = 0.002) and LDL cholesterol (Δ %: − 23.16 ± 18.82, p = 0.002) decreased significantly compared to baseline.

Table 2 Biochemical parameters of the study population at baseline and after 28 days of the active phase of VLCKD

Of note, after 28 days of the active phase of VLCKD, both the DLQI score (Δ%: − 44.62 ± 35.74, p = 0.001), and the Sartorius score (Δ%: -24.37 ± 16.64, p < 0.001. Figure 3) decreased significantly compared to baseline.

Fig. 3
figure 3

Sartorius score of the study population at baseline and after 28 days of the active phase of VLCKD. VLCKD, very low-calorie ketogenic diet; Δ%, percentage change

Inflammation, oxidative stress, and dysbiosis parameters in the study population at baseline and after 28 days of the active phase of VLCKD are reported in Table 3. After 28 days of the active phase of VLCKD, in the entire study population, we observed significant reductions in ox-LDL (Δ%: − 25.53 ± 7.64, p < 0.001), dROMs (Δ%: − 21.10 ± 12.86, p = 0.001), and TMAO (Δ%: − 23.67 ± 13.26, p < 0.001) levels compared to baseline.

Table 3 Parameters of inflammation and oxidative stress of the study population at baseline and after 28 days of the active phase of VLCKD

Table 4 reports the simple correlations among changes in the Sartorius scores and changes in the study parameters after 28 days of the active phase of VLCKD. Changes in the Sartorius score positively correlated with changes in ox-LDL (p = 0.002), dROMs (p < 0.001), and TMAO (p < 0.001) levels, and negatively with PhA (p < 0.001).

Table 4 Simple correlations among the Sartorius scores and changes in the study parameters after 28 days of the active phase of VLCKD


In this prospective pilot study, a cohort of 12 women with HS and overweight or obesity underwent the active phase of VLCKD for 28 days. As expected, at the end of the active phase of VLCKD, anthropometric measurements showed significant reductions in both BMI and WC, and, for body composition, FM decreased significantly, while FFM showed a slight increase. This result was in line with a 12-week study on women with polycystic ovary syndrome (PCOS) undergoing a ketogenic diet, where the authors found significant weight loss primarily in FM [42]. In fact, despite a slight absolute decrease in FFM (kg), the key highlight was a substantial and statistically significant increase in its percentage value [42]. Merra et al. also demonstrated that, after 3 weeks of dietary intervention, VLCKD was effective in reducing body weight without inducing muscle mass loss, thus preventing the risk of sarcopenia [43]. In line with the current literature, this observation pointed out the importance of ensuring an adequate intake of protein, both in terms of quantity (1.2–1.5 g/kg ideal body weight) and quality, with high-biological-value protein preparations such as those we used in this study. Nutritional ketosis, as evidenced in rat hearts and diaphragms, inhibits the oxidation of branched-chain amino acids and reduces the release of the gluconeogenic amino acid alanine [44, 45]. Sherwin et al. observed decreased nitrogen excretion and hypoalaninemia in fasting men with BHB infusion, indicating potential anti-catabolic effects [46]. Koutnik et al. further support this notion, suggesting that nutritional ketosis may attenuate muscle protein breakdown, allowing for the maintenance or even gain of skeletal muscle mass despite lower insulin levels [47]. Finally, the preservation of muscle mass has been included among the benefits of ketogenic diets [48], due to the synergistic effects exerted by the reduction in visceral adipose tissue and obesity-related pro-inflammatory status and the modulation of the gut microbiota [49,50,51].

In addition, there were also notable increments observed in PhA, and this was consistent with previous research [22, 30, 31]. PhA is a BIA parameter that serves as an indicator of cellular health and the distribution of body fluids. It has been recognized as a prognostic marker for both the incidence of illnesses and the likelihood of mortality in cases of chronic inflammatory conditions [52]. It is worth noting that PhA values tend to be diminished in a significant portion of inflammatory disorders, which encompass conditions like psoriasis and HS [19, 53].

For the first time, our study demonstrated a significant decrease in the Sartorius score, index of HS severity, after 28 days of the active phase of VLCKD compared to baseline. Notably, this reduction coincided with significant decreases in TMAO, dROMs, and LDLox, markers indicative of dysbiosis, oxidative stress, and cardiovascular risk, respectively. Our correlation analysis further strengthened this association. Specifically, changes in the Sartorius score exhibited positive correlations with changes in TMAO, dROMs, and LDLox. These findings carry significant implications regarding the potential benefits of VLCKD, particularly for patients struggling with HS along with overweight or obesity, a category of patients particularly exposed to dysbiosis, oxidative stress, and a high risk of cardiovascular diseases [54,55,56]. In this regard, our prior study revealed heightened circulating levels of TMAO, a gut-derived metabolite linked to inflammation and cardiometabolic risk, in 35 patients with HS and with overweight or obesity compared to control subjects [14]. Remarkably, TMAO levels were correlated with the clinical severity of HS, and this correlation remained significant even after adjusting for common confounding factors [14]. In this context, the reduction of inflammation and oxidative stress (as evidenced by the reduction of ox-LDL and dROMs levels, respectively) and the improvement of intestinal dysbiosis (as represented by the reduction of TMAO levels) induced by VLCKD, taken together, may represent the pathophysiological mechanism that is associated with the beneficial effects of this dietary therapy in reducing the clinical severity of HS.

Current research explores how dietary choices can complement traditional treatments for inflammatory disorders, notably HS [57]. Patients with HS are increasingly interested in managing their condition through dietary adjustments, though scientific evidence for specific dietary interventions remains scarce. Anecdotal reports suggest strategies like eliminating dairy, reducing simple carbs, avoiding nightshade vegetables, and certain supplements may benefit some patients with HS [57]. During a VLCKD, there is an increase in the levels of ketone bodies. These compounds are believed to have the potential to counteract inflammation and provide antioxidant effects within the body [58]. This, in turn, could potentially reduce the occurrence of age-related diseases and viral infections like COVID-19 [59, 60]. However, the exact molecular mechanisms responsible for how ketone bodies alleviate oxidative stress and inflammation remain a topic of ongoing investigation. Recent research, drawing from preclinical and clinical studies, has put forth the idea that ketone bodies may induce a controlled level of stress in the mitochondria [58]. This stress, in a subsequent step, activates specific factors such as Nrf2, sirtuins 1 and 3, and AMP-activated kinases, thereby initiating an adaptive response. This adaptive response results in an anti-oxidative and anti-inflammatory state, an improved function of the mitochondria, and the activation of mechanisms for cell repair and regeneration [58].

Finally, we would like to emphasize some safety results that emerged from our study. Glucose and lipid profiles, electrolytes, uric acid, liver enzymes, and markers of kidney function were assessed at both baseline and upon completion of the active phase of VLCKD. Notably, by the end of this active phase, total cholesterol and LDL cholesterol showed significant reductions compared to baseline, indicating a transient enhancement in cardiovascular risk. As for the non-significant changes observed in the HoMA-IR index, despite the decreased carbohydrate intake and weight loss, these are likely attributable to the short treatment duration, which may not allow for substantial improvements in glucose metabolism to manifest. Nevertheless, the absence of significant changes in biochemical parameters such as sodium, potassium, uric acid, and creatinine is an encouraging sign of the VLCKD's safety in patients with HS.

In the present study, it is essential to recognize certain limitations: (a) The sample was limited, and this may have affected the generalizability of the results. However, HS is a relatively rare disease with an overall incidence of approximately 0.00033–4.1% [61]; (b) Lack of a control group. However, for the short treatment period, a comparison with another diet, such as the Mediterranean diet, would have been ineffective, requiring a longer period for comparable results; (c) The sample included only women, limiting consideration of the effect of VLCKD on men. However, HS afflicts women more, and our results could be better applied based on this sex disproportion [62]; (d) A comprehensive analysis of safety and interactions with drugs used to treat HS has not been conducted. Assessing these interactions will be crucial to ensuring the safety of the treatment; (e) Furthermore, this prospective pilot study has the sole purpose of reporting the efficacy of VLCKD in women with HS and not its superiority over other dietary treatments. Further studies, preferably randomized, are needed to compare the efficacy and safety of VLCKD with other dietary approaches available for patients with HS.

We also outline the strengths of the study: (a) VLCKD used highly controlled replacement meals, ensuring a strictly monitored caloric and nutritional intake. This contributed to maintaining a highly controlled and standardized diet for all participants; (b) The patients were followed by a specialized multidisciplinary team that continuously monitored adherence to VLCKD. Ultimately, the results can be used to inform future studies, that is the real strength of this study.


This prospective pilot study is the first evidence of the efficacy and safety of a VLCKD in reducing the clinical severity of HS only after 28 days of dietary therapy. Taken together, our data suggest that a VLCKD can be considered a successful dietary strategy and a safe therapeutic option for the management of women with HS. The main effects depend on the reduction of inflammation and oxidation and the improvement of the intestinal microbiota, which, together, alter the inflammatory and oxidative environment typical of this skin disease.

Availability of data and materials

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.


  1. Napolitano M, Megna M, Timoshchuk EA, Patruno C, Balato N, Fabbrocini G, et al. Hidradenitis suppurativa: from pathogenesis to diagnosis and treatment. Clin Cosmet Investig Dermatol. 2017;10:105–15.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  2. Nguyen TV, Damiani G, Orenstein LAV, Hamzavi I, Jemec GB. Hidradenitis suppurativa: an update on epidemiology, phenotypes, diagnosis, pathogenesis, comorbidities and quality of life. J Eur Acad Dermatol Venereol. 2021;35(1):50–61.

    Article  CAS  PubMed  Google Scholar 

  3. Napolitano M, Fabbrocini G, Marasca C, Monfrecola G. Update on pathogenesis of hidradenitis suppurativa. G Ital Dermatol Venereol. 2018;153(3 Suppl 2):3–7.

    PubMed  Google Scholar 

  4. Revuz JE, Canoui-Poitrine F, Wolkenstein P, Viallette C, Gabison G, Pouget F, et al. Prevalence and factors associated with hidradenitis suppurativa: results from two case-control studies. J Am Acad Dermatol. 2008;59(4):596–601.

    Article  PubMed  Google Scholar 

  5. Edlich RF, Silloway KA, Rodeheaver GT, Cooper PH. Epidemiology, pathology, and treatment of axillary hidradenitis suppurativa. J Emerg Med. 1986;4(5):369–78.

    Article  CAS  PubMed  Google Scholar 

  6. Vazquez BG, Alikhan A, Weaver AL, Wetter DA, Davis MD. Incidence of hidradenitis suppurativa and associated factors: a population-based study of Olmsted County. Minnesota J Invest Dermatol. 2013;133(1):97–103.

    Article  CAS  PubMed  Google Scholar 

  7. Bettoli V, Naldi L, Cazzaniga S, Zauli S, Atzori L, Borghi A, et al. Overweight, diabetes and disease duration influence clinical severity in hidradenitis suppurativa-acne inversa: evidence from the national Italian registry. Br J Dermatol. 2016;174(1):195–7.

    Article  CAS  PubMed  Google Scholar 

  8. Canoui-Poitrine F, Revuz JE, Wolkenstein P, Viallette C, Gabison G, Pouget F, et al. Clinical characteristics of a series of 302 French patients with hidradenitis suppurativa, with an analysis of factors associated with disease severity. J Am Acad Dermatol. 2009;61(1):51–7.

    Article  PubMed  Google Scholar 

  9. Sartorius K, Emtestam L, Jemec GB, Lapins J. Objective scoring of hidradenitis suppurativa reflecting the role of tobacco smoking and obesity. Br J Dermatol. 2009;161(4):831–9.

    Article  CAS  PubMed  Google Scholar 

  10. Mintoff D, Agius R, Benhadou F, Das A, Frew JW, Pace NP. Obesity and Hidradenitis Suppurativa: targeting meta-inflammation for therapeutic gain? Clin Exp Dermatol. 2023.

    Article  PubMed  Google Scholar 

  11. Kromann CB, Ibler KS, Kristiansen VB, Jemec GB. The influence of body weight on the prevalence and severity of hidradenitis suppurativa. Acta Derm Venereol. 2014;94(5):553–7.

    Article  PubMed  Google Scholar 

  12. Luck ME, Tao J, Lake EP. The skin and gut microbiome in hidradenitis suppurativa: current understanding and future considerations for research and treatment. Am J Clin Dermatol. 2022;23(6):841–52.

    Article  PubMed  Google Scholar 

  13. Barrea L, Muscogiuri G, Annunziata G, Laudisio D, Pugliese G, Salzano C, et al. From gut microbiota dysfunction to obesity: could short-chain fatty acids stop this dangerous course? Hormones. 2019;18(3):245–50.

    Article  PubMed  Google Scholar 

  14. Barrea L, Muscogiuri G, Pugliese G, de Alteriis G, Maisto M, Donnarumma M, et al. Association of trimethylamine N-Oxide (TMAO) with the clinical severity of hidradenitis Suppurativa (Acne Inversa). Nutrients. 2021.

    Article  PubMed  PubMed Central  Google Scholar 

  15. Khan A, Chang MW. The role of nutrition in acne vulgaris and hidradenitis suppurativa. Clin Dermatol. 2022;40(2):114–21.

    Article  PubMed  Google Scholar 

  16. Ingram JR, Collier F, Brown D, Burton T, Burton J, Chin MF, et al. British Association of Dermatologists guidelines for the management of hidradenitis suppurativa (acne inversa) 2018. Br J Dermatol. 2019;180(5):1009–17.

    Article  CAS  PubMed  Google Scholar 

  17. Alikhan A, Sayed C, Alavi A, Alhusayen R, Brassard A, Burkhart C, et al. North American clinical management guidelines for hidradenitis suppurativa: a publication from the United States and Canadian Hidradenitis Suppurativa Foundations: Part I: diagnosis, evaluation, and the use of complementary and procedural management. J Am Acad Dermatol. 2019;81(1):76–90.

    Article  PubMed  PubMed Central  Google Scholar 

  18. Yamanaka-Takaichi M, Revankar R, Shih T, Gall M, Hsiao JL, Shi VY, et al. Expert consensus on priority research gaps in dietary and lifestyle factors in hidradenitis suppurativa: a Delphi consensus study. Arch Dermatol Res. 2023;315(7):2129–36.

    Article  PubMed  Google Scholar 

  19. Barrea L, Fabbrocini G, Annunziata G, Muscogiuri G, Donnarumma M, Marasca C, et al. Role of nutrition and adherence to the Mediterranean diet in the multidisciplinary approach of hidradenitis suppurativa: evaluation of nutritional status and its association with severity of disease. Nutrients. 2018.

    Article  PubMed  PubMed Central  Google Scholar 

  20. Barrea L, Verde L, Simancas-Racines D, Zambrano AK, Frias-Toral E, Colao A, et al. Adherence to the Mediterranean diet as a possible additional tool to be used for screening the metabolically unhealthy obesity (MUO) phenotype. J Transl Med. 2023;21(1):675.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  21. Barrea L, Caprio M, Watanabe M, Cammarata G, Feraco A, Muscogiuri G, et al. Could very low-calorie ketogenic diets turn off low grade inflammation in obesity? Emerging evidence. Crit Rev Food Sci Nutr. 2022.

    Article  PubMed  Google Scholar 

  22. Barrea L, Muscogiuri G, Aprano S, Vetrani C, de Alteriis G, Varcamonti L, et al. Phase angle as an easy diagnostic tool for the nutritionist in the evaluation of inflammatory changes during the active stage of a very low-calorie ketogenic diet. Int J Obes. 2022;46(9):1591–7.

    Article  CAS  Google Scholar 

  23. Zambrano AK, Cadena-Ullauri S, Guevara-Ramirez P, Frias-Toral E, Ruiz-Pozo VA, Paz-Cruz E, et al. The impact of a very-low-calorie ketogenic diet in the gut microbiota composition in obesity. Nutrients. 2023.

    Article  PubMed  PubMed Central  Google Scholar 

  24. Barrea L, Caprio M, Watanabe M, Cammarata G, Feraco A, Muscogiuri G, et al. Could very low-calorie ketogenic diets turn off low grade inflammation in obesity? Emerging evidence. Crit Rev Food Sci Nutr. 2023;63(26):8320–36.

    Article  CAS  PubMed  Google Scholar 

  25. Monda V, Polito R, Lovino A, Finaldi A, Valenzano A, Nigro E, et al. Short-Term physiological effects of a very low-calorie ketogenic diet: effects on adiponectin levels and inflammatory States. Int J Mol Sci. 2020.

    Article  PubMed  PubMed Central  Google Scholar 

  26. Jonasson L, Guldbrand H, Lundberg AK, Nystrom FH. Advice to follow a low-carbohydrate diet has a favourable impact on low-grade inflammation in type 2 diabetes compared with advice to follow a low-fat diet. Ann Med. 2014;46(3):182–7.

    Article  CAS  PubMed  Google Scholar 

  27. Barrea L, Di Somma C, Macchia PE, Falco A, Savanelli MC, Orio F, et al. Influence of nutrition on somatotropic axis: milk consumption in adult individuals with moderate-severe obesity. Clin Nutr. 2017;36(1):293–301.

    Article  CAS  PubMed  Google Scholar 

  28. Muscogiuri G, Barrea L, Di Somma C, Altieri B, Vecchiarini M, Orio F, et al. Patient empowerment and the Mediterranean diet as a possible tool to tackle prediabetes associated with overweight or obesity: a pilot study. Hormones. 2019;18(1):75–84.

    Article  PubMed  Google Scholar 

  29. Verde L, Dalamaga M, Capo X, Annunziata G, Hassapidou M, Docimo A, et al. The antioxidant potential of the mediterranean diet as a predictor of weight loss after a very low-calorie ketogenic diet (VLCKD) in women with overweight and obesity. Antioxidants. 2022.

    Article  PubMed  PubMed Central  Google Scholar 

  30. Barrea L, Verde L, Santangeli P, Luca S, Docimo A, Savastano S, et al. Very low-calorie ketogenic diet (VLCKD): an antihypertensive nutritional approach. J Transl Med. 2023;21(1):128.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  31. Verde L, Barrea L, Docimo A, Savastano S, Colao A, Muscogiuri G. Chronotype as a predictor of weight loss and body composition improvements in women with overweight or obesity undergoing a very low-calorie ketogenic diet (VLCKD). Clin Nutr. 2023;42(7):1106–14.

    Article  PubMed  Google Scholar 

  32. Barrea L, Verde L, Di Lorenzo C, Savastano S, Colao A, Muscogiuri G. Can the ketogenic diet improve our dreams? Effect of very low-calorie ketogenic diet (VLCKD) on sleep quality. J Transl Med. 2023;21(1):479.

    Article  PubMed  PubMed Central  Google Scholar 

  33. Kyle UG, Bosaeus I, De Lorenzo AD, Deurenberg P, Elia M, Manuel Gomez J, et al. Bioelectrical impedance analysis-part II: utilization in clinical practice. Clin Nutr. 2004;23(6):1430–53.

    Article  PubMed  Google Scholar 

  34. Kushner RF. Bioelectrical impedance analysis: a review of principles and applications. J Am Coll Nutr. 1992;11(2):199–209.

    Article  MathSciNet  CAS  PubMed  Google Scholar 

  35. Muscogiuri G, El Ghoch M, Colao A, Hassapidou M, Yumuk V, Busetto L, et al. European guidelines for obesity management in adults with a very low-calorie ketogenic diet: a systematic review and meta-analysis. Obes Facts. 2021;14(2):222–45.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  36. Lorenz MW, Graf M, Henke C, Hermans M, Ziemann U, Sitzer M, et al. Anthropometric approximation of body weight in unresponsive stroke patients. J Neurol Neurosurg Psychiatry. 2007;78(12):1331–6.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Shashaj B, Luciano R, Contoli B, Morino GS, Spreghini MR, Rustico C, et al. Reference ranges of HOMA-IR in normal-weight and obese young Caucasians. Acta Diabetol. 2016;53(2):251–60.

    Article  CAS  PubMed  Google Scholar 

  38. Iamele L, Fiocchi R, Vernocchi A. Evaluation of an automated spectrophotometric assay for reactive oxygen metabolites in serum. Clin Chem Lab Med. 2002;40(7):673–6.

    Article  CAS  PubMed  Google Scholar 

  39. Wang Z, Levison BS, Hazen JE, Donahue L, Li XM, Hazen SL. Measurement of trimethylamine-N-oxide by stable isotope dilution liquid chromatography tandem mass spectrometry. Anal Biochem. 2014;455:35–40.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  40. Beale R, Airs R. Quantification of glycine betaine, choline and trimethylamine N-oxide in seawater particulates: minimisation of seawater associated ion suppression. Anal Chim Acta. 2016;938:114–22.

    Article  CAS  PubMed  Google Scholar 

  41. Barrea L, Muscogiuri G, Pugliese G, Graziadio C, Maisto M, Pivari F, et al. Association of the chronotype score with circulating trimethylamine N-Oxide (TMAO) concentrations. Nutrients. 2021.

    Article  PubMed  PubMed Central  Google Scholar 

  42. Paoli A, Mancin L, Giacona MC, Bianco A, Caprio M. Effects of a ketogenic diet in overweight women with polycystic ovary syndrome. J Transl Med. 2020;18(1):104.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  43. Merra G, Gratteri S, De Lorenzo A, Barrucco S, Perrone MA, Avolio E, et al. Effects of very-low-calorie diet on body composition, metabolic state, and genes expression: a randomized double-blind placebo-controlled trial. Eur Rev Med Pharmacol Sci. 2017;21(2):329–45.

    CAS  PubMed  Google Scholar 

  44. Buse MG, Biggers JF, Friderici KH, Buse JF. Oxidation of branched chain amino acids by isolated hearts and diaphragms of the rat. The effect of fatty acids, glucose, and pyruvate respiration. J Biol Chem. 1972;247(24):8085–96.

    Article  CAS  PubMed  Google Scholar 

  45. Palaiologos G, Felig P. Effects of ketone bodies on amino acid metabolism in isolated rat diaphragm. Biochem J. 1976;154(3):709–16.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  46. Sherwin RS, Hendler RG, Felig P. Effect of ketone infusions on amino acid and nitrogen metabolism in man. J Clin Invest. 1975;55(6):1382–90.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  47. Koutnik AP, D’Agostino DP, Egan B. Anticatabolic effects of ketone bodies in skeletal muscle. Trends Endocrinol Metab. 2019;30(4):227–9.

    Article  CAS  PubMed  Google Scholar 

  48. Yakupova EI, Bocharnikov AD, Plotnikov EY. Effects of ketogenic diet on muscle metabolism in health and disease. Nutrients. 2022.

    Article  PubMed  PubMed Central  Google Scholar 

  49. Paoli A, Cancellara P, Pompei P, Moro T. Ketogenic diet and skeletal muscle hypertrophy: a frenemy relationship? J Hum Kinet. 2019;68:233–47.

    Article  PubMed  PubMed Central  Google Scholar 

  50. Rondanelli M, Faliva MA, Gasparri C, Peroni G, Spadaccini D, Maugeri R, et al. Current opinion on dietary advice in order to preserve fat-free mass during a low-calorie diet. Nutrition. 2020;72: 110667.

    Article  CAS  PubMed  Google Scholar 

  51. Rondanelli M, Gasparri C, Peroni G, Faliva MA, Naso M, Perna S, et al. The potential roles of very low calorie, very low calorie ketogenic diets and very low carbohydrate diets on the gut microbiota composition. Front Endocrinol. 2021;12: 662591.

    Article  Google Scholar 

  52. da Silva BR, Orsso CE, Gonzalez MC, Sicchieri JMF, Mialich MS, Jordao AA, et al. Phase angle and cellular health: inflammation and oxidative damage. Rev Endocr Metab Disord. 2023;24(3):543–62.

    Article  PubMed  Google Scholar 

  53. Barrea L, Macchia PE, Di Somma C, Napolitano M, Balato A, Falco A, et al. Bioelectrical phase angle and psoriasis: a novel association with psoriasis severity, quality of life and metabolic syndrome. J Transl Med. 2016;14(1):130.

    Article  PubMed  PubMed Central  Google Scholar 

  54. Chopra D, Arens RA, Amornpairoj W, Lowes MA, Tomic-Canic M, Strbo N, et al. Innate immunity and microbial dysbiosis in hidradenitis suppurativa—vicious cycle of chronic inflammation. Front Immunol. 2022;13: 960488.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  55. Lelonek E, Bouazzi D, Jemec GBE, Szepietowski JC. Skin and gut microbiome in hidradenitis suppurativa: a systematic review. Biomedicines. 2023.

    Article  PubMed  PubMed Central  Google Scholar 

  56. Tzellos T, Zouboulis CC, Gulliver W, Cohen AD, Wolkenstein P, Jemec GB. Cardiovascular disease risk factors in patients with hidradenitis suppurativa: a systematic review and meta-analysis of observational studies. Br J Dermatol. 2015;173(5):1142–55.

    Article  CAS  PubMed  Google Scholar 

  57. Silfvast-Kaiser A, Youssef R, Paek SY. Diet in hidradenitis suppurativa: a review of published and lay literature. Int J Dermatol. 2019;58(11):1225–30.

    Article  PubMed  Google Scholar 

  58. Bae HR, Kim DH, Park MH, Lee B, Kim MJ, Lee EK, et al. beta-Hydroxybutyrate suppresses inflammasome formation by ameliorating endoplasmic reticulum stress via AMPK activation. Oncotarget. 2016;7(41):66444–54.

    Article  PubMed  PubMed Central  Google Scholar 

  59. Boleslawska I, Kowalowka M, Boleslawska-Krol N, Przyslawski J. Ketogenic diet and ketone bodies as clinical support for the treatment of SARS-CoV-2-review of the evidence. Viruses. 2023.

    Article  PubMed  PubMed Central  Google Scholar 

  60. Pugliese G, Liccardi A, Graziadio C, Barrea L, Muscogiuri G, Colao A. Obesity and infectious diseases: pathophysiology and epidemiology of a double pandemic condition. Int J Obes. 2022;46(3):449–65.

    Article  CAS  Google Scholar 

  61. Alotaibi HM. Incidence, risk factors, and prognosis of hidradenitis suppurativa across the globe: insights from the literature. Clin Cosmet Investig Dermatol. 2023;16:545–52.

    Article  PubMed  PubMed Central  Google Scholar 

  62. Garg A, Lavian J, Lin G, Strunk A, Alloo A. Incidence of hidradenitis suppurativa in the United States: a sex- and age-adjusted population analysis. J Am Acad Dermatol. 2017;77(1):118–22.

    Article  PubMed  Google Scholar 

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Authors and Affiliations



Conceptualization: LB, SC and GM; data curation; LV; formal analysis LB; methodology LB; supervision: ACm SS and GT; roles/Writing—original draft: LV, PC, MM, FM, AC, MM and MM; writing—review & editing. LV, SC, GM and LB. All authors have read and agreed to the published version of the manuscript.

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Correspondence to Luigi Barrea.

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The study was conducted in accordance with the guidelines outlined in the Declaration of Helsinki, which provides ethical principles for medical research involving human subjects. Additionally, the Ethics Committee of the Federico II University of Naples reviewed the study procedures and granted a positive opinion on the study protocol (reference no. 50/20).

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Supplementary Information

Additional file 1.

Example of VLCKD diet therapy with meal replacement.

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Verde, L., Cacciapuoti, S., Caiazzo, G. et al. Very low-calorie ketogenic diet (VLCKD) in the management of hidradenitis suppurativa (Acne Inversa): an effective and safe tool for improvement of the clinical severity of disease. Results of a pilot study. J Transl Med 22, 149 (2024).

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